Download Acutely Decompensated Heart Failure: Diagnostic and Therapeutic

December 2006
Acutely Decompensated Heart
Failure: Diagnostic and
Therapeutic Strategies
Volume 8, Number 12
Authors
Joshua M. Kosowsky, MD
Clinical Director, Department of Emergency
Medicine, Brigham & Women’s Hospital, Assistant
Professor Harvard Medical School, MA
You start your shift. An elderly woman with shortness of breath has congestive
heart failure written all over her and her chart. She takes beta-blockers, an ACE
inhibitor, and Lasix®. She looks and sounds “wet.” She receives oxygen,
furosemide, morphine, and nitrate therapy. When you return 20 minutes later, she
looks and feels much better. As you reach for the phone to speak with the admitting physician, you ask yourself, “Do I need to get cardiac enzymes? She really
looks so good now—does she even need to be admitted?”
In the next room, you see an obese woman with shortness of breath, COPD,
CAD, but no known history of CHF, and she does not take Lasix®. Her lungs
sound “wheezy” and you hear crackles. Her legs are edematous and she describes
orthopnea. Does she have a COPD exacerbation or new onset CHF? Should you
send a BNP level? Will her obesity affect this test?
The next evening you see a patient with “severe CHF” and an ejection fraction of 20%. Her family describes recent fatigue and progressive mild confusion.
She is not edematous and her lungs are clear. Her creatinine has increased from
2.5 to 3.2 g/dl. Is this a CHF exacerbation? What are your treatment options?
Are ionotropes indicated?
A
cutely Decompensated Heart Failure (ADHF) is one of the
most common cardiac emergencies encountered in the emergency department (ED). Because patients with heart failure are
seen so frequently, there can be a tendency for the emergency
physician to become complacent with a perfunctory diagnostic
evaluation and a one-size-fits-all therapeutic approach. The fact is,
patients with ADHF represent a diverse group with a single common feature: High morbidity and mortality. Heart failure accounts
for 286,700 deaths a year, and, in 2006, the treatment of heart failure
is expected to cost approximately $29.6 billion. Failure to appreci-
Editor-in-Chief
Andy Jagoda, MD, FACEP, Professor
and Vice-Chair of Academic Affairs,
Department of Emergency Medicine;
Mount Sinai School of Medicine;
Medical Director, Mount Sinai Hospital,
New York, NY.
Associate Editor
Health Science Center, New Orleans,
LA.
Wyatt W Decker, MD, Chair and
Associate Professor of Emergency
Medicine, Mayo Clinic College of
Medicine, Rochester, MN.
Francis M Fesmire, MD, FACEP,
Director, Heart-Stroke Center,
Erlanger Medical Center; Assistant
Professor, UT College of Medicine,
Chattanooga, TN.
HSC/Jacksonville, FL.
Gregory L Henry, MD, FACEP, CEO,
Medical Practice Risk Assessment,
Inc; Clinical Professor of Emergency
Medicine, University of Michigan, Ann
Arbor.
Keith A Marill, MD, Instructor,
Department of Emergency Medicine,
Massachusetts General Hospital,
Harvard Medical School, Boston, MA.
John M Howell, MD, FACEP, Clinical
Charles V Pollack, Jr, MA, MD, FACEP,
Professor of Emergency Medicine,
Michael J Gerardi, MD, FAAP, FACEP,
Professor and Chair, Department of
George Washington University,
Director, Pediatric Emergency
Emergency Medicine, Pennsylvania
Washington, DC; Director of Academic
Medicine, Children’s Medical Center,
Hospital, University of Pennsylvania
Affairs, Best Practices, Inc, Inova
Atlantic Health System; Department of
Health System, Philadelphia, PA.
Fairfax Hospital, Falls Church, VA.
Emergency Medicine, Morristown
Memorial Hospital, NJ.
Michael S Radeos, MD, MPH,
Editorial Board
Assistant Professor of Emergency
Michael A Gibbs, MD, FACEP, Chief,
Medicine, Lincoln Health Center,
William J Brady, MD, Associate
Department of Emergency Medicine,
Bronx, NY.
Professor and Vice Chair, Department
Maine Medical Center, Portland, ME.
of Emergency Medicine, University of
Robert L Rogers, MD, FAAEM,
Steven A Godwin, MD, FACEP,
Virginia, Charlottesville, VA.
Assistant Professor and Residency
Assistant Professor and Emergency
Director, Combined EM/IM Program,
Peter DeBlieux, MD, LSUHSC
Medicine Residency Director,
University of Maryland, Baltimore,
Professor of Clinical Medicine; LSU
University of Florida
MD.
Jennifer L. Chan, MD, MPH
Senior Resident, Harvard Affiliated Emergency
Medicine Residency, Brigham and Women’s
Hospital/ Massachusetts General Hospital, Boston,
MA
Peer Reviewers
Luke K. Hermann, MD
Director, Chest Pain Unit, Assistant Professor,
Department of Emergency Medicine, Mount Sinai
School of Medicine, New York, NY
Joseph D. Toscano, MD
Emergency Physician
San Ramon, CA
CME Objectives
Upon completion of this article, you should be able to:
1. Describe the basic pathophysiology of acutely
decompensated heart failure and identify its common and life-threatening precipitants.
2. Understand the diagnostic tools used in differentiating ADHF from other disease entities.
3. Understand the management of ADHF in the prehospital and ED settings, including the role of
diuretics, vasodilators, inotropes, and non-invasive ventilatory support.
4. Appreciate the role of risk-stratification in determining the disposition of patients with acutely
decompensated heart failure.
Date of original release: December 1, 2006.
Date of most recent review: November 20, 2006.
See “Physician CME Information” on back page.
Alfred Sacchetti, MD, FACEP,
Assistant Clinical Professor,
Department of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M Slovis, MD, FACP, FACEP,
Professor and Chair, Department of
Emergency Medicine, Vanderbilt
University Medical Center, Nashville,
TN.
Jenny Walker, MD, MPH, MSW,
Assistant Professor; Division Chief,
Family Medicine, Department of
Community and Preventive Medicine,
Mount Sinai Medical Center, New
York, NY.
Beth Wicklund, MD, Regions Hospital
Emergency Medicine Residency,
EMRA Representative.
International Editors
Valerio Gai, MD, Senior Editor,
Professor and Chair, Dept of EM,
University of Turin, Italy.
Peter Cameron, MD, Chair, Emergency
Medicine, Monash University; Alfred
Hospital, Melbourne, Australia.
Amin Antoine Kazzi, MD, FAAEM,
Associate Professor and Vice Chair,
Department of Emergency Medicine,
University of California, Irvine;
American University, Beirut, Lebanon.
Ron M Walls, MD, Professor and Chair,
Hugo Peralta, MD, Chair of Emergency
Department of Emergency Medicine,
Services, Hospital Italiano, Buenos
Brigham & Women’s Hospital, Boston,
Aires, Argentina.
MA.
Research Editors
Nicholas Genes, MD, PhD, Mount
Sinai Emergency Medicine Residency.
Maarten Simons, MD, PhD,
Emergency Medicine Residency
Director, OLVG Hospital, Amsterdam,
The Netherlands.
ate and address the subtleties of a patient with
ADHF can have dire consequences.
This issue of Emergency Medicine Practice presents
a comprehensive, evidence-based approach to the
management of acutely decompensated heart failure.
It focuses on the identification of major syndromes of
ADHF, stabilization, treatment, and appropriate disposition of the individual patient while highlighting
emergency diagnostic and therapeutic options.
diagnosis and treatment of ADHF.3 Although the
American Heart Association and the American
College of Cardiology (AHA/ACC) provide comprehensive guidelines on chronic heart failure, they have
yet to publish guidelines that focus upon ADHF.
Since the February 2002 issue of Emergency
Medicine Practice: “Acutely Decompensated Heart
Failure,” multi-center ED and hospital-based studies
have contributed data on the epidemiology, diagnosis, and treatment of ADHF. The Acute
Decompensated Heart Failure National Registry is a
registry of medical information from patients with
ADHF from over 275 hospitals.4 Results from this
registry have confirmed the high prevalence of
underlying comorbidities such as coronary artery
disease and renal dysfunction. It has also shown
that many patients with ADHF have preserved ventricular systolic function. Results from the registry
also highlight the importance of early accurate management beginning in the ED.
The Breathing Not Properly Multinational Study
investigated the diagnostic role of B-natriuretic peptide (BNP) in patients presenting to EDs with acute
dyspnea.5 At least 13 studies have been published
from the multinational data. Results from this study
continue to provide data on the diagnostic power of
BNP and its role in determining the prognosis of
patients presenting with ADHF.
The B-Type Natriuretic Peptide for Acute
Shortness of Breath Evaluation (BASEL) study found
that using BNP as a diagnostic tool decreases length
of stay and cost of treatment among patients presenting to the ED with acute dyspnea.6
The Organized Program to Initiate Lifesaving
Treatment in Hospitalized Patients with Heart
Failure (OPTIMIZE-HF) registry collects data on
demographics, treatment approaches, and follow
up of patients with heart failure.7 Data from
OPTIMIZE-HF will be used to measure current
treatment outcomes and therefore improve the
quality of care for patients admitted with heart failure. Lastly, the Vasodilation in the Management of
Acute CHF (VMAC) trial was a randomized doubleblind trial of dyspneic patients with ADHF. This
study compared two vasoactive agents, nesiritide
and nitroglycerin with a placebo, and their effect
upon pulmonary capillary wedge pressure (PCWP)
and dyspnea. Nesiritide was shown to be superior
to placebo but of marginal benefit compared to intravenous nitrates. (Discussed in depth in the
Treatment section).8
Abbreviations In This Article
ACC: American College of Cardiology
ACE: Angiotensin Converting Enzyme
ACS: Acute Coronary Syndrome
ADHERE: The Acute Decompensated Heart
Failure National Registry
ADHF: Acutely Decompensated Heart Failure
AHA: American Heart Association
BiPAP: Biphasic Positive Airway Pressure
BNP: B-Type Natriuretic Peptide:
CBC: Complete Blood Count
CHF: Congestive Heart Failure
CPAP: Continuous Positive Airway Pressure
COPD: Chronic Obstructive Pulmonary Disease
CVP: Central Venous Pressure
HFSA: The Heart Failure Society of America
IABC: Intra-Aortic Balloon Counterpulsation
ESC: European Society of Cardiology
ETCO2: End-Tidal Carbon Dioxide Levels
ICG: Impedence Cardiography
JVD: Jugular Venous Distension
NIV: Noninvasive Ventilation
PCWP: Pulmonary Capillary Wedge Pressure
PEEP: Positive End-Expiratory Pressure
RSI: Rapid Sequence Intubation
VMAC: Vasodilation in the Management of
Acute CHF
Critical Appraisal Of The Literature
Despite its overwhelming prevalence and burden on
the healthcare system, evidence-based literature for
ADHF continues to lag behind that of other emergent
conditions such as acute coronary syndrome and
stroke. Although consensus guidelines provide
instruction to practicing physicians, there are few
controlled studies that have determined the optimal
treatment regimen for ADHF. The Heart Failure
Society of America (HFSA), and the European Society
of Cardiology (ESC) provide recommendations on the
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December 2006 • EBMedicine.net
Table 1. Guidelines, Registries, And Studies
reflecting at least in part its heterogeneous pathophysiology and presentation. Some experts describe
decompensated heart failure as a syndrome whereby; “ a patient with an established diagnosis of heart
failure develops increasing signs and symptoms of
the disease after a period of relative stability,”17 while
others define acute heart failure syndrome as, “[the]
gradual or rapid change in heart failure signs and
symptoms resulting in the need for urgent therapy.”
Additional terms used by physicians for this syndrome are CHF exacerbation” and “acute CHF.” The
common theme among these definitions is an abrupt
Epidemiology
As a result of the aging of the United States’ population and improved survival following myocardial
infarction, the overall prevalence of heart failure is
rising.9,10 At the same time, advances in outpatient
medical therapy are allowing patients with chronic
heart failure to live longer. Over 5 million
Americans with heart failure are alive today, and by
2037, an estimated 10 million people in the United
States will have a diagnosis of heart failure.1,11 Heart
failure now accounts for over one million in-patient
admissions annually, and is the number one reason
for hospitalization among the growing elderly population.1 In 2006, the estimated cost of direct hospital
management for heart failure will be $15.4 billion
dollars.13 According to data from ADHERE, 80% of
patients hospitalized for ADHF will initially present
to the emergency department.14 One retrospective
analysis of 2 million ED visits over an eleven-year
period revealed approximately 1.1% of visits to have
a primary diagnosis of heart failure or pulmonary
edema.15
The Euro Heart Failure survey and the Acute
Decompensated Heart Failure National Registry
(ADHERE) add to the current knowledge on the epidemiology of heart failure. The mean age of patients
with ADHF is between 71-75 years with an equal
ratio of men to women.4, 16 New studies have shown
that almost half of all patients presenting with ADHF
have preserved systolic function, coronary artery disease, hypertension and diabetes.4
Table 2. Etiologies Of Heart Failure
• Coronary artery disease
• Hypertension
• Valvular disease
• Cardiomyopathy
Š Idiopathic cardiomyopathy
Š Alcoholic cardiomyopathy
Š Toxin-related cardiomyopathy
(e.g., adriamycin)
Š Post-partum cardiomyopathy
Š Hypertrophic obstructive cardiomyopathy
(HOCM)
Š Tachyarrhythmia-induced cardiomyopathy
• Infiltrative disorders (e.g., amyloid)
• Congenital heart disease
• Pericardial disease
• Hyperkinetic states
Š Anemia
Š Arterio-venous fistula
Š Thyroid disease
Š Beri-beri
Definitions, Etiology
There is no universally accepted definition of ADHF,
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Each episode of ADHF contributes to disease
progression and the gradual decline in clinical status
that characterizes chronic heart failure. Non-adherence to medications, dietary indiscretion, physiologic
stress, or lack of access to medication are frequent
precipitants of ADHF (Table 4).
clinical change from baseline affecting the cardiopulmonary system that requires emergent or urgent
intervention. Regardless of terminology, this article
will refer to this acute clinical presentation as
Acutely Decompensated Heart Failure or ADHF.
Chronic heart failure is itself a complex syndrome, and is characterized by inadequate cardiac
output at physiologic filling pressures. The etiologies of chronic heart failure are numerous and
diverse (Table 2). In the United States, the vast
majority of heart failure arises as a consequence of
coronary artery disease and/or long-standing hypertension. Table 3 describes the American Heart
Association classification and the commonly used
New York Heart Association (NYHA) classification
system. Understanding the differences in both classification systems can be helpful in evaluating and
managing individual patients when they present
with ADHF.
In the ED, heart failure can present de novo as
an acute process or as an acute decompensation of
chronic heart failure. For example, acute myocardial
infarction (MI) with or without valvular dysfunction
can cause acute heart failure. More commonly,
patients seen in the ED have chronic heart failure
that has decompensated as the result of one or more
precipitating factors.
Pathophysiology
Regardless of etiology, inadequate cardiac function
Table 4. Common Precipitants of
Acutely Decompensated Heart Failure
• Medication non-compliance
• Dietary indiscretion
• Myocardial ischemia / infarction
• Uncontrolled hypertension
• Cardiac arrhythmias
• Pulmonary and other infections
• Administration of inappropriate medications
(e.g., negative inotropes)
• Fluid overload
• Thyrotoxicosis
• Anemia
• Alcohol withdrawal
Table 3. Classifications Of Heart Failure
American Heart Association Classification
Class
Description
Stage A
Patients are at high risk for heart failure but have not developed structural heart disease
and have no symptoms.
Stage B
Patients have developed structural heart disease but have not (yet) developed symptoms.
Stage C
Patients with past or current heart failure symptoms in association with structural damage
to the heart.
Stage D
Patients with end-stage, or terminal, heart failure requiring specialized treatment strategies.
New York Heart Association Classification
Class
Functional state
I
No limitation
II
Slight limitation
III
IV
Moderate limitation
Severe limitation
Symptoms
Asymptomatic during usual daily activities
Mild symptoms (dyspnea, fatigue, or chest pain) with
ordinary daily activities
Symptoms noted with minimal activity
Symptoms at rest
Sources: Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart
Failure in the Adult: 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): developed in collaboration with
the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart
Rhythm Society. Circulation 2005; 112:e154-235.
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Figure 1: Heart Failure Pathophysiology Diagram
dromes. Systemic volume overload, acute diastolic
dysfunction, and low-output failure (Figure 2 and
Table 5).
Systemic volume overload, accounting for the
majority of cases of ADHF, occurs commonly in the
setting of non-adherence to medical regimens,
dietary indiscretion, and/or progression of disease.
Volume overload combined with poor left ventricular performance results in gradual worsening of congestive symptoms. Patients with ADHF due primarily to systemic volume overload will often describe
a slow increase in lower extremity edema, dyspnea,
and fatigue.
Acute diastolic dysfunction results in an abrupt
increase in left ventricular pressure producing symptoms of congestion. Contrary to the common perception that a depressed ejection fraction is the main
cause of ADHF, acute diastolic dysfunction often
occurs in the setting of a preserved ejection fraction.
Many situations cause de novo or worsening diastolic dysfunction. Myocardial infarction causes ventricular wall stiffness that can maintain cardiac output but result in congestive symptoms. Patients with
long standing hypertension may have existing diastolic dysfunction as a result of left ventricular hyper-
sets in motion a common set of compensatory mechanisms, brought about by neurohormonal activation
and characterized by elevated sympathetic tone,
fluid and salt retention, and ventricular remodeling.
These adaptations can allow heart failure to remain
stable (or “compensated”) for a period of time, but
also provide the final common pathway for decompensation—a downward spiral that can accelerate
dramatically in response to a particular precipitant
or stress. High circulating levels of aldosterone, vasopressin, epinephrine, and norepinephrine are ultimately maladaptive, as tachycardia and vasoconstriction compromise the intrinsic performance of the
left ventricle (LV) and simultaneously worsen
myocardial oxygen balance. Deterioration of left
ventricular function results in further neurohormonal activation and self-perpetuation of this adverse
cycle (Figure 1). An acute decompensation can
develop over a period of minutes, hours, or days and
can range in severity from mild symptoms of volume
overload or decreased cardiac output to frank pulmonary edema or cardiogenic shock.
ADHF can be viewed as three overlapping syn-
Figure 2: Syndromes of Acutely
Decompensated Heart Failure
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Table 5. Syndromes of Acutely
Decompensated Heart Failure
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trophy. During events such as sepsis, trauma, and
arrhythmias, myocardial relaxation is impaired preventing proper ventricular filling resulting in pulmonary congestion and pulmonary edema. The
coexistence of hypertension, CAD and even ACS can
cause a complex pathophysiological picture during
acute diastolic dysfunction.
Low output heart failure refers to severely
depressed left ventricular function which impairs
end organ perfusion. Patients with low output heart
failure may or may not have congestive symptoms
but may present with worsening fatigue, decline in
renal function, and confusion all due to decreased
perfusion of vital organs.
The severity of failure can be described in many
ways, which may include a measure of how chronic
heart failure affects the quality of life or more acute
clinical parameters.
prevalence of these coexisting diseases varies
depending on the particular population.
Nevertheless, in almost all cases, the possibility of an
acute coronary syndrome should be considered.
Other cardiovascular precipitants, such as arrhythmia, high-grade heart block, severe valvular dysfunction, or hypertensive crisis, must not be overlooked. It should also be recognized that ADHF
could arise as a consequence of non-cardiac conditions such as sepsis, anemia, alcohol withdrawal,
uncontrolled diabetes, or thyroid disease (Tables 4
and 6).
Prehospital Care
Even before patients reach the hospital, ADHF is
associated with significant morbidity and mortality
including malignant arrhythmias and prehospital
cardiac arrest.28 All patients should have continuous
cardiac monitoring and intravenous access established if possible (See also “Clinical Pathway:
Prehospital Therapy For Acutely Decompensated
Heart Failure”). Because successful management
depends on reversal of hypoxia, pulse oximetry and
supplemental oxygen should be utilized routinely in
the prehospital care of patients with ADHF.
Prehospital personnel should alert ED staff of any
Differential Diagnosis
Acutely decompensated heart failure can coexist
with or closely mimic a number of other cardiac, respiratory, and systemic illnesses (Table 6). In fact,
when patients present to the ED with undifferentiated dyspnea, the diagnosis of heart failure is often
overlooked.18 Patients who present with mild or
non-specific symptoms pose a particular diagnostic
challenge. Symptoms such as weakness, lethargy,
fatigue, anorexia, or lightheadedness may actually be
a manifestation of decreased cardiac output and low
output ADHF. Older patients frequently lack typical
signs and symptoms of heart failure.20 These features
may be obscured by the aging process itself or by the
presence of coexisting medical conditions.
Patients presenting with acute exacerbations of
either cardiac dysfunction or COPD may have
wheezing on pulmonary auscultation with signs of
chronic right-sided heart failure and non-diagnostic
chest radiographs. In heart failure patients, pulmonary embolism may be clinically indistinguishable from ADHF.21
Precipitating factors for decompensation
should be sought in a careful and deliberate fashion
(Table 4). Myocardial ischemia or infarction and
non-compliance with medications or dietary indiscrition are the most common causes of clinical decompensation.22-27 Often, the cause-effect relationship of
ADHF is difficult to determine due to the co-prevalence of diseases such as coronary artery disease,
hypertension, and atrial fibrillation.14 The exact
Emergency Medicine Practice©
Table 6. Differential Diagnosis Of
Acutely Decompensated Heart Failure
Cardiovascular
Acute Coronary Syndrome
Acute valvular / septal rupture
Aortic dissection
Arrhythmia
Critical aortic stenosis
Endocarditis / Myocarditis
Hypertensive crisis
Pericardial tamponade / effusion
Pulmonary
COPD (chronic obstructive pulmonary disease)
Pulmonary thromboembolism
Multi-lobar pneumonia
ARDS (acute respiratory distress syndrome)
Other
Pure volume overload
renal failure
iatrogenic (e.g., post-transfusion)
Sepsis
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patient presenting with symptoms suggestive of pulmonary edema or cardiogenic shock, and receive online medical advice when appropriate. Prehospital
staff trained to interpret electrocardiograms should
obtain a 12-lead electrocardiogram and, if ACS is
identified, ED staff or medical control should be
immediately informed.
The decision to treat a patient in the relatively
uncontrolled prehospital environment carries some
risks that must be weighed against expected benefits.
With few exceptions, the safety and efficacy of prehospital medications have been poorly studied.29
Prehospital therapy for ADHF should be undertaken
with particular caution in light of the relatively high
number of inaccurate diagnoses made in the field.
As many as 50% of patients with assumed cardiac
associated respiratory distress are diagnosed with a
different condition once they arrive at the hospital.28,30,31
Despite these concerns, evidence suggests that prehospital therapy for presumed ADHF can prevent
serious complications and improve survival, particularly for critically ill patients.28,30,31 In a large retrospective case series of 493 patients, there was a
decrease in mortality among critical and non critical
patients who received treatment (nitroglycerin,
Lasix® and/or morphine) compared to no pharmacologic intervention.30 In European countries, where
physicians commonly staff ambulances, intensive
prehospital treatment of patients with severe heart
failure confers short-term benefits.32-34 A retrospective
review of 640 patients that presented in the prehospital setting with acute pulmonary edema (APE)
revealed that the use of nitrates were associated with
a trend toward decreased mortality.32
Sublingual nitroglycerin appears to be the safest
and most effective of the prehospital medications
used for presumed pulmonary edema.31 A prospective, randomized, double blind study of 57 patients
comparing morphine, nitroglygerin, and furosemide
found nitroglycerin to be the safest and most effective intervention in the prehospital management of
ADHF.31 Prehospital intravenous (IV) nitrates also
yield positive short-term results. The role of other
medications for heart failure in the prehospital setting is less clear. Early administration of furosemide
appears to have very little benefit, and may result in
short-term complications.31,35 The prehospital use of
morphine sulfate for presumed pulmonary edema is
associated with an increased rate of endotracheal
intubation, particularly among patients who turn out
to have been misdiagnosed in the field.31,36 A
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prospective, randomized study of 57 patients administered four different drug regimens found that the
administration of morphine and Lasix® showed little
improvement.31
Emergency Department Evaluation
Initial Approach
The approach to the patient with ADHF begins with
stabilization of respiratory and hemodynamic status
and with the rapid exclusion or treatment of
reversible conditions. Clinical evaluation and empiric therapy begin simultaneously with supplemental
oxygen, cardiac monitoring, pulse oximetry, and
intravenous access. Patients with clinical signs of
exhaustion or cyanosis, despite supplemental oxygen,
require respiratory support by either invasive or noninvasive means. Those with hypotension, obtundation, cool extremities, or other signs of poor perfusion
should be presumed to be in or near cardiogenic
shock and managed accordingly (see Special
Circumstances). Once the initial resuscitation is
underway, further efforts should be made to identify
the underlying cause of acute decompensation.
History
Most patients presenting with heart failure complain
of dyspnea; therefore, determining its degree and
precipitants are important. Dyspnea with exertion
and at rest, paroxysmal nocturnal dyspnea (PND),
and orthopnea are common symptoms. Inquiring
about the number of pillows used while sleeping
may help identify the presence of orthopnea. A large
meta-analysis in 2005 reported that these symptoms
are not only specific, but are more likely to occur
during ADHF37 (Table 8). Patients who present with
PND, orthopnea, or edema are two time mores likely
than others to have ADHF.37 The rapidity of symptom onset may suggest an underlying etiology for
the decompensation. An abrupt deterioration should
raise concern for arrhythmia, acute MI, or valvular
rupture (see Special Circumstances). Prior episodes
of a similar nature can provide important clues.
Associated symptoms are important and the EP
should determine whether the patient has had any
chest pain or other anginal equivalent such as shoulder, neck, arm or epigastric discomfort. In a retrospective analysis of 491 patients, the combination of
syncope and heart failure was found to be associated
with a mortality rate of 50%, which was ten times
greater than those patients without ADHF.38 Recent
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weight gain, leg swelling, change in urinary output,
exercise tolerance, fatigue, and compliance with diet
should be elicited.
Medication history is also important in determining the etiology of ADHF and may also guide therapy. Non-adherence with prescribed medications is
often a precipitating factor and is associated with 15
to 64% of cases of ADHF.39,40 New prescriptions or
changes in dosage of medications such as NSAIDs,
ophthalmic beta-blockers, herbals, and over the
counter drugs are important as well. Male patients
with congestive failure may take sildenafil (Viagra),
and the administration of nitrates may cause lifethreatening hypotension in such individuals.41
The most valuable historical information to elicit
from patients with ADHF is a prior history of heart
failure, myocardial infarction, and/or coronary
artery disease37 (Table 8). A history of heart failure
has a specificity of 90%, and patients with prior heart
failure are approximately four times more likely to
have ADHF when presenting to the ED with acute
dyspnea.37 Prior myocardial infarction is one of the
best predictors of impaired left ventricular systolic
dysfunction.42 Patients often can tell you if they have
had prior episodes of ADHF. A common term synonymous to ADHF for patients with the syndrome of
systemic volume overload or acute diastolic dysfunction is “fluid on the lungs.” More sophisticated
patients may be able to provide details of previous
echocardiograms or cardiac catheterizations.
Table 7. Key Historical Questions
• Have you been able to take your prescribed
medications?
• Have you adhered to a prescribed diet
regimen?
• Has your primary care doctor or cardiologist
changed any of your medications lately?
• Have you gained or lost weight in the past
3 to 5 days?
• Do you have difficulty breathing? While lying
flat? While walking? In the middle of the night?
• Do these symptoms feel like any prior episodes
of “fluid in your lungs,” or “heart failure?
• Are you having any chest pain? Have you
passed out?
Physical
Vital signs provide a sense of the severity of illness
and can suggest etiologic factors for decompensation. Hyperthermia or hypothermia may indicate
sepsis or thyroid disease. In the absence of rate-controlling pharmacologic agents, tachycardia is nearly
universal in ADHF. Bradycardia should raise concern for high-degree AV block, hyperkalemia, drug
toxicity (digoxin, calcium channel, beta blocker), or
severe hypoxia. Hypertension is commonly seen in
both systemic volume overload and acute diastolic
dysfunction syndromes of ADHF. Hypotension can
be baseline for patients with end-stage cardiomyopathy or low output heart failure, but otherwise should
raise concern for sepsis, massive pulmonary
embolism, or cardiogenic shock.
Signs of congestion may be detected by careful
attention to heart and lung sounds, jugular venous
distention (JVD), hepatomegaly, and peripheral
edema. Elevated central venous pressure (CVP) is
present when the top of the external or internal jugular veins is more than 3 cm of vertical distance above
the sternal angle.43 The diagnostic utility of this physical exam finding is well documented for chronic heart
failure, but less so for ADHF in the ED setting.44, 45
JVD, abdominojugular reflux, and an audible 3rd
heart sound are very specific. Patients who present
with these exam findings are at least five times more
likely to have ADHF37 (Table 8). A new cardiac murmur in the proper context must be presumed to signal acute valvular or papillary muscle dysfunction.
Table 8. Signs, Symptoms And
Diagnostic Studies In Determining
Acutely Decompensated Heart Failure.
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The pulmonary exam is usually helpful, but can
be misleading. Rales, a classic finding in heart failure, may also occur with pneumonia, interstitial lung
disease, or COPD. The presence of rales has moderate specificity and is more likely to occur in ADHF
(Table 8). Wheezing, or “cardiac asthma,” is common in ADHF but has poor sensitivity37 (Table 8).
The leg exam is routine in the evaluation of
patients with suspected heart failure and may represent a degree of systemic volume overload. While
peripherial edema is moderately specific for
increased filling pressures, it has poor sensitivity37,45
(Table 8). Unilateral extremity swelling and especially the presence of a venous cord should raise suspicion for deep venous thrombosis and possible pulmonary embolism.
B-Natriuretic Peptide and NT-proBNP
B-type natriuretic peptide (BNP) and NT-proBNP
correlate with the presence and severity of heart failure. BNP is produced by cardiac myocytes in
response to myocardial stretch and increased enddiastolic pressure and occurs in the setting of heart
failure. Pre-proBNP is synthesized within myocytes
and is cleaved to proBNP. The latter is released into
the circulation and then cleaved to the active BNP
and an inactive N-terminal fragment, called NTproBNP.48 The half-life of BNP is approximately 20
minutes and the half-life of NT-proBNP is three to
six times that of BNP.
BNP is a counter-regulatory hormone that offsets
the effects of neurohormonal activation by promoting diuresis, natriuresis, and vasodilation and suppressing the renin-angiotensin system. Plasma levels
of BNP have been shown to correlate with the degree
of left ventricular overload, severity of clinical heart
failure, and both short- and long-term cardiovascular
mortality.49-53
Plasma BNP and NT-proBNP levels can be used
to distinguish between cardiac and non-cardiac causes of dyspnea.5,54-56 Studies have shown that the two
peptides have a high degree of correlation.57-60
Acutely dyspneic patients with plasma BNP levels of
less than 100 pg/dl and NT-proBNP levels less than
300 pg/dl are unlikely to have ADHF, and those
with BNP greater than 500 pg/dl and NT-proBNP
levels greater than 1000 pg/dl are very likely to have
ADHF. BNP levels above 100 pg/dl have 90% sensitivity for identifying ADHF, and BNP levels of 500
pg/dl have 87% specificity for identifying ADHF.61
A BNP cut point of 100 pg/ml predicts the diagnosis
ADHF with 81 to 91% accuracy.5,10,61 Fewer studies
have been performed on NT-proBNP, but a prospective, observational study showed a cut point of 300
pg/ml with 99% sensitivity.62
In general, clinicians are 80% accurate in clinically differentiating ADHF from other disease processes.10,63 Data from the Breathing Not Properly
Multinational Study indicate that BNP levels can be
used to improve diagnostic accuracy beyond clinical
judgment.5,10,61 BNP levels will not add significant
diagnostic value for patients with classic findings
from history and physical exam of ADHF; therefore,
diagnostic BNP levels should be used on a case-bycase basis. It is unclear how indeterminate BNP levels affect the management of patients with suspected
ADHF.
BNP and NT-proBNP levels are elevated in non-
Diagnostic Studies
Laboratory tests
The majority of patients who present with complaints suggestive of ADHF will need basic laboratory testing. A complete blood count (CBC) is useful
for ruling out anemia as a cause for decompensation.
Some believe that an elevated white blood count
may suggest the presence of an infectious process,
especially if bands are present. However, this is not
well studied in the patient who presents with dyspnea. Serum chemistries help assess renal function
and overall fluid and electrolyte balance.
Cardiac Markers
The question as to which patients with ADHF
require screening for cardiac enzymes is not well
studied. Additional information from the history
(e.g., chest discomfort, new-onset heart failure, or
significant risk factors for coronary artery disease)
should heighten the suspicion of associated cardiac
ischemia. Although not always clear, a high level of
suspicion for acute coronary syndrome (ACS) should
be considered in patients presenting with ADHF.
Several studies have shown that elevated cardiac troponins are found in up to one-third of patients with
severe heart failure and help to identify those with
worse short-term prognosis.46, 47 According to one
review of 151 patients with a discharge diagnosis of
heart failure, 70% of patients did not report chest
pain.47 Therefore, the ED physician should strongly
consider screening for cardiac enzymes in any
patient who presents with ADHF, regardless of the
presence or absence of chest pain.
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cardiac conditions (i.e., age, renal insufficiency, pulmonary embolism, and cor pulmonale).58, 64-67 Since
BNP and NT-proBNP levels increase with age, cutpoints for diagnosing ADHF are elevated among the
elderly and have discriminatory value.58,65,67 Data
from the Breathing Not Properly Multinational Study
indicate that BNP is a better indicator at younger
ages.65 In a prospective, observational study of elderly patients greater than 65 years of age with acute
dyspnea, a higher BNP level of 250 pg/ml has a
specificity of 90% in diagnosing ADHF.58
The role of BNP in patients with severe renal
failure is less studied. Patients with severe renal failure have reduced ability to clear metabolites and volume overload resulting in higher levels of circulating
BNP. These proposed elevated cut-points have discriminatory value, but actual cut points are yet to be
determined.59
Obese patients with elevated filling pressures
may have less myocardial stretch which lowers
measured BNP and NT-proBNP levels. This may be
due to increased extracardiac pressure associated
with an elevated BMI. The sensitivity of BNP and
NT-proBNP at existing cut points for obese patients
may be lower than expected and a true cut-point in
this setting is unclear.68 The Breathing Not Properly
Multinational Study found an inverse relationship
between BMI and BNP.69 For overweight and obese
patients, BNP is 80% sensitive at a cut point of 100
pg/ml. In addition, 20% of these patients with
ADHF had BNP levels less than the standard cut
off.68 NT-proBNP may also lose discriminatory value
among obese patients. The ProBNP Investigation of
Dyspnea in the Emergency Department (PRIDE)
study identified significantly lower ProBNP and
BNP levels in overweight and obese patients presenting with ADHF.68
For patients with classic signs of ADHF (i.e.
prior episodes of ADHF, volume overload, dyspnea,
and orthopnea) or those with shortness of breath
consistent with other etiologies (i.e. asthma, COPD),
BNP is not likely to assist in the diagnostic workup.
Checking BNP levels in indeterminate cases may aid
in diagnosing or excluding ADHF, but results may
leave the EP with additional questions.
A provocative single-center study used BNP to
diagnose ADHF and showed beneficial effects on
patient outcomes. In the B-Type Natriuretic Peptide
for Acute Shortness of Breath Evaluation (BASEL)
study, patients presenting to the ED with acute dyspnea were randomized to standard clinical evaluation
Emergency Medicine Practice©
versus a clinical evaluation including BNP. The BNP
group had reduced time to treatment, reduced hospital costs, and reduced time to discharge.6
Approximately one-third of the cost saving was associated with identifying an alternate diagnosis.
ECG
While the ECG is admittedly a relatively insensitive
tool, it remains useful for detecting ischemia,
arrhythmias, and electrolyte disturbances. Given the
high proportion of heart failure exacerbations precipitated or accompanied by ischemia, it is difficult to
justify not obtaining an ECG on all such patients.22
In a meta-analysis of 22 studies differentiating cardio-pulmonary cause of dyspnea, atrial fibrillation
was the most likely associated ECG finding among
patients presenting to the ED with ADHF37 (Table 8).
The ECG is likely to be abnormal in patients
with chronic heart failure. In a clinic population,
approximately 40% of 19,877 clinic patients had ECG
with left ventricular hypertrophy, and approximately
70% had electrocardiographic evidence of cardiac
ischemia or a prior MI.70 Conversely, an entirely normal ECG is strong evidence against the presence of
left ventricular dysfunction and should therefore
prompt consideration of alternative diagnoses.20,37,71
Also, a prolonged QRS has been shown to be an
independent predictor of LV dysfunction.
Chest X-ray
The chest x-ray should be obtained in patients with
suspected ADHF.3 Findings suggestive of ADHF
include cardiomegaly, vascular redistribution (e.g.,
cephalization, fullness of hilar vessels), interstitial or
pulmonary edema, and pleural effusions. Pleural
effusions in heart failure tend to be bilateral or localized to the right side.73 The presence of pulmonary
congestion and cardiomegaly is associated with a
very high likelihood of ADHF37 (Table 8). The chest
film may also be useful in identifying alternative or
contributing causes of the patient’s symptomatology.
There are several pitfalls that await the unwary
physician who uses the chest film to diagnose acute
heart failure. Heart size may be normal in acute failure, especially if the failure originates from acute
diastolic dysfunction.45 COPD patients may have
minimal radiographic evidence of concurrent heart
failure. Also, patients with longstanding chronic
heart failure may have well developed lymphatic
drainage of the pulmonary interstitium and, therefore, little radiographic evidence of congestion.
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Recent studies have shown that a normal chest radiograph alone cannot exclude ADHF. According to a
recent ADHERE study, one in five patients without
radiographic findings of interstitial edema, pulmonary edema, or vascular congestion received a
final diagnosis of ADHF.73
Other Diagnostic Modalities
Peak Flow/End Tidal CO2
Peak flow and end tidal CO2 are two additional diagnostic modalities that may help identify ADHF in the
undifferentiated patient. In a study of 56 acutely
dyspneic patients, peak expiratory flow rates of
those with heart failure were found to be twice those
of patients with COPD; however, no single cut-off
provided for perfectly accurate classification.80 While
end-tidal carbon dioxide levels (ETCO2) for heart
failure patients differ significantly from those of
asthma/COPD patients, there is no single ETCO2
level that can reliably differentiate between the two
conditions.81
Cardiac Echocardiography
Echocardiography is invaluable and is, in some
sense, considered the “gold standard” for assessing
the status of left ventricular function, distinguishing
between systolic and diastolic failure, and identifying regional wall motion abnormalities.
Echocardiography can also assist in diagnosing or
excluding potentially reversible etiologies of an acute
decompensation such as pericardial tamponade,
massive pulmonary embolus, ruptured chordae
tendineae, or ruptured ventricular septum (see
Special Circumstances).
Echocardiography is probably not indicated in all
instances of ADHF, particularly if a patient has had a
recent echocardiogram and a clear precipitant for
decompensation. ACC/AHA guidelines recommend
transthoracic echocardiography as soon as possible
after initial stabilization for any patient who presents
with acute pulmonary edema, unless there are obvious precipitating factors and the patient’s cardiac status has been adequately evaluated previously.74
Guidelines for establishing an effective system for
emergency echocardiography have been published.75
Experience with emergency physicians performing
bedside echocardiography has generally been limited
to ruling out pericardial effusion / tamponade.76-78
Treatment
As with any ill patient, the initial focus of treatment
will be on airway and breathing (see Clinical
Pathway: Treatment For Acutely Decompensated
Heart Failure). Although many patients can be managed with oxygen, with or without non-invasive
ventilatory support, the presence of agonal respirations or profoundly depressed mental status will
mandate emergent intubation with the caveat that
the respiratory symptoms that accompany ADHF
reflect cardiovascular rather than pulmonary pathology and are therefore often rapidly reversible with
aggressive medical therapy (see Respiratory
Therapy).
Sitting the patient upright may reduce pulmonary
congestion and improve respiratory dynamics.
Studies in patients with chronic heart failure show a
large rise in airflow resistance after lying supine for
five minutes, a condition that is reversed by sitting
erect.82 Practice guidelines recommend early use of
pulse oximetry, noninvasive blood pressure monitoring, and continuous cardiac monitoring as these can
provide early warnings of decompensation.3
Pulmonary Artery Catheterization (Swan-Ganz)
Swan-Ganz catheters provide considerable data on
cardiopulmonary function that are thought to
improve management and clinical outcomes; however, recent trials have not demonstrated significant
patient benefit associated with their use.79 The
Evaluation Study of Congestive Heart Failure and
Pulmonary Artery Catheterization Effectiveness
(ESCAPE) trial, a randomized, controlled trial of 433
patients, showed no difference in six-month mortality or return for hospitalization compared to clinical
assessment.79 On the other hand, the use of invasive
monitoring in this study was associated with more
adverse events. Nevertheless, published consensus
guidelines advise the use of PA catheters in patients
who do not respond to initial therapies.2,3
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Pharmacologic Therapy
The main objectives of pharmacologic therapy for
ADHF are relief of pulmonary congestion and
improvement in systemic tissue perfusion. The goal
of therapy is to reduce preload and enhance left ventricular function, while maintaining or improving
myocardial oxygen balance. While the basic
approach to treating ADHF has not changed over the
past two decades, there has been increasing emphasis on afterload reduction and other means of counteracting the adverse cycle of neurohormonal activa11
Emergency Medicine Practice©
tion (see Table 9 and Clinical Pathway: Emergency
Department Therapy for Acutely Decompensated
Heart Failure).
ticularly for patients with hypertension or with
presumed pulmonary edema.2,3 The beneficial hemodynamic effects of nitrates in the setting of heart failure have long been appreciated.83,84 At low doses,
nitroglycerin induces venodilation; at high doses,
nitroglycerin causes arteriodilation including dilation
of the coronary arteries.85 Significantly, in patients
with severe underlying left ventricular dysfunction,
Nitrates
Nitrates are recommended as initial therapy for
ADHF of both ischemic and non-ischemic origin, par-
Table 9. Medications For Acutely Decompensated Heart Failure
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December 2006 • EBMedicine.net
afterload reduction appears to predominate over
preload reduction, even at moderate doses of nitroglycerin.86
Despite its common use, few studies have rigorously addressed the role of nitrates in the treatment
of ADHF. To date, no prospective studies on its
effects on mortality have been published. In the
Vasodilation in the Management of Acute Congestive
Heart failure (VMAC) trial, intravenous nitroglycerin
improved dyspnea scores compared to placebo during early therapy.8 In another randomized, controlled
trial involving subjects with pulmonary edema, a regimen of high-dose nitrates and low-dose diuretics
provided more consistent clinical improvement than
a regimen of high-dose diuretic and low-dose
nitrates. It was also associated with lower rates of
mechanical ventilation and MI.87 Because many of
the patients in this study had underlying coronary
artery disease, it is likely that the anti-ischemic effects
of nitrates also played a role. Data from ADHERE
show a lower mortality rate among patients treated
with nitrates compared to inotropic agents, but did
not compare nitrates to diuretic therapy.88
Single doses of 0.4 mg sublingual nitroglycerin
can be given repeatedly every five to ten minutes,
provided the patient has stable blood pressures. In
the hospital setting, continuous IV administration of
nitroglycerin is generally more convenient and
allows for titration to specific clinical or hemodynamic end-points. Nitroglycerin can be started at 0.3
to 0.5 mcg/kg/min but may require much higher
doses (up to 3 to 5 mcg/kg/min), so long as the
blood pressure is above 95 to 100 mm Hg.89
Alternative regimens and formulations for administering IV nitrates have been described, but offer no
clear advantages.83,90,91 Oral or transdernal nitroglycerin have comparable hemodynamic effects to IV
nitroglycerin but are less amenable to rapid titration
and may be less effective in patients with poor gastrointestinal absorption or poor skin perfusion.92
Hypotension with standard nitrate therapy is
generally mild and transient. Severe or persistent
hypotension should raise suspicion for hypovolemia,
stenotic valvular disease such as aortic stenosis, cardiac tamponade, right ventricular infarction, or
recent use of sildenafil (Viagra®). If these conditions
are known or suspected, nitrates should be avoided
or used with extreme caution. Nitrate therapy may
not be particularly effective in patients with massive
peripheral edema.93 In such cases, aggressive diuretic therapy is more likely to be of benefit.
EBMedicine.net • December 2006
The European Society of Cardiology (ESC) recommends sodium nitroprusside for patients with
marked systemic hypertension, severe mitral or aortic valvular regurgitation, or pulmonary edema not
responsive to standard nitrate therapy.3
Nitroprusside directly dilates resistance vessels,
rapidly reducing blood pressure and afterload.83
Typically, nitroprusside is started at a dose of 0.1 to
0.3 mcg/kg/min and advanced as needed to
improve clinical and hemodynamic status, maintaining a SBP greater than 90 or mean arterial pressure
greater than 65 mm Hg. In patients with renal failure, long-term use of nitroprusside carries the potential for cyanide toxicity as metabolites accumulate.
Diuretics
Diuretics are the mainstay of therapy for patients
with systemic volume overload.2,3 Although this
practice is recommended by societies and is a commonly accepted approach, there have not been multiple randomized, controlled trials or meta-analysis to
support it use. On the other hand, it is important to
recognize that patients who present with ADHF are
not always volume overloaded. Patients with acute
diastolic dysfunction may benefit more from redistribution of circulating volume by using vasodilators.
The indiscriminate use of diuretics carries the risk of
overdiuresis and detrimental effects on renal function, particularly among elderly patients. Even without overdiuresis, there is growing evidence that
the higher doses of diuretics required to treat
advanced heart failure correlate to worsening renal
function, which has been tied to both longer hospitalizations and increased mortality after discharge.
This adds strength to the argument that the focus
should be on changing loading conditions with
vasodilators rather than diuresis as the stand alone
therapy it often is.
Evidence from a large number of in vitro and in
vivo experiments suggest that direct vascular actions
also contribute to the clinical effects of furosemide.94-97
These actions are not necessarily advantageous, in
that their net effect may promote further activation
of the sympathetic and renin-angiotensin systems
characterized by reflex vasoconstriction, worsening
of cardiac loading conditions, and a decline in cardiac output.98,99 Studies comparing the acute effects
of diuretics and nitrates have emphasized the more
favorable overall hemodynamic effects of the latter
group, as described earlier.
(continued on page 18)
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followed by a continuous drip of 0.01 mcg/kg/hr.
Randomized, controlled trials of NYHA class IIIV patients with ADHF have shown nesiritide to be
more effective than placebo in improving hemodynamics.110-112 The VMAC trial compared nesiritide to
nitroglycerin in the treatment of ADHF. At three
hours, PCWP was lower in the nesiritide group versus the nitroglycerin group but dyspnea scores at 3
and 24 hours were not statistically significant
between the two groups.8 A study from ADHERE
showed that treatment with nitroglycerin or nesiritide had lower in-hospital mortality than ionotropic
treatments with milrinone or dobutamine.88 There
was no in-hospital difference in mortality between
nitroglycerin and nesiritide. Studies have yet to
show improvement in length of stay, hospital costs,
or mortality.
Recent studies have emphasized potential risks
associated with nesiritide.113,114 Pooled data and metaanalysis suggest an increase in creatinine levels with
nesiritide, which required additional medical intervention. Another meta-analysis suggested that nesiritide carries a greater 30-day risk of death compared
to conventional therapy.113 Prospective trials addressing these questions have not yet been published.
Although there are recent studies questioning
the safety of nesiritide and consensus guidelines recommend its use, the Heart Failure Society of
America notes the need for additional prospective
studies.2
(continued from page 13)
Depending on the patient’s clinical condition,
state of hydration, and previous use of diuretics, an
initial IV dose of 40 to 200 mg of furosemide can be
administered. For patients on chronic diuretic therapy, a common strategy is to begin with the usual
daily dose (typically 40 to 80 mg) given as an IV
bolus, and to double the dose if there is inadequate
diuresis. Although IV boluses of furosemide are a
common practice, there is a trend toward using IV
furosemide infusions.100-102 A randomized crossover
study compared continuous furosemide to bolus
administration and showed that those treated with
continuous furosemide resulted in greater urine output and fewer adverse effects.96 A recent meta-analysis reviewing eight randomized, controlled trials
compared bolus versus continuous intravenous
diuretics. These small heterogeneous studies
showed that continuous IV diuretics improved
diuresis and carried a better safety profile.103
Although these findings are encouraging, larger
studies to definitively support one over the other are
needed.
In cases of volume overload that fail to respond
to standard therapy, substitute a more potent loop
diuretic such as torsemide (Demadex®) 10 to 20 mg
IV or bumetanide (Bumex®) 1 to 4 mg IV. The use of
these medications among patients with ADHF in the
ED setting has not been published. Combining
furosemide with a thiazide agent such as metolazone
(5 to 20 mg PO) or chlorothiazide (Diuril®) 500 to
1000 mg IV) may improve diuresis.104,105 While not all
patients in ADHF require a Foley catheter, monitoring of urinary output with a urinometer can be helpful in those with severe symptoms.
Electrolyte abnormalities such as hypokalemia
and hypomagnesemia occur with chronic diuretic
use and may worsen with subsequent administration
of diuretics in the ED. Daily monitoring of potassium, magnesium, and sodium levels are recommended for patients admitted to the hospital for ADHF.2
ACE Inhibitors
Angiotensin converting enzyme inhibitors (ACE
inhibitors) represent a logical extension of vasodilator therapy. The beneficial hemodynamic effects of
ACE inhibitors in acute heart failure have been
appreciated for two decades.115 Acutely, ACE
inhibitors reduce both preload and afterload,
improve renal hemodynamics, impair sodium retention, attenuate sympathetic stimulation, and maintain or enhance left ventricular function.116-118
Although not currently recommended by the
European Society of Cardiology or the Heart Failure
Society of America in the setting of acute heart failure, drug regimens that include an ACE inhibitor
appear to have hemodynamic advantages over those
based upon other vasodilators.119-121
For acutely decompensated heart failure, ACE
inhibitors can be administered intravenously (e.g.,
enalaprilat), orally (e.g., captopril) or sublingually
(e.g., emptied captopril capsules contents).
Nesiritide
Nesiritide (recombinant BNP) is FDA approved for
the treatment of ADHF symptoms. BNP has
vasodilatory as well as mild diuretic and natriuretic
properties. When administered in supraphysiologic
doses, it exerts favorable hemodynamic, natriuretic,
and neurohormonal effects.106-109 Nesiritide can be
administered intravenously with a 2 mcg/kg bolus
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December 2006 • EBMedicine.net
Depending on the drug, the dose, and the route of
administration, hemodynamic effects may be seen
within 10 to 60 minutes.116,117,119 Safe dosing regimens
of enalaprilat include 0.004 mg/kg as an intravenous
bolus, or 1 mg by continuous intravenous infusion
over two hours. The suggested one-time dose of oral
or sublingual captopril is 12.5 to 25 mg. The safety
of administering an ACE inhibitor in the setting of
ADHF is of concern to some clinicians who fear
potentially deleterious effects on blood pressure,
renal function, and electrolyte balance. However,
clinical trials have consistently demonstrated the
safety of administering ACE inhibitors to patients
with ADHF.118,122
Few studies of ACE inhibitors for ADHF have
been performed in the ED setting. Small studies
have demonstrated that sublingual captopril is safe
and effective for ED patients with pulmonary
edema.123,124 In one retrospective analysis, the use of
sublingual captopril in the ED was associated with
lower rates of mechanical ventilation and CCU
admission.125
ACE inhibitors are contraindicated in the context
of pregnancy, hyperkalemia, or a history of ACEinhibitor-induced angioedema. For patients with
evidence of poor systemic perfusion, ACE inhibitors
should be used cautiously, because additional
vasodilation may not be tolerated. Unlike nitrates,
ACE inhibitors have a relatively prolonged duration
of action, making dosage less easily titratable.
increase in mortality among patients with volume
overload and diastolic dysfunction who were treated
with ionotropes.88
It is important to understand the expected hemodynamic effects of inotropic agents and to set clear
goals for therapy. Most inotropic agents have multiple pharmacologic actions, some of which may be
deleterious. Undesirable chronotropic effects,
arrhythmogenesis, or ischemia resulting from
increased myocardial oxygen consumption may curtail the use of any particular drug.
Digoxin has a very limited role in the ED management of heart failure. The inotropic effects of
digoxin are modest, unpredictable, and delayed for
at least 90 minutes after intravenous loading.128 For
patients with ADHF, the only reasonable use for
digoxin is to help control the ventricular response to
atrial fibrillation (see Special Circumstances–Atrial
Fibrillation).
Morphine
Morphine is one of the oldest drugs still in use for
the treatment of acute heart failure and remains an
adjunct for treating the anxiety and discomfort associated with pulmonary edema. With high doses of
morphine, direct vasodilation may result from histamine release, but the predominant hemodynamic
effects of morphine appear to be mediated through
the central nervous system.129 Morphine can be
administered safely to most patients. However,
because of its sedative properties and potential to
depress respirations, caution should be exercised
when administering morphine in the setting of
chronic pulmonary insufficiency or suspected acidosis. One retrospective study found that ED administration of morphine to patients with pulmonary
edema was associated with an increased rate of
endotracheal intubation and CCU admission.125
Inotropes
Short-term therapy with ionotropes may benefit
patients presenting with low output failure, which
are considered acceptable treatment modalities,
although with notable risks.2,3 Classically, inotropic
agents have been reserved for the treatment of cardiogenic shock. However, short-term inotropic support may also be seen as beneficial for patients with
low output failure who fail to respond to conventional therapy. While short-term inotropic therapy
clearly improves hemodynamic performance, the
impact on clinical outcomes is less sanguine.
Inotropic therapy has deleterious effects upon
patients with preserved or moderately depressed
ventricular function and congestion. The Outcomes
of a Prospective Trial of Intravenous Milrinone for
Exacerbations of Chronic Heart Failure, a randomized, controlled trial, showed no increased benefit
over standard therapy with the use of milrinone.126,127
ADHERE also supports this finding indicating an
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Respiratory Therapy
The majority of patients with respiratory distress
respond to supplemental oxygen and standard pharmacologic therapy, but patients with persistent
hypoxemia or progressive fatigue will require at least
temporary respiratory support (see also the July
2001 issue of Emergency Medicine Practice,
“Noninvasive Airway Management Techniques:
How And When To Use Them”).
Continuous positive airway pressure (CPAP)
improves lung mechanics by recruiting atelectatic
alveoli, improving pulmonary compliance, and
19
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reducing the work of breathing.130 At the same time,
particularly in patients with congestive heart failure,
CPAP improves hemodynamics by reducing preload
and afterload, thereby enhancing left ventricular performance.131-134 Nasal or face mask-applied CPAP of 5
to 10 cm H20 has been shown to improve oxygenation, reduce heart rate and reduce blood pressure
compared to standard oxygen treatment.135-141 In several randomized, controlled clinical trials, CPAP
reduced the need for endotracheal intubation in
patients with severe cardiogenic pulmonary
edema.135,137,138,142 Pooled data and one randomized,
controlled trial also suggest that the use of CPAP in
this setting may be associated with decreased mortality.142,143
Biphasic positive airway pressure (BiPAP)—or
non-invasive positive pressure ventilation (NPPV)—
provides the physiological advantages of CPAP during expiration and also provides additional assistance
with the inspiratory work of breathing. Evidence
from several case series and a recent randomized trial
support the use of this therapy in patients with acute
cardiogenic pulmonary edema;144-147 however, another
randomized, controlled trial and small series did not
show benefit.148,149 A small, randomized trial comparing BiPAP with CPAP demonstrated a more rapid
clinical improvement with BiPAP but no difference in
the rates of intubation.150 Of concern in this trial was
an unexpectedly high rate of acute MI associated
with the use of BiPAP, which prompted premature
termination of the study. One other clinical trial
involving BiPAP was also terminated early because
Cost Effective Strategies For Acutely Decompensated Heart Failure
who are agitated or those who have altered mental status, unstable vital signs, or evidence of
acute MI.
1. Don’t admit every patient with heart failure.
Some patients with acutely decompensated heart
failure may only require an ED “tune-up” and
will be appropriate for discharge. Patients with
a past history of failure who have a reassuring
history and physical examination, normal laboratory values, and an ECG unchanged from previous tracings may be candidates for outpatient
follow up (especially if their decompensation
occurred because they ran out of their medicine).
If discharge is considered, communicating with
the patient’s cardiologist and/or primary care
provider is necessary for close follow-up. ED
observation units for select patients may also be
a cost-effective alternative to traditional admission.
3. Consider the use of furosemide infusions.
While many patients in acutely decompensated
heart failure respond quickly to nitrates and
bolus diuretics, some do not. Some studies do
show that intravenous infusions of furosemide
for NYHA class IV heart failure are a safe, effective, and economic mode of therapy, especially in
the elderly. The increased cost of the infusion
would be more than offset by savings accrued by
a shorter hospital stay. Since this trial was small
and non-randomized, further study is needed to
ensure the cost-effectiveness of this intervention.
Caveat: Most patients who present with acutely
decompenesated heart failure will need hospital
admission—especially those with abnormal vital
signs, worsening renal function, or chest pain.
4. Utilize BNP or NT-proBNP when appropriate.
Of all of the diagnostic tests available to determine the presence of acutely decompensated
heart failure, BNP may be the single best investigation. It is relatively sensitive and specific and
can be performed at the bedside. In the acute
setting, elevated BNP levels correlate with the
diagnosis of heart failure, reduce time to treatment, decrease length of hospital stay, and
decrease cost of care.
2. Consider the use of CPAP/BIPAP.
CPAP or BIPAP may prevent the need for intubation in some patients with acutely decompensated heart failure and can decrease the cost and
length of stay in the intensive care unit. Keeping
a machine in the ED and using it frequently can
promote early use.
Caveats: Levels of BNP or NT-proBNP are affected by their half-lives. BNP levels may also be
elevated in eldery patients and patients with
renal insufficiency and lower in obese patients.
Caveat: Some patients are not good candidates
for non-invasive ventilation—especially those
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December 2006 • EBMedicine.net
of similar safety concerns.151 Recent studies provide
evidence to suggest no advantage of BiPAP/NPPV
over CPAP for patients with cardiogenic pulmonary
edema and hypoxemic respiratory failure.152-154
However, recent meta-analysis shows a small benefit
in CPAP, but no significant changes in clinical outcomes.155
The success of non-invasive respiratory support
depends upon appropriate patient selection. For
patients with compromised upper airway function or
significantly altered level of consciousness, intubation and mechanical ventilation remain the definitive
therapy. Patients with a history of cardiac arrest,
unstable cardiac rhythms, or cardiogenic shock are
generally not felt to be candidates for non-invasive
approaches. Likewise, in the setting of severe
myocardial ischemia or infarction, full ventilatory
support may be preferable in order to decrease the
myocardial oxygen demand associated with respiratory effort.
Although the decision to initiate non-invasive
respiratory support is dependent on a variety of factors, the presumption is that the earlier therapy is
instituted, the greater the likelihood of averting intubation. Recent studies suggest that the use of noninvasive ventilatory support in the prehospital setting is feasible and potentially beneficial for patients
with presumed cardiogenic pulmonary edema.156, 157
A small case series showed an increase in mean
pulse oximetry of patients treated with CPAP.157 In
one convenience sample, matched control study,
patients presumed to have congestive heart failure
(CHF) were given BiPAP by the medics during transport and compared to matched controls treated without NIV. In this trial, 97% of EMTs who used BiPAP
on patients with suspected CHF thought it improved
the patients’ dyspnea; however, data analysis
showed no statistical difference between groups in
the length of subsequent hospital stay, intubation, or
mortality.156
In either the prehospital or ED setting, if there is
progressive respiratory failure in spite of non-invasive support, the patient requires intubation and
mechanical ventilation. In general, airway management should be accomplished with rapid sequence
intubation (RSI). This involves using an induction
agent in combination with a short-acting paralytic
such as succinylcholine so as to maximize the rate of
success on the initial attempt.158 Maintaining the
patient in an upright position as long as possible
prior to intubation may assist in maximizing preEBMedicine.net • December 2006
oxygenation. Prolonged episodes of hypoxia or
hypotension during intubation risk further cardiac
decompensation and cardiopulmonary arrest. In one
study, all induction agents used (thiopental, fentanyl,
and midazolam) were associated with a significant
risk of hypotension for patients with pulmonary
edema. However, the authors admit that the small
numbers of patients with pulmonary edema in this
study preclude a valid post hoc comparison.159 On the
other hand, induction with etomidate appears to be
safe and effective for a range of patients undergoing
RSI, including those with underlying heart disease.160
Once mechanical ventilation is instituted for cardiogenic pulmonary edema, it is not certain whether
positive end-expiratory pressure (PEEP) confers any
additional hemodynamic benefit.161-164
Special Circumstances
Cardiogenic Shock
Cardiogenic shock in the setting of heart failure is
most often seen in the setting of acute ST-segment
elevation MI and acute valvular diseases. Mortality
rates for patients with frank cardiogenic shock
remain alarmingly high, ranging from 50 to 80%165
Stat echocardiograms play a pivotal role in diagnostics and treatment, as many etiologies of cardiogenic
shock will require surgical management. In the context of acute MI, emergent cardiac catheterization
and revascularization have been shown to be of benefit.3,166,167
Other potentially reversible causes of cardiogenic
shock, such as acute valvular dysfunction, ventricular septal wall rupture, and pericardial tamponade,
need to be excluded or addressed promptly. Acute
valvular dysfunction can occur in the setting of ACS
(ischemic papillary muscle dysfunction/rupture) or
independently in acute mitral/aortic insufficiency,
aortic dissection, or prosthetic valve thrombosis
causing cardiogenic shock. Free wall rupture and
ventricular septal wall rupture are uncommon complications of AMI that require rapid recognition.
Once the diagnosis is made, surgical management
provides an opportunity for survival. Again, the etiology of these types of cardiogenic shock should be
promptly identified with emergent echocardiography.2 Once acute surgical causes of cardiogenic
shock are ruled out, non-cardiac etiologies of shock,
such as hypovolemia, sepsis, poisoning, and massive
pulmonary embolism must also be entertained.
Aside from addressing reversible causes of car21
Emergency Medicine Practice©
diogenic shock, the overarching goal in treating
patients who present with evidence of inadequate
tissue perfusion (i.e., cool skin, altered mental status)
from acute heart failure or ADHF should be to
restore and maintain perfusion of vital organs.
Patients who present in shock with a normal
blood pressure or with mild hypotension may
respond favorably to dobutamine (starting at 2 to 3
mcg/kg/min). Prior to initiation of vasopressor
agents or ionotropes, small fluid bolus can be administered as an initial measure. Compared with
dopamine, dobutamine is associated with a lower
incidence of arrhythmias, less peripheral vasoconstriction, and more consistent reduction in left ventricular filling pressure for a comparable rise in cardiac output.168 Dopamine is required for patients
who have severe hypotension (SBP less than 70 to 80
mm Hg) in the presence of volume overload or after
bolus administration of saline. At moderate doses (4
to 5 mcg/kg/min), dopamine improves cardiac output without causing excessive systemic vasoconstriction. If the patient can be stabilized with dopamine,
dobutamine can then be added and the dose of
dopamine reduced, with the goal of reducing
myocardial oxygen demand.
Intra-aortic balloon counterpulsation (IABC)
should be considered for patients with a potentially
reversible condition, when initial management of
ADHF fails, or when stabilizing measures are needed
as a bridge to definitive management.3 IABC can be
an effective temporizing measure in anticipation of
coronary revascularization or cardiac valve repair.
The patients least likely to benefit from the IABC are
those with multiple previous infarctions, massive
irreversible myocardial necrosis, aortic dissection,
advanced stages of cardiogenic shock, and elderly
patients with peripheral vascular disease (because of
complications from insertion of the device). If IABC
is not immediately available, norepinephrine can be
added to increase systolic pressure to acceptable levels (80 or more mm Hg). Because of the adverse
effects on renal and mesenteric perfusion, the use of
high-dose dopamine or norepinephrine should be
considered only as a temporizing measure until a
definitive therapy can be substituted.
It is important for the EP to distinguish between
acute heart failure with cardiogenic shock and low
output ADHF, both which present with hypotension.
Low output ADHF tends to present subacutely in
patients with end stage systolic heart failure (see
Pathophysiology section, and Figure 1 on page 5).
Emergency Medicine Practice©
Patients may describe symptoms of fatigue, loss of
appetite and lethargy. Management of these patients
can be extremely challenging for the EP; therefore,
optimal treatment may require the involvement of a
heart failure specialist. Frequently, the key to management is identifying the etiology of decompensation. Although the EP’s impulse may be to aggressively fluid bolus or aggressively diurese patients
with low output ADHF, a “do nothing” management
style is often the best approach.
Renal Dysfunction
ADHF and chronic renal insufficiency frequently coexist.169,170 One out of every three patients admitted
for ADHF have renal insufficiency, with one of every
five patients with creatinine levels greater than 2.0
mg/dl. Renal hypoperfusion from poor cardiac output is aggravated by the use of diuretics and ace
inhibitors which, in turn, contribute to worsening
renal function. Both pre-existing renal insufficiency
and decline in renal function while managing ADHF
are associated with increased mortality. There is a
greater risk of in-hospital mortality among patients
treated for ADHF with interval worsening of renal
function.171
Heart failure is present in about one third of
patients who begin dialysis and will develop over
time in an additional 25%.172 Among anuric
hemodialysis patients, heart failure is the most common cause of ED visits.173 In these patients, ADHF is
most often due to volume overload between dialysis
treatments. Although hemodialysis is the treatment
of choice for these patients, it may not be immediately available. ED treatment is directed at stabilizing
these patients until hemodialysis can be performed
(Table 10). Because of their direct vascular effects,
diuretics may still have a role in managing anuric
patients with volume overload.174 Vasodilator therapy with nitrates and ACE inhibitors has been shown
to be particularly effective.123 In a descriptive study
of 46 renal dialysis patients, the administration of
preload and afterload reducing agents including captopril and nitroglycerin resulted in no deaths. In any
dialysis patient with an unstable cardiac rhythm,
hyperkalemia and digoxin toxicity must be considered.
Atrial Fibrillation
Atrial fibrillation is commonly seen in patients with
chronic heart failure and its co-prevalence is likely
associated with underlying hypertension and coro22
December 2006 • EBMedicine.net
nary artery disease. In patients presenting with
ADHF, atrial fibrillation is seen in approximately
one-third of patients.3,4,8
In the context of normal ventricular function,
loss of synchronized atrial contractions is of minimal
hemodynamic significance. However, in patients
who have abnormal systolic or diastolic function, the
loss of “atrial kick” can have profound consequences. When atrial fibrillation is accompanied by
a rapid ventricular response, the reduced filling time
and increased myocardial oxygen demand lead to
further decline in cardiac performance.
When assessing the patient with rapid atrial fibrillation and ADHF, it is often difficult to attribute
cause and effect. While new onset rapid atrial fibrillation may be the precipitant of ADHF, more commonly atrial fibrillation is a response to worsening
heart failure (e.g., via neurohormonal activation
and/or increased atrial stretch). This distinction can
often only be made clinically. In either case, management focuses upon the treatment of both conditions.175
Management of atrial fibrillation in the context
of ADHF should focus upon treating the underlying
cause of ADHF and controlling the ventricular rate
to allow for improved ventricular filling / contraction and improved myocardial oxygen balance2,3
(Table 10). In general, digoxin, diltiazem, and amiodarone are considered acceptable therapies for rate
control in patients with left ventricular systolic dysfunction.176-178 The EP should exercise some caution
with beta-blockers or calcium-channel blockers for
rate control because of potential negative inotropic
effects that could worsen existing systolic dysfunction. Although not specifically studied in the setting
of ADHF, esmolol would be a reasonable option,
given its short duration of action and demonstrated
safety in patients with severe chronic heart failure.
Cardioversion, whether electrical or chemical, is a
reasonable treatment alternative for unstable or
“new” atrial fibrillation, but maintaining sinus
rhythm may not be possible if the underlying heart
failure is not addressed.
ICG has been investigated in a variety of clinical settings and has been found to compare moderately
well with other modalities for assessing hemodynamics (e.g., echocardiography, Swan-Ganz catheterization).179,180 Because the technique is non-invasive,
portable, and capable of providing beat-to-beat information, potential applications in the ED are numerous. ICG is less accurate in patients with underlying
heart disease; however, serial measurements may
still provide useful information, such as monitoring
response to therapy. In a small study of 38 patients
with undifferentiated dyspnea, incorporation of ICG
data increased diagnostic accuracy of patients with
cardiac causes of dyspnea.181 In the Emergency
Department Impedance Cardiography–aided
Assessment Changes Therapy (ED-IMPACT) trial,
the use of ICG affected treatment plans for 24% of
patients with acute dyspnea.182 However, more studies are necessary to determine the overall utility of
this diagnostic tool and its effects on morbidity, mortality, cost, and length of stay.
Beta-blockers
Large, randomized, controlled trials have demonstrated clear morbidity and mortality benefits of
long-term beta-blocker therapy in patients with systolic heart failure.183-185 In contrast, short-term administration of beta-blockers to patients with severe systolic dysfunction can cause life-threatening clinical
deterioration.186 There has been no study that specifically addresses the potential benefits of beta-blocker
therapy in the setting of ADHF. Therefore, beta-blockers are not routinely recommended by the ESC for treatment of acutely decompensated heart failure and caution is
advised during its use.3 In the setting of an acute
decompensation, chronic beta-blocker therapy
should either be temporarily discontinued or administered cautiously at a reduced dose, according to the
ESC. On the other hand, in the context of ongoing
ischemia, tachycardia, and severe hypertension betablockers may be considered.3
Less is known specifically about the safety and
efficacy of beta-blocker therapy for patients with
acute diastolic dysfunction. In theory, the value of
reducing hypertension and tachycardia would outweigh any concern about negative inotropy in these
patients. Further studies are needed to clarify the
role of beta-blockers in this context.
Controversies / Cutting Edge
Impedance Cardiography (ICG)
Impedance cardiography (ICG) is a non-invasive
means of hemodynamic monitoring that provides
real-time estimates of cardiac output and pulmonary
capillary wedge pressure by employing principles of
thoracic bioimpedance. Over the past three decades,
EBMedicine.net • December 2006
Calcium Sensitizers
Calcium sensitizers are a novel class of agents that
23
Emergency Medicine Practice©
modify the configuration of troponin C to promote
myofilament sensitivity to calcium, enhancing contractility without impeding diastolic relaxation.186b
Levosimendan is the best studied of these agents. In
two small, randomized, controlled studies of patients
with severe ADHF, these agents were shown to
improve hemodynamics and decrease mortality.187,188
The Levosimendan Versus Dobutamine Trial (LIDO)
compared levosimendan to dobutamine with
improved hemodynamics and six month mortality
among 203 patients.187 Although encouraging, the
study population was restricted to low output heart
failure patients and the mortality benefit may be
associated with adverse affects of dobutamine. The
Calcium Sensitizer or Inotrope or None in Low
Output Failure Trial (CASINO) showed a significant
mortality benefit with levosimendan compared to
dobutamine and placebo.188 Although these results
are encouraging, this study was performed on inpatients and the incidence of low output failure requiring ionotropes remains low so its use in the ED is
still unclear. Implications for ED use await additional clinical trials.
Pimobendan is another calcium sensitizer
approved for use in Japan. The Pimobenden in
Congestive Heart Failure Trial (PICO) showed
improved hemodynamics but increased hazards for
death compared to placebo.189 The study population
was stable heart failure patients in the clinic setting.
Generalization of these findings to patients with
ADHF in the ED setting is limited.
Vasopressin Antagonists
Elevated vasopressin levels are found in patients
with ADHF, and vasopressin antagonists have been
proposed as a means to improve diuresis in patients
with ADHF. In a hemodynamic trial, conivaptan, a
V1a and V2 receptor antagonist, decreased PCWP
and right atrial pressures.191 In a randomized controlled trial among patients with ADHF in the setting
of systolic dysfunction, tolvaptan, a V2 receptor
antagonist, has been shown to decrease body weight
with no changes in worsening heart failure at 60
days.192
Endothelin Antagonists
Endothelin one (ET-1), a potent vasoconstrictor and
modulator of the renin-angiotensin-aldosterone system, are elevated in patients with ADHF. In hemodynamic studies, tezosentan, an ET-1 receptor antagonist, reduced preload and afterload, delayed
myocyte hypertrophy, and increased myocardial contractility.193 A randomized, controlled trial comparing
tezosentan with placebo among patients with low
output ADHF showed improved hemodynamics
with the use of tezosentan without significant
changes in dyspnea compared to standard therapies.194 Future studies will clarify tezosentan’s role
in the treatment of ADHF.
Disposition
Even in this era of cost containment, the vast majority of patients who present with ADHF are admitted
to the hospital.195 According to ADHERE, the
majority of patients with ADHF are admitted to
telemetry and step-down units while 14% of patients
are admitted to the ICU during their hospital stay.14
Meanwhile, hospital costs for in-patient care of
ADHF are continuing to rise. In-hospital mortality
remains approximately 2.3 to 7%,14,126,196 with major
adverse events occurring in up to 18% of patients.197,198
In patients with NYHA class III or IV heart failure
who are admitted for ADHF, there is a 9.6% mortality
rate at 60 days and a 30% combined rate of rehospitalization and/or death.6 However, while the realities
of modern healthcare economics may not favor routine hospitalization, premature release of inadequately treated patients are likely to result in increased
short-term morbidity and mortality.199
In general, clinicians have great difficulty judging the prognosis of patients with exacerbations of
heart failure.200 Acutely decompensated heart failure
Novel Natriuretic Peptides
Endogenous natriuretic peptides in addition to nesiritide have been investigated as potential new agents
to treat ADHF. Carperitide, an atrial natriuretic peptide, has vasodilatory effects as well as natriuretic
properties. Preliminary studies indicated that carperitide improves hemodynamic parameters and dyspnea scores among NYHA class III and IV heart failure patients with ADHF.190 Ularitide is a renal natriuretic peptide that has diuretic and natriuretic properties. One small, randomized study evaluated continuous ularitide compared to placebo in predominantly male patients with ADHF. Results showed
improved hemodynamics, and symptoms of dyspnea. The impact of these novel therapies in the ED
setting is unknown because previous studies have
yet to represent ED patients with ADHF.
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December 2006 • EBMedicine.net
is a dynamic entity, and the ED physician often sees
only a snapshot of the patient at any point in time.
Some patients are dramatically ill at presentation but
respond rapidly to treatment, while other patients go
on to develop serious complications after a period of
relative stability.
Previous studies have found that certain patient
characteristics are predictive of in-hospital morbidity
and mortality (Table 11).201-206 In multivariate analysis,
independent correlates of major complications or
death during hospitalization have included hypotension, tachypnea, jugular venous distention, electrocardiographic abnormalities, hyponatremia, and poor
initial diuresis.196,201-204 Recent studies have shown that
troponin elevations, elevated BNP, and worsening
renal function are prognostic factors in post-discharge
mortality and risk for rehospitalization.196,207,208 In one
study, 325 patients with acute dyspnea and those
with BNP levels greater than 230 pg/ml had a relative risk of 24.1 for death and a 51% probability of an
additional episode of ADHF within 6 months.207 Predischarge BNP for patients treated for ADHF are predictive of readmission and mortality.209,210
Two large, recent studies have further investigated characteristics predictive of increased mortality
among patients admitted with heart failure.205,206 The
Enhanced Feedback for Effective Cardiac Treatment
(EFFECT) study, a retrospective, multi-center, community-based study identified predictors of 30-day
and one-year mortality among patients admitted to
the hospital for heart failure.
A clinical tool developed from ADHERE identified patients admitted with ADHF, renal insufficiency (Cr greater than 2.7), elevated BUN (greater than
43) and moderately low systolic blood pressures
(SBP greater than 115) to have a mortality of greater
than 20%.205 A risk stratification tree has been developed to assist clinicians in determining mortality risk
of patients who present with ADHF (Table 12).
Disturbingly, some studies have shown that patients
without any independent risk factors appear to have
substantial rates (6%) of in-hospital morbidity and
mortality.201
The Heart Failure Society of America has established criteria for hospitalization of patients with
heart failure.2 The recent HFSA criterion includes
worsening renal function, altered mentation, and
new onset atrial fibrillation as circumstances that
merit hospitalization. However, in the Agency for
Health Care Policy and Research study, criteria failed
to identify up to one-third of the patients who die
EBMedicine.net • December 2006
within 30 days.195 Studies on the effectiveness of the
HFSA criteria have not yet been studied or published. Thus, while published criteria and guidelines
can help with triage, the significant rate of morbidity
even among “low-risk” patients mandates that clinical judgment be incorporated into the decision-making process.
For patients who are ultimately discharged
home, consultation with the patient’s primary care
physician and/or cardiologist is imperative. The EP
needs to understand that this is a high-risk situation.
Patients and their families need to understand that
there is a substantial chance of outpatient failure
necessitating a repeat ED visit or hospitalization
within the next 30 days.211 Alarmingly, a recent outcome study of 112 patients discharged from the ED
with a primary diagnosis of CHF showed that within
three months of initial visit, more than 60% experienced a recurrent ED visit, hospitalization, or
death.211 Depending on what precipitated the decompensation, the patient’s outpatient drug regimen may
require some adjustment. Intensive outpatient follow-up has been shown to be successful in preventing repeat visits to the ED.212-214 Referral to an outpatient heart failure program, where available, can
reduce the frequency of ED visits and hospitalizations.215
Heart Failure Observation Units
Theoretically, an ED-based observation unit or other
subacute care setting can serve patients with ADHF
Table 10. Treatment Recommendations
For Special Circumstances
Class of evidence definitions from Emergency Medicine Practice; see
back page of this issue.
25
Emergency Medicine Practice©
and accomplish this at substantial cost savings.
These units could monitor for patients’ response to
therapy and the development of potentially serious
adverse events. Observation units have been
advanced as a safe and effective means of reducing
hospital admissions in general and heart failure
admissions in particular.216,217 There have been several studies that suggest ED-based heart failure observation units may decrease ED return visits and readmissions.218 Although there is a growing interest to
provide ED observation units for patients with
ADHF, no randomized studies have been performed
to substantiate their use.
Table 11. Correlates Of In-Hospital
Mortality
• Advanced age
• New onset of heart failure
• Prolonged duration of symptoms
• Poor left ventricular (LV) function
• Chest pain
• Hypotension
• Jugular venous distention
• Non-sinus rhythm and ECG abnormalities
• Elevated creatine kinase levels
• Hyponatremia
• Elevated BUN
• Systolic Blood Pressure less than 115
• BNP level greater than 230 pg/ml
• Digoxin use
• Advanced renal dysfunction
• Poor response to initial therapy
Conclusion: Case Outcomes
The elderly woman who “looked and sounded wet”
felt much better after receiving furosemide and supplemental oxygen. You decided to send off cardiac
enzymes and they were positive. She did not have
Table 12. Predictors of In-Hospital Mortality
Emergency Medicine Practice©
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December 2006 • EBMedicine.net
Ten Pitfalls To Avoid
1. “She was just weak and dizzy. How was I supposed to know she had heart failure?”
You found out when she went into acute pulmonary edema after the aggressive fluid bolus.
Non-specific symptoms such as weakness, lethargy, fatigue, anorexia, or lightheadedness may be a
manifestation of low output acutely decompensated heart failure. Older patients can be particularly difficult to evaluate because they often lack
typical signs and symptoms of heart failure.
6. “She was clearly ‘wet’ and needed to be aggressively diuresed. Is it my fault her creatinine
doubled by the next day?”
Maybe. This elderly woman with acute diastolic
dysfunction was not suffering from volume overload. Her pulmonary congestion may have
responded better to vasodilator therapy than to
aggressive diuresis which ended up impairing her
renal function and prolonging her hospital stay.
7. “I always thought sublingual nitroglycerin was
harmless. I didn’t expect his systolic BP to drop
to single digits.”
Nitrates are fast, effective, and relatively safe;
however, patients with preload-dependent conditions (e.g., valvular stenosis) do not tolerate them
well.
2. “She was only 35, she couldn’t have had heart
failure”
You can’t diagnose post-partum cardiomyopathy
unless you consider it. Myocarditis, alcohol
abuse, and cardiotoxic chemotherapies are among
the other etiologies of heart failure that present in
younger patients. Older age is a major risk factor
for heart failure, but young age should never
exclude it.
8. ”He was in severe respiratory distress so he had
to be intubated. Who would have thought he
would spend a week in the CCU?”
Maybe if you had considered CPAP, the patient
could have avoided the ventilator-associated
pneumonia and prolonged CCU stay. For patients
with severe cardiogenic pulmonary edema, noninvasive ventilatory support, CPAP in particular,
has been shown in multiple controlled trials to
reduce the need for endotracheal intubation and
to decrease length of ICU stay.
3. “He seemed to be wheezing, so I treated him for
COPD.”
Unfortunately, his condition continued to deteriorate and you only learned about his history of
heart failure after he was intubated.
Distinguishing between cardiac and pulmonary
causes of dyspnea remains a fundamental clinical
challenge. Careful diagnostic workup can yield
important clues and using BNP or NT-ProBNP
can aid in diagnostics challenges.
9. “He was in rapid atrial fibrillation and I figured
rate-control would improve his cardiac function.”
Unfortunately, you failed to consider the negative
inotropic effects of verapamil, and the patient’s
heart failure further decompensated. When a
patient presents with acutely decompensated
heart failure in the context of rapid atrial fibrillation, it is important to address the clinical situation as a whole, which means treating for both
conditions simultaneously and recognizing that
the treatment of one may impact the other.
4. “I just assumed he hadn’t been taking his medications.”
Medication non-compliance and dietary indiscretion commonly precipitate decompensated heart
failure, but don’t assume this is the case until
other serious causes have been considered. Acute
decompensation may be brought on by a variety
of cardiac and non-cardiac conditions including
ischemia / infarction, arrhythmias, valvular /
septal rupture, sepsis, anemia, and thyrotoxicosis.
5. “He was wide awake, and looked extremely anxious. I thought he could tolerate the 10 mg of
morphine” ...
Until he stopped breathing and had to be intubated. Injudicious use of opiates can result in excessive sedation and loss of respiratory drive.
Although useful in small doses for relieving anxiety, opiates provide little or no direct hemodynamic benefit in patients with pulmonary edema.
EBMedicine.net • December 2006
10. “She felt a little better after the Lasix, so we
sent her home.”
But when she came back the next day in florid
pulmonary edema, she ended up in the CCU.
There is growing evidence that premature release
of patients with inadequately treated heart failure
is associated with increased short-term morbidity
and mortality. While published guidelines can
help guide the decision to admit, it is important
to recognize that even “low-risk” patients have
considerable potential for morbidity.
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Emergency Medicine Practice©
any ischemic ECG changes, but you changed her disposition to a step-down unit for closer monitoring.
You decided to send a BNP test on the obese
woman in the next room since it was unclear
whether she was presenting with a COPD exacerbation or ADHF. The BNP returned at 1100 pg/dl confirming a diagnosis of ADHF. You informed her of
your clinical diagnosis and she improved after
administration of nitroglycerin and furosemide. She
called you back into the room later to tell you that
she remembers taking a “water pill” in the past for
similar symptoms but was not restarted on this medication when she moved to your town. This further
confirmed your clinical diagnosis.
Remembering that “less is more” for patients
with low output failure, you immediately called the
cardiologist of the woman with recent fatigue, confusion, and an ejection fraction of 20%. You discussed
the role of inotropes with her cardiologist and agreed
to “hold off” on inotropes in the ED, but immediate
admission to the ICU for monitoring was necessary.
Prior to her disposition, you confirmed that her urinalysis and chest x-ray did not show signs of infection to account for her fatigue and mild confusion.
At the end of your busy shift, you reflected upon
the diverse presentation of patients with ADHF and
the importance of tailoring therapy to a specific syndrome.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
References
13.
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight
than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such
as the type of study and the number of patients in
the study, will be included in bold type following the
reference, where available.
1.
2.
14.
15.
16.
Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005
Guideline Update for the Diagnosis and Management of
Chronic Heart Failure in the Adult: 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): developed in collaboration with the American
College of Chest Physicians and the International Society for
Heart and Lung Transplantation: endorsed by the Heart
Rhythm Society. Circulation 2005;112(12):e154-235.
(Conesensus statement)
Heart Failure Society of America. Executive summary: HFSA
Emergency Medicine Practice©
17.
18.
20.
21.
28
2006 Comprehensive Heart Failure Practice Guideline. J Card
Fail 2006:12(1)10-38. (Review)
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(4):384416. (Consensus statement)
Maisel AS, Kirsiknaswany P, Nowak R et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis
of heart failure. N Engl J Med 2002;347:161-169.
(Retrospective, descriptive; 105,388 patients)
Maisel A. B-type natriuretic peptide measurements in diagnosing congestive heart failure in the dyspneic emergency
department patient. Rev Cardiovasc Med 2002;3 Suppl 4:S10-7.
(Prospective, observational; 1586 patients)
Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type
natriuretic peptide in the evaluation and management of
acute dyspnea. N Engl J Med 2004;350(7):647-54. (Prospective,
randomized, controlled; 452 patients)
Fonarow GC. Strategies to improve the use of evidence-based
heart failure therapies: OPTIMIZE-HF. Rev Cardiovasc Med
2004;5 Suppl 1:S45-54. (Review)
Investigators V. Intravenous nesiritide vs nitroglycerin for
treatment of decompensated congestive heart failure: a randomized controlled trial. JAMA 2002;287(12):1531-40.
(Randomized double-blind; 489 patients)
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December 2006 • EBMedicine.net
patients with heart failure. Circulation 2000;101(12):e122.
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87. Which of the following excludes a patient from a
trial of CPAP?
a. Hemodynamic stability
b. Renal failure
c. Normal ECG
d. Severe agitation
88. Which of the following tests has been shown to correlate with left ventricular overload, severity of clinical heart failure, and both short- and long-term cardiovascular mortality in heart failure patients?
a. Pulmonary edema on CXR
b. CRP
c. BNP
d. D-dimer ELISA
CME Questions
89. All of the following indicators are prognostic factors
in post-discharge mortality and risk for re-hospitalization EXCEPT:
a. Elevated troponin
b. Hypokalemia
c. Renal insufficiency (Cr greater than 2.7)
d. Hypotension (SBP less than 115)
81. Acute diastolic dysfunction primarily involves
impairment of:
a. Myocardial contractility
b. Ventricular filling
c. Atrioventricular conduction
d. Systemic vascular resistance
90. What percentage of patients who are admitted with
ADHF have preserved systolic dysfunction?
a. 10%
b. 30%
c. 50%
d. 80%
82. Mild respiratory distress with a normal mental status
and hypertension in the prehospital setting can best
be addressed with which of the following:
a. Prone positioning
b. Continuous high-dose Lasix® infusion
c. CPAP
d. Endotracheal intubation
91. Which of the following is a true statement?
a. A normal ECG makes left diastolic dysfunction
unlikely.
b. ST segment elevations in a patient with decompensated heart failure is a contraindication for
thrombolytic therapy.
c. Clinical findings usually lag behind CXR findings
in heart failure patients.
d. Hilar vessels are usually “full” and the hilum is
convex in heart failure.
83. Which of the following tests is unlikely to be helpful
in patients presenting with acutely decompensated
heart failure?
a. Cardiac enzymes
b. BUN / creatinine
c. Free T4 level
d. CBC
e. BNP or NT-proBNP levels
92. An ideal drug (or drug combination) for the treatment of acutely decompensated heart failure would
do which of the following?
a. Reduce preload
b. Enhance left ventricular function
c. Maintain or improve myocardial oxygen balance
d. All of the above
84. Cardiogenic shock is most often seen in the setting
of:
a. Acute ST-elevation MI
b. Ventricular septal rupture
c. Pericardial tamponade
d. Mitral valve chordae rupture
85. A patient with new cardiac murmur and acute onset
of heart failure needs to have the following study
performed emergently:
a. Chest CT
b. Cardiac MRI
c. Transesophageal echocardiography
d. Transthoracic echocardiography
93. Which of the following statements is true?
a. Morphine’s main effect is through its peripheral
vasodilating effect.
b. Morphine may cause respiratory depression and
increase the incidence of intubation.
c. Diuretics are more important than nitrates in
managing volume overload.
d. Furosemide has no vasodilating properties.
86. Which medication improves congestive symptoms of
heart failure most rapidly?
a. Nitrates
b. Beta-blockers
c. Diuretics
d. Amiodarone
EBMedicine.net • December 2006
94. According to the BASEL study, incorporating BNP in
the diagnosis of ADHF contributes to all of the following outcomes EXCEPT:
a. Reduced hospital costs
b. Decreased admissions to ICU level care
c. Reduced time to treatment
d. Reduced length of stay
35
Emergency Medicine Practice©
Physician CME Information
95. What percentage of patients admitted to the hospital
with ADHF will present to the emergency department?
a. 50%
b. 70%
c. 80%
d. 90%
Accreditation: This activity has been planned and implemented in accordance with
the Essentials and Standards of the Accreditation Council for Continuing Medical
Education (ACCME) through the joint sponsorship of Mount Sinai School of
Medicine and Emergency Medicine Practice. The Mount Sinai School of Medicine
is accredited by the ACCME to provide continuing medical education for physicians.
Credit Designation: The Mount Sinai School of Medicine designates this educational activity for a maximum of 48 AMA PRA Category 1 Credit(s)TM per year.
Physicians should only claim credit commensurate with the extent of their participation in the activity. Credit may be obtained by reading each issue and completing the printed post-tests administered in December and June or online singleissue post-tests administered at EBMedicine.net.
96. All of the following conditions are known to affect
the cut points of BNP in diagnosing ADHF EXCEPT:
a. Diabetes
b. Age
c. Renal function
d. BMI
Target Audience: This enduring material is designed for emergency medicine physicians.
Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of
prior activities for emergency physicians.
Date of Original Release: This issue of Emergency Medicine Practice was published December 1, 2006. This activity is eligible for CME credit through
December 1, 2009. The latest review of this material was November 20, 2006.
Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that is
outside Food and Drug Administration approved labeling. Information presented as
part of this activity is intended solely as continuing medical education and is not
intended to promote off-label use of any pharmaceutical product. Disclosure of OffLabel Usage: This article discusses the administration of calcium sensitizers,
vasopressin antagonists, endothelin antagonists, and novel natriuretic peptide
agents for the treatment of acutely decompensated heart failure. However, it is not
the intention of this article to promote the off-label use of these agents for the
treatment of acute decompensated heart failure outside the context of an
approved clinical trial.
Coming in Future Issues:
Delirium And Agitation
Oncologic Emergencies
Pediatric Toxicology
Class Of Evidence Definitions
Faculty Disclosure: It is the policy of Mount Sinai School of Medicine to ensure
objectivity, balance, independence, transparency, and scientific rigor in all CMEsponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any relevant financial relationships and to assist in resolving any conflict of interest that
may arise from the relationship. Presenters must also make a meaningful disclosure to the audience of their discussions of unlabeled or unapproved drugs or
devices.
Each action in the clinical pathways section of Emergency Medicine
Practice receives a score based on the following definitions.
Class I
• Always acceptable, safe
• Definitely useful
• Proven in both efficacy and
effectiveness
Level of Evidence:
• One or more large prospective
studies are present (with rare
exceptions)
• High-quality meta-analyses
• Study results consistently positive
and compelling
Class II
• Safe, acceptable
• Probably useful
Level of Evidence:
• Generally higher levels of evidence
• Non-randomized or retrospective
studies: historic, cohort, or casecontrol studies
• Less robust RCTs
• Results consistently positive
Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative
treatments
Level of Evidence:
• Generally lower or intermediate
levels of evidence
• Case series, animal studies, consensus panels
• Occasionally positive results
In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for
this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Kosowsky, Dr. Chan, Dr. Toscano, and Dr. Hermann
report no significant financial interest or other relationship with the manufacturer(s)
of any commercial product(s) discussed in this educational presentation.
Indeterminate
• Continuing area of research
• No recommendations until further
research
For further information, please see The Mount Sinai School of Medicine website at
www.mssm.edu/cme.
ACEP Accreditation: Emergency Medicine Practice is approved by the American
College of Emergency Physicians for 48 hours of ACEP Category 1 credits per
annual subscription.
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling
AAFP Accreditation: Emergency Medicine Practice has been reviewed and is
acceptable for up to 48 Prescribed credits per year by the American Academy of
Family Physicians. AAFP Accreditation begins August 1, 2006. Term of approval is
for two years from this date. Each issue is approved for 4 Prescribed credits.
Credits may be claimed for two years from the date of this issue.
Significantly modified from: The
Emergency Cardiovascular Care
Committees of the American Heart
Association and representatives
from the resuscitation councils of
ILCOR: How to Develop EvidenceBased Guidelines for Emergency
Cardiac Care: Quality of Evidence
and Classes of Recommendations;
also: Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency
Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring effectiveness of community-wide emergency cardiac care. JAMA
1992;268(16):2289-2295.
AOA Accreditation: Emergency Medicine Practice has been approved for 48
Category 2B credit hours per year by the American Osteopathic Association.
Earning Credit: Two Convenient Methods
• Print Subscription Semester Program: Paid subscribers with current and valid
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Medicine Practice six-month testing period, complete the post test and the CME
Evaluation Form distributed with the December and June issues, and return it
according to the published instructions are eligible for up to 4 hours of Category 1
credit toward the AMA Physician’s Recognition Award (PRA) for each issue. You
must complete both the post test and CME Evaluation Form to receive credit.
Results will be kept confidential. CME certificates will be delivered to each participant scoring higher than 70%.
• Online Single-Issue Program: Paid subscribers with current and valid licenses in
the United States who read this Emergency Medicine Practice CME article and
complete the online post test and CME Evaluation Form at EBMedPractice.net are
eligible for up to 4 hours of Category 1 credit toward the AMA Physician’s
Recognition Award (PRA). You must complete both the post-test and CME
Evaluation Form to receive credit. Results will be kept confidential. CME certificates may be printed directly from the Web site to each participant scoring higher
than 70%.
Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.
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Emergency Medicine Practice (ISSN Print: 1524-1971, ISSN Online: 1559-3908) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions
expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein
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December 2006 • EBMedicine.net