Download Full Topic PDF

EMERGENCY MEDICINE PRACTICE
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
February 2002
Acutely Decompensated
Heart Failure: Diagnostic
And Therapeutic Strategies
For The New Millennium
Volume 4, Number 2
Authors
Joshua M. Kosowsky, MD
Department of Emergency Medicine, Brigham and
Women’s Hospital, Boston, MA.
11 p.m.: You begin your shift. An elderly patient with shortness of breath has “CHF”
written all over her. She looks and sounds “wet.” She gets the usual: oxygen, furosemide, and nitrates. 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 start to wonder,
“Do I need to get cardiac enzymes? She really looks so good now—does she even need to
be admitted?”
A
CUTELY decompensated heart failure is one of the most common
cardiac emergencies encountered in the ED. Because patients with heart
failure are seen so frequently, our evaluations can become perfunctory and our
therapy homogenized. The fact is, patients with acutely decompensated heart
failure represent a diverse group that share common features, among them high
morbidity and mortality. Failure to appreciate and address the subtleties of an
individual exacerbation of heart failure 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 stabilization, differential diagnosis, pharmacologic and
adjunctive therapies, and appropriate disposition of the individual patient.
Epidemiology, Etiology, And Definitions
As a result of the aging of the U.S. population, the overall prevalence of heart
failure is rising.1 At the same time, advances in outpatient medical therapy are
allowing patients with chronic heart failure to survive despite advanced stages
of hemodynamic compromise. Nearly 5 million Americans have heart failure,
and approximately 550,000 new cases arise each year.2 Heart failure now
accounts for close to 1 million inpatient admissions annually and represents the
Editor-in-Chief
Stephen A. Colucciello, MD, FACEP,
Assistant Chair, Director of
Clinical Services, Department of
Emergency Medicine, Carolinas
Medical Center, Charlotte, NC;
Associate Clinical Professor,
Department of Emergency
Medicine, University of North
Carolina at Chapel Hill, Chapel
Hill, NC.
Associate Editor
Andy Jagoda, MD, FACEP, Professor
of Emergency Medicine; Director,
International Studies Program,
Mount Sinai School of Medicine,
New York, NY.
Editorial Board
Judith C. Brillman, MD, Residency
Director, Associate Professor,
Department of Emergency
Medicine, The University of
New Mexico Health Sciences
Center School of Medicine,
Albuquerque, NM.
W. Richard Bukata, MD, Assistant
Clinical Professor, Emergency
Medicine, Los Angeles County/
USC Medical Center, Los Angeles,
CA; Medical Director, Emergency
Department, San Gabriel Valley
Medical Center, San Gabriel, CA.
Francis M. Fesmire, MD, FACEP,
Director, Chest Pain—Stroke
Center, Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Valerio Gai, MD, Professor and Chair,
Department of Emergency
Medicine, University of Turin, Italy.
Michael J. Gerardi, MD, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Children’s Medical
Center, Atlantic Health System;
Vice-Chairman, Department of
Emergency Medicine, Morristown
Memorial Hospital.
Michael A. Gibbs, MD, FACEP,
Residency Program Director;
Medical Director, MedCenter Air,
Department of Emergency
Medicine, Carolinas Medical
Center; Associate Professor of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine, University
of Michigan Medical School, Ann
Arbor, MI; President, American
Physicians Assurance Society, Ltd.,
Bridgetown, Barbados, West Indies;
Past President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/
Emergency Medicine, UCLA
School of Medicine; Attending
Leo Kobayashi, MD
Department of Emergency Medicine, Brigham and
Women’s Hospital, Boston, MA.
Peer Reviewers
Francis M. Fesmire, MD
Director, Heart-Stroke Center, Chattanooga, TN.
Christopher J. Rosko, MD, FACEP
Medical Director, Department of Emergency
Medicine, University of Alabama at Birmingham,
Birmingham, AL.
CME Objectives
Upon completing this article, you should be able to:
1. describe the basic pathophysiology of acutely
decompensated heart failure;
2. identify the common and life-threatening
precipitants of acutely decompensated
heart failure;
3. explain the management of acutely
decompensated heart failure in the prehospital
and ED settings, including the role of
diuretics, vasodilators, inotropes, and
noninvasive ventilatory support; and
4. describe the role of risk stratification in
determining the disposition of patients with
acutely decompensated heart failure.
Date of original release: February 1, 2002.
Date of most recent review: January 18, 2002.
See “Physician CME Information” on back page.
Physician, UCLA Emergency
Medicine Center; Co-Director,
The Doctoring Program,
UCLA School of Medicine,
Los Angeles, CA.
John A. Marx, MD, Chair and Chief,
Department of Emergency
Medicine, Carolinas Medical
Center, Charlotte, NC; Clinical
Professor, Department of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Michael S. Radeos, MD, MPH, FACEP,
Attending Physician in
Emergency Medicine, Lincoln
Hospital, Bronx, NY; Research
Fellow in Emergency Medicine,
Massachusetts General Hospital,
Boston, MA; Research Fellow in
Respiratory Epidemiology,
Channing Lab, Boston, MA.
Steven G. Rothrock, MD, FACEP, FAAP,
Associate Professor
of Emergency Medicine, University
of Florida; Orlando Regional
Medical Center; Medical Director of
Orange County Emergency
Medical Service, Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Department of Emergency
Medicine, Vanderbilt University
Hospital, Nashville, TN.
Mark Smith, MD, Chairman,
Department of Emergency
Medicine, Washington Hospital
Center, Washington, DC.
Charles Stewart, MD, FACEP,
Colorado Springs, CO.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
Emergency Medicine, University
of Alabama at Birmingham,
Birmingham, AL.
patients. Systolic failure is a physiologic state characterized
by impaired cardiac contractility—typically defined as an
ejection fraction less than 40%. In the case of diastolic failure,
the ejection fraction is normal or supranormal, but myocardial relaxation is impaired, preventing proper filling of
the ventricle.
Forward failure is a clinical constellation of symptoms
representing inadequate tissue perfusion, the extreme
example of which is cardiogenic shock. Pulmonary edema,
peripheral edema, and congestive hepatomegaly distinguish backward failure.
Right heart failure involves impaired return of blood to
central venous circulation (as evidenced by neck vein
distention, dependent extremity edema, and hepatomegaly).
It is most commonly a consequence of severe left heart failure
but can also occur in isolation (as in the case of cor pulmonale) or result from right ventricular infarction. High-output
failure is caused by excessive demand for tissue perfusion
resulting in hyperdynamic cardiac dysfunction, as seen with
sepsis, thyrotoxicosis, and beri-beri. Low output failure,
distinguished by a low cardiac output, is the more common
presentation of heart failure.
The severity of failure can be described in many ways,
which may include a measure of how chronic failure affects
the quality of life or more acute clinical parameters. Table 2
on page 3 describes the new American Heart Association
classification, the commonly used New York Heart Association (NYHA) classification, and the Killip classification
(originally used to predict outcome after acute MI).
number-one reason for hospitalization among the growing
elderly population.2
Symptoms of decompensated heart failure commonly
cause patients to seek emergency care. The National
Hospital Ambulatory Medical Care Survey reported 1.5
million ED visits in 1999 for non-ischemic heart disease, of
which a significant proportion were related to heart failure.3
One retrospective analysis of 2 million ED visits over an 11year period revealed approximately 1.1% of visits to have a
primary diagnosis of heart failure or pulmonary edema.4
Short-term outcomes for patients admitted to the
hospital with decompensated heart failure have held fairly
constant over the past two decades. In-hospital mortality
remains approximately 7%, with major adverse events
occurring in up to 18% of patients.5-7 For those patients who
present with frank pulmonary edema, the corresponding
rates of morbidity and mortality are approximately
double.8-11 Patients who present with acute myocardial
infarction and cardiogenic shock have a mortality rate of
70% or more despite aggressive therapy.12 Less is known
about the outcomes of patients who are sent home from the
ED. In a recent study of 112 patients discharged from the ED
with a primary diagnosis of heart failure, more than 60%
experienced another ED visit, hospitalization, or death
within 90 days of the index visit.13
The etiologies of heart failure are numerous and
diverse. (See Table 1.) In the United States, the vast majority
of heart failure arises as a consequence of coronary artery
disease and/or long-standing hypertension. In the ED,
acute heart failure can present de novo—for example, in
acute myocardial infarction (MI) or with acute valvular
insufficiency. Much more commonly, patients seen in the ED
have chronic heart failure that has decompensated as the
result of one or more precipitating factors.
Chronic heart failure is a complex and multifaceted
syndrome with variable clinical presentations and overlapping systems of classification. Differentiating among these
can be helpful in evaluating and managing individual
Pathophysiology
Regardless of etiology, inadequate cardiac function triggers
a common set of compensatory mechanisms. These are
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 resulting from
some precipitant or stress.
High circulating levels of aldosterone, vasopressin,
epinephrine, and norepinephrine are ultimately maladaptive, as tachycardia and vasoconstriction compromise the
performance of the left ventricle (LV) and simultaneously
worsen myocardial oxygen balance. Deteriorating left
ventricular function results in further neurohormonal
activation and self-perpetuation of this adverse cycle. (See
Figure 1 on page 3.)
Pathophysiologic considerations notwithstanding,
acutely decompensated heart failure is a poorly defined
clinical entity, and no universal definition exists.14 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. However it is
defined, the number of heart failure patients who present to
the ED with clinical decompensation is likely to increase
over the coming years.
Table 1. Etiologies Of Heart Failure.
Coronary artery disease
Hypertension
Valvular disease
Cardiomyopathy
• Idiopathic cardiomyopathy
• Alcoholic cardiomyopathy
• Toxin-related cardiomyopathy (e.g., adriamycin)
• Postpartum cardiomyopathy
• Hypertrophic obstructive cardiomyopathy (HOCM)
• Tachyarrhythmia-induced cardiomyopathy
Infiltrative disorders (e.g., amyloid)
Congenital heart disease
Pericardial disease
Hyperkinetic states
• Anemia
• Arteriovenous fistula
• Thyroid disease
• Beri-beri
Emergency Medicine Practice
2
February 2002
State Of The Literature
empiric or based on observational studies and small caseseries reports. The American College of Cardiology/
American Heart Association (ACC/AHA) and the Agency
for Health Care Policy and Research (AHCPR) have
published practice guidelines that are based, in part, on the
aforementioned literature.16,17
Unfortunately, controlled trials provide few data to direct
the optimal diagnosis and management of patients with
acutely decompensated heart failure. In general, clinical
trials have focused on heart failure arising in the context of
acute MI, although this subgroup represents 15% or fewer of
patients hospitalized with heart failure.11,15 Much of the
literature on severely decompensated heart failure concerns
the management of patients after they have been admitted
to the CCU. Care of patients in the ED—particularly for
those with mild-to-moderate symptoms—remains largely
Differential Diagnosis
Decompensated heart failure can coexist with or closely
mimic a number of other cardiac, respiratory, and systemic
illnesses. (See Table 3 on page 4.) In fact, when patients
Table 2. Classifications Of Heart Failure.
American Heart Association Classification
Class
Stage A
Stage B
Stage C
Stage D
Description
Patients are at high risk for heart failure but have not developed structural heart disease and have no symptoms.
Patients have developed structural heart disease but have not (yet) developed symptoms.
Patients with past or current heart failure symptoms in association with structural damage to the heart.
Patients with end-stage, or terminal, heart failure requiring specialized treatment strategies.
New York Heart Association Classification
Class
I
II
III
IV
Functional state
No limitation
Slight limitation
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
Killip Classification
Class
Killip class I
Killip class II
Killip class III
Killip class IV
Description
No evidence of pulmonary congestion or shock.
Mild pulmonary congestion (patients had rales up to 50% of each lung field ) or an isolated S3 gallop.
Pulmonary edema (rales more than 50% up).
Hypotension and evidence of shock.
Sources: Hunt HA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive
summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the
1995 Guidelines for the Evaluation and Management of Heart Failure). Circulation 2001;104: 2996-3007; and Killip T, Kimball JT. Treatment of
myocardial infarction in coronary care unit. A two-year experience with 250 patients. Am J Cardiol 1967;20:457-467.
Figure 1. Heart Failure Pathophysiology Diagram.
decreased cardiac output
increased pulmonary capillary wedge pressure
➤
➤
➤
symptomatic
decompensation
activation of renin-angiotensin system
activation of sympathetic nervous system
➤
cardiac ischemia
decreased left ventricle function
➤
increased heart rate
increased systemic vascular resistance
increased preload
February 2002
3
Emergency Medicine Practice
and non-diagnostic chest radiographs. Bedside peak flow
measurements may prove useful in these cases.22 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.22 While ETCO2 levels for
heart failure patients differ significantly from those of
asthma/COPD patients, once again, there is no single
ETCO2 level that can reliably differentiate between the two
conditions.23 In heart failure patients, pulmonary embolism
may be clinically indistinguishable from an acute deterioration of underlying failure.24
Precipitating factors for decompensation should be
sought in a careful and deliberate fashion. (See Table 4.)
Ischemia/infarction and noncompliance with medications
or dietary restrictions are the most common causes of
clinical decompensation.10,15,25-28 The exact prevalence of such
precipitants 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
decompensated heart failure can arise as a consequence of
non-cardiac conditions such as sepsis, anemia, alcohol
withdrawal, uncontrolled diabetes, or thyroid disease.
present to the ED with undifferentiated dyspnea, the
diagnosis of heart failure is often overlooked.19 Patients
who present with mild or nonspecific symptoms pose
a particular diagnostic challenge. Symptoms such as
weakness, lethargy, fatigue, anorexia, or lightheadedness
may actually be a manifestation of decreased cardiac
output.20 Older patients frequently lack typical signs and
symptoms of heart failure.21 These features may be obscured
by the aging process itself or by the presence of coexisting
medical conditions.
Distinguishing heart failure from other life-threatening
conditions may be as difficult as identifying its atypical or
subtle presentations. However, if an adequate history and
physical exam are not suggestive of heart failure, and both the
chest radiograph and the ECG are normal, heart failure is unlikely.
Patients presenting with acute exacerbations of either
cardiac dysfunction or chronic obstructive pulmonary
disease (COPD) may have wheezing on pulmonary
auscultation with signs of chronic right-sided heart failure
Table 3. Differential Diagnosis Of Acutely
Decompensated Heart Failure.
Cardiovascular
• Acute myocardial infarction
• Unstable angina
• Acute valvular/septal rupture
• Aortic dissection
• Arrhythmia
• Critical aortic stenosis
• Endocarditis/myocarditis
• Hypertensive crisis
• Pericardial tamponade/effusion
“Out-worn heart, in a time out-worn,
Come clear of the nets of wrong and right;
Laugh, heart, again in the gray twilight.”
—William Butler Yeats (1865–1939), “Into the Twilight.”29
Prehospital Care
Pulmonary
• COPD
• Pulmonary thromboembolism
• Multilobar pneumonia
• Acute respiratory distress syndrome (ARDS)
Even before patients reach the hospital, decompensated
heart failure is associated with significant morbidity and
mortality, including malignant arrhythmias and prehospital
cardiac arrest.30 All patients should have continuous cardiac
monitoring and intravenous access established if possible.
(See also “Clinical Pathway: Prehospital Therapy For
Acutely Decompensated Heart Failure” on page 13.)
Because successful management depends on reversal of
hypoxia, pulse oximetry and supplemental oxygen should
be utilized routinely in the prehospital care of patients with
decompensated heart failure. Prehospital personnel should
radio ED staff for any patient presenting with symptoms
suggestive of pulmonary edema or cardiogenic shock and
receive on-line medical advice when appropriate.
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.32 Prehospital therapy for decompensated
heart failure requires particular caution in light of the
relatively high number of inaccurate diagnoses made in the
field. Nearly 30% of patients with respiratory distress
(presumed in the field to be cardiac in origin) are diagnosed
with a different condition once they arrive at the hospital.30,33,34 Despite these concerns, available evidence suggests
Other
• Pure volume overload
• Renal failure
• Iatrogenic (e.g., post-transfusion)
• Sepsis
Table 4. Common Precipitants Of
CHF Decompensation.
•
•
•
•
•
•
•
•
•
•
•
•
•
Medication noncompliance
Dietary indiscretion
Uncontrolled hypertension
Myocardial ischemia/infarction
Acute valvular dysfunction
Cardiac arrhythmias
Pulmonary and other infections
Administration of inappropriate medications
(e.g., negative inotropes)
Fluid overload
Missed dialysis
Thyrotoxicosis
Anemia
Alcohol withdrawal
Emergency Medicine Practice
4
February 2002
ED Evaluation
that prehospital therapy for presumed heart failure can
prevent serious complications and improve survival,
particularly for critically ill patients.30,33,34 In European
countries, where physicians commonly staff ambulances,
intensive prehospital treatment of patients with severe heart
failure confers short-term benefits.35,36
Sublingual nitroglycerin appears to be safest and most
effective of the prehospital medications used for presumed
pulmonary edema.33 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.33
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.33,37
There are few data on the prehospital use of
noninvasive ventilation (NIV). In one non-randomized
study, patients presumed to have congestive heart failure
(CHF) were given biphasic positive airway pressure (BiPAP)
by the medics during transport and compared to matched
controls treated without NIV.38 In this trial, 97% of emergency medicine technicians who used BiPAP 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.
Initial Approach
The approach to the patient with acutely decompensated
heart failure begins with stabilization of respiratory and
hemodynamic status. The emergency physician must then
rapidly exclude or treat reversible conditions. Clinical
evaluation and empiric therapy begin simultaneously with
supplemental oxygen, cardiac monitoring, pulse oximetry,
and IV access. Patients with clinical signs of exhaustion or
cyanosis despite supplemental oxygen require respiratory
support by either invasive or noninvasive means (which is
described later in the text). 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 (which is also described
later in the text). Once the initial resuscitation is under way,
further efforts should be made to identify the underlying
cause of decompensation.
History
Most patients with heart failure complain of dyspnea or
trouble sleeping. It is important to determine the degree of
dyspnea and its precipitants. Does it occur at rest? Does the
patient have paroxysmal nocturnal dyspnea (PND)? Ask the
patient how he or she has been sleeping and on how many
pillows. (Spending the night erect on the sofa is a suspicious
finding except in the most severe addict of CNN.)
The rapidity of symptom onset may suggest an
etiology for the decompensation. An abrupt deterioration
raises concern for arrhythmia, acute coronary syndrome, or
“The heart monitor, the death cricket bleeping.”
—Anne Sexton (1928-1974), U.S. poet.
“The Twelve Dancing Princesses.”29
Cost-Effective Strategies For Acutely Decompensated Heart Failure
noninvasive ventilation—especially those 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.
Certain patients with heart failure may require only an
ED “tune-up” and 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 medicines). ED
observation units for select patients may also be a costeffective alternative to traditional admission.202,203
Caveat: Most patients who present with acutely
decompensated heart failure will need hospital
admission—especially those with abnormal vital signs,
chest pain, or acute exacerbations.
3. Consider the use of furosemide infusions.
While many patients in acute heart failure respond quickly
to nitrates and bolus diuretics, some do not. According to one
study, intravenous infusions of furosemide for class IV heart
failure are a safe, effective, and economic mode of therapy,
especially in the elderly.98 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.
2. Consider the use of CPAP.
CPAP may prevent the need for intubation in some patients
with acute 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.
Caveat: Some patients are not good candidates for
4. Utilize BNPs when appropriate.
Of all of the tests available to determine the presence of
acute heart failure, BNP may be the single best investigation.
It is very sensitive and specific and can be performed at
the bedside. In the acute setting, elevated BNP levels
correlate with the diagnosis of heart failure.58 ▲
February 2002
5
Emergency Medicine Practice
tion (JVD), hepatomegaly, and peripheral edema. The
diagnostic utility of these physical exam findings and
related maneuvers is well-documented for chronic heart
failure.42,43 Studies performed in the acute setting are scarce
and tend to be limited by the lack of “gold-standard”
diagnostic criteria. Inter-observer agreement on some of
these findings is marginal, even in ideal settings.44,45
The pulmonary exam is usually helpful, but it can
sometimes be misleading. Rales, a classic finding in heart
failure, may also occur with pneumonia, interstitial lung
disease, or COPD. On the other hand, wheezing, or
“cardiac asthma,” is not uncommon in acute heart failure.
In acutely dyspneic patients, the sensitivity and specificity
of rales for LV dysfunction appears to be quite poor,
whereas the constellation of rales, an S3 gallop, and JVD is
more accurate.24
Elevated CVP is present when the top of the external or
internal jugular veins is more than 3 cm vertical distance
above the sternal angle.46 A positive hepatojugular reflux
sign is defined by a rise in the neck veins of greater than 3
cm, sustained for more than 15 seconds, that occurs when
the physician pushes firmly on the patient’s epigastrium.47
In one study, ED patients with acute dyspnea, presence of
hepatojugular reflux had a reported sensitivity and specificity of 24% and 96%, respectively, for heart failure.19 A
MEDLINE review of the hepatojugular sign found that it is
positive in a variety of conditions, including constrictive
pericarditis, right ventricular infarction, restrictive cardiomyopathy, and left ventricular failure (but only when the
pulmonary capillary wedge pressure is greater than 15).47
Heart sounds can be helpful in confirming the diagnosis of heart failure. In one study of patients with chronic
heart failure, an S3 gallop was highly predictive of an
abnormal ejection fraction. The absence of an S3, however,
was not uncommon in those with a mildly impaired
ejection fraction.48 A new cardiac murmur in the proper
context must be presumed to signal acute valvular or
papillary muscle dysfunction.
The leg examination is routine in the evaluation of
patients with suspected heart failure. While pedal edema is
highly specific for increased filling pressures, it has poor
sensitivity.43 Unilateral extremity swelling and especially the
presence of a venous cord should raise suspicion for deep
venous thrombosis and possible pulmonary embolism.
valvular rupture. Prior episodes of a similar nature can
provide important clues.
Associated symptoms are also important. Determine
whether the patient has had any chest pain or other anginal
equivalent such as shoulder, neck, arm or epigastric
discomfort. The combination of syncope and heart failure is
worrisome and is associated with high one-year mortality
rate.39 Ask the patient and family about recent weight gain,
leg swelling, urinary output, exercise tolerance, fatigue, and
compliance with diet and medications. New prescriptions or
changes in dosage of suspect drugs such as NSAIDs,
ophthalmic beta-blockers, herbals, and over-the-counter
agents should be sought.
Medication history is also important in determining
therapy. Specifically ask male patients with congestive
failure if they are currently taking sildenafil (Viagra). The
administration of nitrates may cause life-threatening
hypotension in such individuals.40
Most patients presenting with decompensated
heart failure will have a prior cardiac history. Patients
can generally tell you if they have had “fluid on the lungs”
in the past. More sophisticated patients may be able
to provide details of previous echocardiograms or
cardiac catheterizations.
“heart, n. Figuratively, this useful organ is said to be
the seat of emotions and sentiments . . . .
It is now known that sentiments and emotions
reside in the stomach, being evolved from food
by chemical action of the gastric fluid.”
—Ambrose Bierce (1842-1914) U.S. journalist,
short-story writer; The Devil’s Dictionary, 1911.29
Physical Examination
The patient’s degree of distress should be determined early
in the encounter; severe pulmonary edema can be a
“doorway diagnosis.” Confusion, cyanosis, diaphoresis,
inability to speak, falling over on the stretcher, and so on
should prompt a call for the airway cart.
Vital signs not only suggest the severity of illness but
can also indicate etiologic factors. Hyperthermia or hypothermia can occur with sepsis or thyroid disease. In the
absence of rate-controlling pharmacologic agents, tachycardia is nearly universal in decompensated heart failure.
Bradycardia should raise concern for high-degree AV block,
hyperkalemia, digoxin (or other drug) toxicity, or severe
hypoxia. Hypertension is common in both systolic and
diastolic failure. While hypotension can be baseline for
patients with end-stage cardiomyopathy, in the symptomatic patient it should raise concern for sepsis, massive
pulmonary embolism, or cardiogenic shock. The proportional pulse pressure (PPP)—i.e., pulse pressure (systolic
minus diastolic pressure) divided by systolic blood pressure—provides an approximation of left ventricular
function, a PPP of less than 25% correlating with a cardiac
index less than 2.2 L/min/m2.19,41
Signs of congestion may be detected by careful
attention to heart and lung sounds, jugular venous disten-
Emergency Medicine Practice
Diagnostic Studies
Laboratory Tests
The majority of patients who present with complaints
consistent with heart failure will need basic laboratory
testing. A complete blood count (CBC) or other measurement of hemoglobin is useful for ruling out anemia as a
cause for decompensation. Some believe that an elevated
white blood cell count may suggest an infectious process,
especially if bands are present. However, this is not wellstudied in the patient who presents with dyspnea. Serum
chemistries help assess renal function and overall fluid and
electrolyte balance.
6
February 2002
Cardiac Markers
Electrocardiogram
The question as to which patients with acutely decompensated heart failure should get cardiac enzymes is not wellstudied. If an acute coronary syndrome is a consideration
(e.g., history of chest discomfort or other anginal equivalent,
new-onset heart failure, or significant risk factors for
coronary artery disease), serum markers for cardiac
ischemia/infarction (CK, CK-MB, and troponin) are
indicated. Elevated troponins may detect cardiac myolysis
(possibly secondary to myocardial wall strain) even in the
absence of coronary artery disease.49 Other studies show
that elevated cardiac troponins may be found in the blood of
25%-33% of patients with severe heart failure and help to
identify those with poor short-term prognosis.50
While the ECG is admittedly a relatively insensitive
tool, it remains useful for detecting ischemia, arrhythmias,
or electrolyte disturbances. Given the high proportion
of heart failure exacerbations precipitated by ischemic
events, it is difficult to justify not obtaining an ECG on all
such patients.15
The ECG is likely to be abnormal in patients with heart
failure. In one study using a clinic population, left ventricular hypertrophy on resting ECG was noted in 42% and
electrocardiographic evidence of cardiac ischemia or a prior
MI was present in approximately 70%.62 Comparison with
prior ECGs may be critical, especially with patients who
have subtle changes or “baseline abnormal” tracings.
Patients with ECG evidence of acute ischemia or
infarction should be considered for emergent coronary
reperfusion therapy. Importantly, a completely normal
ECG is strong evidence against the presence of left ventricular
dysfunction and should therefore prompt consideration of
alternative diagnoses.24,63
B-Natriuretic Peptide
B-type natriuretic peptide (BNP) is an endogenous hormone
released from the ventricles in response to stretch. BNP is a
counter-regulatory hormone, offsetting the effects of
neurohormonal activation by promoting diuresis and
vasodilation. Plasma levels of BNP have been shown to
correlate with degree of left ventricular overload, severity of
clinical heart failure, and both short- and long-term
cardiovascular mortality.51-55
Of significance from an ED standpoint, plasma BNP
levels can be used to distinguish between cardiac and noncardiac causes of dyspnea.56,57 Among patients presenting
with acute dyspnea, a serum BNP level above 94 pg/mL
predicts a diagnosis of heart failure with 91% accuracy.58 In a
prospective study of 250 patients with acute dyspnea
possibly due to CHF, the mean BNP level was 1076 pg/mL
in the CHF group compared with 38 pg/mL in patients
without CHF. In this study, BNP measurement was more
accurate than any other single variable, including history,
physical, chest x-ray, or ECG.58 Using standard clinical
criteria, the treating physicians misdiagnosed heart failure
in 15 patients subsequently found to have other conditions
and failed to recognize it in 15 additional patients. BNP
would have accurately classified 29 of these 30 patients
using an 80 pg/mL cut-off.59
For patients with known heart failure, BNP levels
at any given point in time can be compared with baseline
measurements to form an independent assessment
of clinical severity and may be useful for tailoring
specific therapies.60,61,164
Chest X-ray
Combined with a clinical assessment, chest radiography has
been reported to be 92% sensitive and 91% specific for
detecting systolic dysfunction.24 The chest film may also be
useful in identifying alternative or contributing causes of
the patient’s symptomatology.
Findings on chest radiograph can 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.64
There are several pitfalls that await the unwary
physician who uses the chest film to diagnose acute heart
failure. Most importantly, heart size may be normal in acute
failure, especially if the failure originates from acute diastolic
dysfunction.43 It is also important to recognize that radiographic findings can lag several hours behind clinical signs
and symptoms.64 COPD patients may have minimal
radiographic evidence of concurrent heart failure, and
patients with prior lung injury may develop focal infiltrates
mimicking pneumonia.
Cardiac Echocardiography
Formal echocardiography is invaluable 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.
Whether or not echocardiography is indicated in all
instances of decompensated heart failure remains open to
debate.24,64 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
Other Tests
Arterial blood gases should not be routine in those with
acutely decompensated heart failure. They may be useful if
there is a concern for hypoxia and pulse oximetry is not
available or if the physician suspects hypercapnia. Patients
on digoxin should have serum levels checked.
“But the heart refuses to be imprisoned;
in its first and narrowest pulses it already tends outward
with a vast force and to immense and innumerable expansions.”
—Ralph Waldo Emerson (1803–1882), U.S. essayist, poet,
philosopher. “Circles,” in Essays, First Series (1841, repr. 1847).29
February 2002
7
Emergency Medicine Practice
the patient’s cardiac status has been adequately evaluated
previously.16 With the availability of on-call sonographers
and timely interpretation via telemedicine,
echocardiography can be made operational around the
clock.65 Guidelines for establishing an effective system for
emergency echocardiography have recently been published.66 Experience with emergency physicians performing
bedside echocardiography has generally been limited to
ruling out pericardial effusion/tamponade.67-69
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.78 Early application of monitors
such as pulse oximetry, noninvasive blood pressure, and
continuous cardiac monitoring may provide early warnings
of decompensation. While not all patients in acutely
decompensated heart failure require a Foley catheter,
monitoring of urinary output with a urinometer can be
helpful in those with severe symptoms.
Once immediate threats to airway and breathing are
addressed, the physician must deal with blood pressure
emergencies. While hypertensive emergencies resulting in
pulmonary edema are life-threatening, they are in general
more easily amenable to pharmacologic therapy than
hypotensive emergencies associated with acute heart failure.
In most cases of shock, fluid challenge is routine and
generally not harmful, yet in the case of cardiogenic shock
the literature is mute.
Pulmonary Artery Catheterization
Most patients with decompensated heart failure can be
evaluated and stabilized in the ED without the introduction
of a pulmonary artery (PA) catheter. The literature on the
risks and benefits of PA catheterization (also called SwanGanz catheterization) in critical illness continues to evolve,
but in the case of patients with decompensated heart failure,
little is known. ACC/AHA guidelines recommend placement of a PA catheter in the setting of acutely decompensated heart failure if improvement is not proceeding as
expected, if high-dose nitrates are required for clinical
stabilization, or if inotropic support is needed to augment
systemic perfusion.16 However, these guidelines were first
issued in 1995, before the publication of more recent data
regarding the dangers of PA catheterization in the critically
ill.70,71 When it is believed necessary, invasive hemodynamic
monitoring can generally be initiated in the CCU.
Pharmacologic Therapy
The twin objectives of pharmacologic therapy for acutely
decompensated heart failure are relief of pulmonary
congestion and improvement in systemic tissue perfusion.
An ideal drug (or drug combination) would reduce preload,
enhance left ventricular function, and at the same time
maintain or improve myocardial oxygen balance. While the
basic approach to treating acutely decompensated heart
failure 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
activation. (See Table 5 on page 9; see also “Clinical
Pathway: Emergency Department Therapy For Acutely
Decompensated Heart Failure” on page 14.)
“I am dying from the treatment of too many physicians.”
—Alexander the Great
Treatment
The most important initial interventions will involve
management of the airway. Patients with inadequate
respirations will most likely need emergent intubation. 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.72 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.73 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.74 Once mechanical ventilation is instituted for
cardiogenic pulmonary edema, it is not certain whether
positive end-expiratory pressure (PEEP) confers any
additional hemodynamic benefit.75-77
For patients in respiratory distress, application of highflow oxygen appears beneficial. Although there have been
reports that excessive oxygen can adversely affect left
ventricular function, hypoxia is by far the greater concern in
the acute setting.31 Sitting the patient bolt upright may
Emergency Medicine Practice
Nitrates
Nitrates are recommended as first-line therapy for acutely
decompensated heart failure of both ischemic and nonischemic origin.16 The beneficial hemodynamic effects of
nitrates in the setting of heart failure have long been
appreciated.80,81 At low doses, nitroglycerin induces
venodilation; at high doses, nitroglycerin causes
arteriodilation, including dilation of the coronary arteries.82
Significantly, in patients with severe underlying left
ventricular dysfunction, afterload reduction appears to
predominate over preload reduction, even at moderate
doses of nitroglycerin.83
A number of studies have compared the hemodynamic
effects of nitrates and diuretics in acutely decompensated
heart failure. In contrast to furosemide, nitrates reduce both
preload and afterload, and maintain or improve cardiac
output.84-86 In one head-to-head comparison, a regimen of
high-dose nitrates and low-dose diuretics provided more
consistent clinical improvement than a regimen of high-dose
diuretics and low-dose nitrates and was 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 played a role.
8
February 2002
to standard nitrate therapy.16 Nitroprusside directly dilates
resistance vessels, rapidly reducing blood pressure and
afterload.80 Typically, nitroprusside is started at a dose of 0.1
mcg/kg/min and advanced as needed to improve clinical
and hemodynamic status. Use a systolic pressure of 85-90
mmHg as a lower limit provided that adequate systemic
perfusion is maintained. In patients with renal failure, longterm use of nitroprusside carries the potential for cyanide
toxicity, as metabolites accumulate. However, this is
extremely unlikely during the course of emergency therapy.
Nitroprusside has been safely used in the ED treatment of
dialysis patients who presented in acute heart failure.95
No other group of agents improves the symptoms of
congestion as rapidly as nitrates. Treatment with sublingual
nitroglycerin (tablets or spray) results in noticeable hemodynamic and clinical improvement within five minutes.88-90
Single doses of 0.4 mg can be given repeatedly every 5-10
minutes provided the patient has stable blood pressures. In
the hospital setting, continuous IV administration of
nitroglycerin is generally more convenient and appropriate
for the more severely ill patient and allows for titration to
specific clinical or hemodynamic end-points. Nitroglycerin
can be started at 0.3-0.5 mcg/kg/min so long as the blood
pressure is above 95-100 mmHg.16 Alternative regimens and
formulations for administering IV nitrates have been
described, but they offer no clear advantages.80,91,92
Transdermal nitroglycerin has comparable hemodynamic
effects to IV nitroglycerin but is less amenable to
rapid titration and may be less effective in patients
with poor skin perfusion.93
Hypotension with standard nitrate therapy is generally
mild and transient. Severe or persistent hypotension should
raise suspicion for hypovolemia, stenotic valvular disease,
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.94 In such cases,
aggressive diuretic therapy is more likely to be of benefit.
Sodium nitroprusside is recommended for patients
with marked systemic hypertension, severe mitral or aortic
valvular regurgitation, or pulmonary edema not responsive
Diuretics
Diuretics represent the mainstay of therapy for patients with
volume overload. On the other hand, it is important to
recognize that patients who present with acutely decompensated
heart failure are not necessarily volume overloaded. Patients with
acute diastolic dysfunction, for example, may benefit more
from redistribution of circulating volume (using nitrates)
rather than from diuresis. The indiscriminate use of
diuretics carries the risk of overdiuresis, particularly among
elderly patients.
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.104-107 These
actions are not necessarily altogether advantageous, in that
their net effect tends to promote further activation of the
sympathetic and renin-angiotensin systems.108,109 Studies
comparing the acute effects of diuretics and nitrates have
Table 5. Medications For Acutely Decompensated Heart Failure.
Oxygen
Action: Improvement in systemic and myocardial
oxygen balance
Indications: Hypoxia and/or dyspnea
Cautions/Adverse Effects: Respiratory depression (COPD)
Dosing: Titrate to pulse oximetry
Indications: Severe hypertension; refractory
pulmonary edema
Cautions/Adverse Effects: Hypotension; myocardial
ischemia; cyanide toxicity
Dosing: Start 0.1-0.2 mcg/kg/min IV and titrate
upward
Morphine
Action: Relief of anxiety; preload reduction
Indications: Pulmonary edema
Cautions/Adverse Effects: Respiratory depression;
hypotension
Dosing: 2-4 mg IV boluses
Enalaprilat
Action: Afterload reduction
Indications: Pulmonary edema; hypertension
Cautions/Adverse Effects: Hypotension; hyperkalemia
Dosing: 1.25 mg IV
Dobutamine
Action: Positive inotropy; afterload reduction
Indications: Low-output heart failure; refractory
pulmonary edema
Cautions/Adverse Effects: Tachycardia; arrhythmia;
hypotension; bronchoconstriction
Dosing: Start 2.5 mcg/kg/min IV and titrate upward
Furosemide
Action: Preload reduction
Indications: Volume overload
Cautions/Adverse Effects: Hypotension; pre-renal azotemia
Dosing: Start 20-40 mg (or twice daily oral dose as IV bolus )
Nitroglycerin
Action: Preload and afterload reduction; anti-ischemic
Indications: Pulmonary edema; myocardial ischemia
Cautions/Adverse Effects: Hypotension; tolerance
Dosing: Start 0.3–0.5 mcg/kg/min IV and titrate upward
Milrinone
Action: Positive inotropy; afterload reduction
Indications: Low-output heart failure; refractory
pulmonary edema
Cautions/Adverse Effects: Arrhythmia; hypotension
Dosing: Bolus 50 mcg/kg over 10 min, then start
0.375 mcg/kg/min IV and titrate upward
Nitroprusside
Action: Afterload reduction
February 2002
9
Emergency Medicine Practice
of spironolactone substantially reduces the risk of both
morbidity and death.110 However, there is no evidence
supporting its use in the ED during an acute episode of
decompensated failure.
emphasized the more favorable overall hemodynamic
effects of the latter group (as described earlier).
Depending on the patient’s clinical condition,
state of hydration, and previous use of diuretics, an
initial IV dose of 20-200 mg of furosemide can be administered. For patients on chronic diuretic therapy, a common
strategy is to begin with the usual daily dose (typically
40-80 mg) given as an IV bolus, and to double the dose
if there is inadequate diuresis. In cases of volume overload
that fail to respond to standard therapy, substitute a
more potent loop diuretic such as torsemide (Demadex)
10-20 mg IV or bumetanide (Bumex) 1-4 mg IV. Combining
furosemide with a thiazide agent such as metolazone (5-20
mg PO) or chlorothiazide (Diuril 500-1000 mg IV) may
improve diuresis.96,97
If the patient does not respond to an initial dose or two
of diuretics, another alternative is to administer a high-dose,
continuous furosemide infusion at 20-40 mg/hr titrated to a
urine output of 100 mL/hr. This will maximize diuresis
while minimizing the toxicity of comparable bolus furosemide therapy.98 Other studies support the superiority of
continuous furosemide therapy over bolus injection,99,100
with some patients receiving up to 2 grams (yes, 2 grams) of
furosemide per day.101 (For a more detailed discussion of this
topic and further references, see the Cochrane Database of
Systematic Reviews.102)
In patients with severe chronic heart failure, regular use
ACE Inhibitors
Angiotensin-converting enzyme (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.111 Acutely, ACE
inhibitors reduce both preload and afterload, improve renal
hemodynamics, impair sodium retention, attenuate
sympathetic stimulation, and maintain or enhance left
ventricular function.112-114 In the setting of acute heart failure,
drug regimens that include an ACE inhibitor appear to
have hemodynamic advantages over those based on
other vasodilators.115-117
For acutely decompensated heart failure, ACE inhibitors can be administered intravenously (e.g., enalaprilat
[Vasotec IV]), orally (e.g., captopril), or sublingually (e.g.,
emptied captopril capsules contents). Depending on the
drug, dose, and route of administration, hemodynamic
effects may be seen within 10-60 minutes.112,113,115 Safe dosing
regimens of enalaprilat include 0.004 mg/kg as an IV bolus,
or 1.25 mg by infusion over five minutes. The suggested
one-time dose of oral or sublingual captopril is 12.5-25.0 mg.
The safety of administering an ACE inhibitor in the setting
Ten Excuses That Don’t Work In Court
important clues. Consider the use of BNP if the diagnosis is
not clear.
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! Nonspecific symptoms
such as weakness, lethargy, fatigue, anorexia, or
lightheadedness may be a manifestation of decreased
cardiac output, especially in the older patient. Geriatric
patients can be particularly difficult to evaluate because
they often lack typical signs and symptoms of heart failure.
4. “I just assumed he hadn’t been taking his medications.”
Medication noncompliance 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.
2. “She was only 35—she couldn’t have had heart failure!”
You can’t diagnose postpartum cardiomyopathy unless
you consider it. Myocarditis, cocaine or alcohol abuse,
and cardiotoxic chemotherapies are important causes of
heart failure in younger patients. While advanced age is a
major risk factor for heart failure, young age should never
exclude it.
5. “He was wide awake and looked extremely anxious. I
thought he could tolerate the 10 mg bolus of morphine!”
This patient stopped breathing and had to be precipitously
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
hemodynamic benefit in patients with pulmonary edema.
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. A careful diagnostic work-up can yield
Emergency Medicine Practice
6. “She was clearly ‘wet’ and needed to be aggressively
diuresed. Is it my fault her creatinine doubled by the
next day?”
Continued on page 11
10
February 2002
While the role of long-term inotropic therapy for chronic
heart failure remains controversial, short-term therapy in
acutely decompensated failure appears to benefit select
patients. Classically, inotropic agents have been reserved for
the treatment of cardiogenic shock. However, short-term
inotropic support may also be beneficial for patients who
fail to respond to (or who are not candidates for) conventional therapy with diuretics and vasodilators.16 While
short-term inotropic therapy clearly improves hemodynamic performance, data on clinical outcomes are limited.
In the absence of frank cardiogenic shock, inotropic
support is typically initiated using an agent that both
increases myocardial contractility and reduces afterload.
This class of “vasodilator inotropes” includes beta-agonists
such as dobutamine as well as the phosphodiesterase
inhibitors amrinone, milrinone, and enoximone. (See Table 5
on page 9.) Small trials with each of these agents have
demonstrated short-term hemodynamic improvement in
patients with acutely decompensated heart failure, most
commonly in the setting of MI.123-127 The addition of lowdose nitrate therapy to an inotropic regimen may confer
additional hemodynamic benefits.128,129 In one head-to-head
comparison in patients who sustained heart failure following an acute MI, milrinone (50 mcg/kg bolus over 10
minutes, infusion at 0.25-0.75 mcg/kg/min) appeared to
confer more consistent short-term hemodynamic improvement than dobutamine (infusion at 2.5-15.0 mcg/kg/min).130
Other evidence suggests some advantage in milrinone over
dobutamine in patients with severe heart failure even in the
absence of acute MI.131 As we see more heart failure patients
maintained on chronic beta-blocker therapy, the theoretical
Ten Excuses That Don’t Work In Court
(continued)
of acutely decompensated heart failure 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 acutely
decompensated heart failure.114,118
Few studies of ACE inhibitors for acutely decompensated heart failure have been performed in the ED setting.
Small studies have demonstrated that sublingual captopril
is safe and effective for ED patients with pulmonary
edema.95,119 In one retrospective analysis, the use of sublingual captopril in the ED was associated with lower rates of
mechanical ventilation and CCU admission.120
ACE inhibitors are contraindicated in the context of
pregnancy, hyperkalemia, or a history of ACE-inhibitorinduced 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.
Inotropes
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
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
the one may impact upon the other. If the emergency
physician believes that new-onset atrial fibrillation has
precipitated acute pulmonary edema, emergent
cardioversion is indicated.
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 that ended up
impairing her renal function and prolonging her
hospital stay.
7. “I always thought sublingual nitroglycerines were
harmless. I didn’t expect his systolic BP to drop to
single digits!”
Nitrates are fast, effective, and relatively safe, but patients
with preload-dependent conditions (e.g., valvular stenosis)
do not tolerate them well. Nor do patients taking Viagra!
10. “She felt a little better after the Lasix, so we sent
her home 10 minutes later. Her short length of stay
was impressive!”
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. ▲
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, CPAP can reduce the need for
endotracheal intubation and decrease length of ICU stay.
9. “He was in rapid atrial fibrillation, and I figured rate-
February 2002
11
Emergency Medicine Practice
case series and a recent randomized trial supports the use of
this therapy in patients with acute cardiogenic pulmonary
edema.143-147 A small, randomized trial comparing BiPAP
with CPAP demonstrated a more rapid clinical improvement with BiPAP but no difference in the rates of intubation.148 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 of similar safety concerns.149 At present, it seems
prudent to employ CPAP rather than BiPAP for patients
with cardiogenic pulmonary edema and hypoxemic
respiratory failure.150
The success of noninvasive respiratory support
depends on 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 noninvasive
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 noninvasive 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.38,151 If there is progressive respiratory failure in spite
of noninvasive support, the patient requires intubation and
mechanical ventilation.
advantages to phosphodiesterase inhibitors over betaagonists increase.132
It is important to understand the expected hemodynamic effects of inotropic agents and 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 IV
loading.123 For patients with acutely decompensated heart
failure, the only reasonable use for digoxin is to help control
the ventricular response to atrial fibrillation (as described
later in the text).
Morphine
Morphine is one of the oldest drugs still in use for the
treatment of acute heart failure and remains an important
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.133
Morphine can be administered safely to most patients.
However, because of its sedative properties and potential to
depress respirations, exercise caution 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.120
Respiratory Therapy
Special Circumstances
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.”)
Mask-applied continuous positive airway pressure
(CPAP) of 5-10cm H2O has been shown in several randomized, controlled clinical trials to reduce the need for endotracheal intubation in patients with severe cardiogenic
pulmonary edema.134-136 Pooled data also suggest that the
use of CPAP in this setting may be associated with decreased mortality.137 CPAP improves lung mechanics by
recruiting atelectatic alveoli, improving pulmonary compliance, and reducing the work of breathing.138 At the same
time, particularly in patients with CHF, CPAP improves
hemodynamics by reducing preload and afterload, thereby
enhancing left ventricular performance.139-142
BiPAP—or noninvasive positive pressure ventilation
(NPPV)—provides the physiological advantages of CPAP
during expiration but provides additional assistance with
the inspiratory work of breathing. Evidence from several
Emergency Medicine Practice
“But his flawed heart / (Alack, too weak the conflict to support!) /
‘Twixt two extremes of passion, joy and grief, / Burst smilingly.”
—William Shakespeare (1564–1616),
in King Lear, act 5, sc. 3, l. 197-200.
Cardiogenic Shock
Hypotension in the setting of decompensated heart failure is
presumed to be due to cardiogenic shock and requires
aggressive management. Regardless of blood pressure,
patients who present with evidence of inadequate tissue
perfusion (i.e., cool skin, altered mental status) should be
approached in the same manner. Mortality rates for patients
with frank cardiogenic shock remain alarmingly high,
ranging from 50% to 80%.152 Although there is a lack of data
from controlled trials regarding the optimal management of
these patients, consensus guidelines offer some direction.16
Cardiogenic shock is most often seen in the setting of
acute ST-segment elevation MI, but it occurs in other acute
coronary syndromes as well.153 In the context of acute MI,
emergent cardiac catheterization and revascularization improves
outcome and should be strongly considered.154 In the absence of
Continued on page 19
12
February 2002
Clinical Pathway: Prehospital Therapy
For Acutely Decompensated Heart Failure
• Upright sitting position (Class indeterminate)
• Oxygen therapy (Class I)
• Cardiac monitor (12-lead ECG if available; Class
indeterminate)
• IV access (Class I)
→
Impending respiratory failure?
→
• Endotracheal intubation (Class I) or CPAP if available
and no contraindications (see text) (Class II)
• Alert ED regarding patient status
→
→
→
Pulmonary edema?
Chest pain?
Arrhythmia?
→
• ASA (Class I)
• SL TNG/Nitro-Spray (Class II)
• IV morphine (Class II)
• ACLS interventions (Class I-III;
use caution with calciumchannel blockers and betablockers)
→
→
→
* These drugs can cause complications if patient is misdiagnosed as
pulmonary edema in the field
→
→
• SL TNG/Nitro-Spray (Class II)
• IV furosemide* (Class III)
• IV morphine* (Class III)
Expedite transport to the ED
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
February 2002
13
Emergency Medicine Practice
Clinical Pathway: Emergency Department Therapy
For Acutely Decompensated Heart Failure
•
•
•
•
•
•
•
Upright sitting position (Class indeterminate)
Oxygen therapy (Class I)
Chest x-ray (Class I)
Cardiac monitor and 12-lead ECG (Class I)
Pulse oximetry (Class I-II)
IV access (Class I)
Foley catheter if significant distress (Class indeterminate)
→
• Persistent respiratory distress?
Yes
→
Compromised upper airway function?
Altered level of consciousness?
Hemodynamic instability/cardiogenic shock?
Myocardial infarction or severe ischemia?
→
Yes
Endotracheal
intubation (Class I)
• Cardiogenic shock?
Yes
→
→
No
→
→
No
•
•
•
•
No
Consider CPAP
(Class II)
• Pressors/inotropes (Class II)
• Inra-aortic balloon counterpulsation (IABC) if potentially
reversible etiology (Class II)
• Cardiology consult (Class indeterminate)
→
• Acute MI, persistent cardiac
ischemia?
Yes
→
→
No
→
• Unstable tachycardia?
• ASA (Class I)
• percutaneous transluminal coronary angioplasty (PTCA)
(Class I)
• Thrombolytics (Class I-II for ST-elevation MI)
Yes
→
→
No
• Determine if patient is a candidate for cardioversion
(ventricular tachycardia or acute-onset atrial fibrillation, atrial flutter) (Class II)
• Antiarrhythmic therapy* (Class II)
*Special caution needed with beta-blockers and calciumchannel blockers due to negative inotropy
→
Go to top of next page
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
Emergency Medicine Practice
14
February 2002
Clinical Pathway: Emergency Department Therapy
For Acutely Decompensated Heart Failure
(continued)
Nitrates*
• Sublingual while starting IV or if moderate symptoms (Class II)
• Transdermal if good skin perfusion no significant diaphoresis (Class III)
• Intravenous nitroglycerin if severe distress or significant hypertension (Class I-II): start at 0.3-0.5 mcg/kg/min and titrate to
blood pressure and symptoms
*Do not use if patient taking sildenafil (Viagra)
→
Add diuretics*
• Furosemide twice daily dose intravenously or start with 40-80 mg IV (Class II)
• If inadequate urinary output, consider one or more of the following:
• Double furosemide dose (Class II)
• Add different loop diuretic (torsemide [Demadex] or bumetanide [Bumex]) (Class III)
• Add thiazide diuretic (Chlorothiazide [Diuril] or other) (Class II)
• Begin furosemide infusion: start at 20-40 mg/h, titrate to achieve urine output of 100 cc/h (Class II)
*Avoid diuretics in case of acute diastolic dysfunction (flash pulmonary edema with presumed ischemia) and in case of hypotension
→
If inadequate clinical improvement
→
Consider morphine sulfate (2-3 mg boluses) for anxiety as needed (Class II-III)
→
If inadequate clinical improvement
→
Add ACE inhibitors*
• Enalapril 1.25 mg IV given over 5 minutes (Class II-III)
• Captopril 12.5-25.0 mg PO or SL (Class II-III)
*Avoid in hypotension, pregnancy, hyperkalemia, or a history of ACE-inhibitor-induced angioedema
→
If inadequate clinical improvement
→
Add inotropes
• Milrinone (50-mcg/kg bolus over 10 minutes, infusion at 0.25-0.75 mcg/kg/min) (Class I-II)
• Dobutamine (infusion at 2.5-15.0 mcg/kg/min) (Class I-II)
→
Go to top of next page
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
February 2002
15
Emergency Medicine Practice
Clinical Pathway: Emergency Department Therapy
For Acutely Decompensated Heart Failure
(continued)
Diagnostic studies
• Cardiac enzymes: Sudden/rapid onset, anginal pain, ischemic changes on ECG, or significant risk factors for coronary artery
disease (Class II)
• B-natriuretic peptide: Possible competing diagnosis or unclear clinical picture (Class II)
• Electrolytes (Class II)
• CBC or hemoglobin (Class II-III)
→
•
•
•
•
New murmur?
Unexplained etiology for pulmonary edema?
Clinical exam suspicious for tamponade?
Shock?
→
Yes
Emergent or urgent transthoracic echocardiography depending on clinical stability (Class II)
→
Valve/septal rupture?
→
→
Pericardiocentesis (Class II)
Cardiothoracic consult (Class II)
→
→
→
→
Pericardial tamponade?
Disposition according to clinical status
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
Emergency Medicine Practice
16
February 2002
Clinical Pathway: Emergency Department Therapy
For Acutely Decompensated Heart Failure—Special Circumstances
• Atrial fibrillation/atrial flutter?
Yes
• Consider cardioversion for new-onset atrial fibrillation
(Class II; Class I if unstable patient with new-onset atrial
fibrillation)
• Rate control:
• IV/PO diltiazem (Class II)
• IV amiodarone (Class II)
• IV/PO digoxin (Class II)
Yes
•
•
•
•
•
Dialysis (Class I)
IV nitroglycerin (Class II)
IV nitroprusside (Class II)
IV/PO ACE inhibitor (Class II)
IV furosemide (Class II)
Yes
•
•
•
•
IV nitroglycerin (Class I-II)
IV nitroprusside (Class I-II)
IV/PO ACE inhibitor (Class II)
IV furosemide (Class II)
Yes
• Antibiotics (Class I)
• Pressors (Class I-II)
• Fluids (Class II)
→
→
No
• Fluid overload in renal failure?
→
→
No
• Uncontrolled hypertension?
→
→
No
• Infection/sepsis?
→
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
February 2002
17
Emergency Medicine Practice
Tool 1. Sample Discharge Instructions For ED Heart Failure Patients.
You have been evaluated and treated for symptoms of heart failure in the emergency department.
Your condition has sufficiently improved or stabilized so that you will be discharged from the
emergency department for outpatient follow-up. However, your heart failure may deteriorate once
again, in which case you should return to the emergency department.
If you experience any of the following, please return to the emergency department immediately:
1.Chest pain or discomfort
2.Progressive shortness of breath
3.Fainting or lightheadedness
4.Persistent palpitations or (new) irregular pulse
5.Significantly reduced amount of urine
6.Persistent cough
7.Wheezing
8.High fever or shaking chills
9.Any new, different, or worsening problem
Follow-up Instructions
• Return to emergency department for re-evaluation in _______ hours/days.
• Check in with your doctor (Primary Care Provider or Cardiologist) if not improved in _______ days.
• Check in with your doctor (Primary Care Provider or Cardiologist) in _______ days.
• You will need to have the following (x-rays/tests) checked in _______ days: ________________
• You may need to have an outpatient (stress test/echocardiogram). This (has/has not) been
discussed with your regular doctor.
Medications
Take the following medicines as prescribed:
__________________________________________________________________________________
__________________________________________________________________________________
__________________________________________________________________________________
__________________________________________________________________________________
Additional Instructions
1.Avoid salty foods.
2.Limit fluid/water intake as instructed (daily fluid restriction: _______ ).
3.Keep a daily measurement of your weight in a logbook for your doctor to see.
4.Visiting Nurse/Home Health Aide/Social Work/Outpatient Heart Failure Team has been arranged.
They will contact and check on you within _______ days.
5.Read through the provided heart failure materials, and contact your regular doctor if you have
any questions.
Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
Emergency Medicine Practice
18
February 2002
Continued from page 12
sis 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.
Because of their direct vascular effects, diuretics may
still have a role in managing anuric patients with volume
overload.162 Vasodilator therapy with nitrates and ACE inhibitors
has been shown to be particularly effective.95 In any dialysis
patient with an unstable cardiac rhythm, hyperkalemia and
digoxin toxicity must be considered.
An older therapy that is sometimes considered when
dialysis is unavailable and other interventions fail is the
administration of oral sorbitol (100 mg PO). This intervention draws intravascular fluid into the gut, which is then
excreted in the diarrheal stool.163
emergent catheterization, thrombolysis may be useful,
especially when given in combination with intra-aortic
balloon counterpulsation (IABC).155 Other potentially
reversible causes of cardiogenic shock, such as acute
valvular dysfunction, septal rupture, and pericardial
tamponade, need to be excluded or addressed promptly.
Non-cardiac etiologies of shock, such as hypovolemia,
sepsis, poisoning, and massive pulmonary embolism, must
also be entertained.
As mentioned previously, the use of a fluid bolus to
treat cardiogenic shock is not well-studied. While conventional wisdom holds that hypotension due to a right
ventricular infarction generally responds well to fluid
infusion, some data call this notion into question.156,157
Patients who present in shock with a normal blood
pressure or with mild hypotension often respond favorably
to dobutamine (starting at 2-3 mcg/kg/min). 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.158
Dopamine is required for patients who have severe or
persistent hypotension (systolic blood pressure < 70-80
mmHg) in the presence of volume overload or after bolus
administration of saline. At moderate doses (4-5 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.
If hypotension or clinical shock persists at dopamine
doses of 15 mcg/kg/min or greater, IABC should be
considered, presuming the patient has a potentially reversible
condition. For example, IABC can be an effective temporizing measure in anticipation of coronary revascularization or
cardiac valve repair. Likewise, a patient with massive betablocker overdose can be maintained on IABC until the drug
is metabolized or otherwise removed from the body.159 The
patients least likely to benefit from the IABC are those with
multiple previous infarctions, massive irreversible myocardial necrosis, 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 mmHg).
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.
Atrial Fibrillation
Atrial arrhythmias, and atrial fibrillation in particular, are
commonly seen in patients with chronic heart failure. In
fact, it is frequently the same underlying condition—e.g.,
hypertension, coronary artery disease, or valvular disease—
that predisposes the patient to both atrial fibrillation and
heart failure. 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. Moreover, when
atrial fibrillation is accompanied by a rapid ventricular
response, the tachycardia itself is problematic because it
means reduced filling time and increased myocardial
oxygen demand.
When assessing the patient with rapid atrial fibrillation
and acutely decompensated heart failure, it is often difficult
to attribute cause and effect. Was the onset of rapid atrial
fibrillation a response to worsening heart failure (e.g., via
neurohormonal activation and/or increased atrial stretch)?
Alternatively, did ventricular function deteriorate because
of the onset of rapid atrial fibrillation? Rather than risk
getting caught up in a “chicken-and-egg” debate, the
important point is to address the patient’s clinical status
as a whole. Often this means treating for both conditions
simultaneously, recognizing that the treatment of the one
may impact upon the other. For example, use of a betablocker or calcium-channel blocker for rate control may
have negative inotropic effects that worsen existing systolic
dysfunction. On the other hand, use of an inotropic agent
like dobutamine to enhance myocardial contractility may
result in a faster ventricular rate. In general, diltiazem
and amiodarone (and, to a lesser extent, digoxin) are
considered first-line therapies for rate control in patients
with left ventricular dysfunction.166-168 Electrical cardioversion
may be life-saving for the unstable patient who has acute atrial
fibrillation. However, maintaining sinus rhythm may not be
possible if the underlying heart failure is not addressed.
Dialysis Patients
Heart failure is present in about one-third of patients who
begin dialysis and will develop over time in an additional
25%.160 Among anuric hemodialysis patients, heart failure is
the most common cause of ED visits.161 In these patients,
acutely decompensated failure is most often due to volume
overload between dialysis treatments. Although hemodialy-
February 2002
Controversies/Cutting Edge
Impedance Cardiography
Impedance cardiography (IC) is a noninvasive means of
19
Emergency Medicine Practice
natriuretic, and neurohormonal effects when administered
in supraphysiologic doses.179-182 Studies show that nesiritide
(Natrecor), a recombinant form of BNP, improves short-term
hemodynamic function and clinical status in patients
hospitalized with decompensated heart failure.183 The FDA
has recently approved this drug for the treatment of heart
failure. Like other vasodilator agents, the major adverse
effect of nesiritide is hypotension.
Whether or not there is a role for nesiritide in the ED
remains unclear. A multicenter, randomized clinical trial of
nesiritide in an ED-based heart-failure observation-unit
setting is currently under way (PROACTION).
hemodynamic monitoring, capable of providing real-time
estimates of cardiac output and pulmonary capillary wedge
pressure by employing principles of thoracic bioimpedance.
Over the past three decades, IC 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).169,170 Because the technique is noninvasive,
portable, and capable of providing beat-to-beat information,
potential applications in the ED are numerous.171 IC is less
accurate in patients with underlying heart disease, but serial
measurements may still provide useful information—for
example, for monitoring response to therapy.170 Also, there
may be a distinct role for IC in helping to differentiate
between systolic and diastolic dysfunction.171
Calcium Sensitizers
Calcium sensitizers (levosimendan, pimobendan) are a
novel class of agents that modify the configuration of
troponin C to promote myofilament sensitivity to calcium,
enhancing contractility without impeding diastolic relaxation.184 In small studies of patients with severe decompensated heart failure, these agents have been shown to be as
effective as dobutamine and milrinone in increasing cardiac
output and reducing pulmonary capillary wedge pressure,
but without increasing myocardial oxygen demand as
conventional inotropes do.185,186 Implications for ED utilization await additional clinical trials.
Beta-blockers
Large randomized, controlled trials have demonstrated
clear benefits for long-term beta-blocker therapy in
patients with systolic heart failure.172-174 In contrast,
short-term administration of beta-blockers to patients
with severe systolic dysfunction can cause life-threatening
clinical deterioration.175 Therefore, beta-blockers are not
routinely recommended for treatment of acutely decompensated
heart failure. In the setting of an acute decompensation,
chronic beta-blocker therapy should either be temporarily
discontinued or administered cautiously at a reduced
dose. When decompensated heart failure occurs in the
context of an acute coronary syndrome, the risk of worsening heart failure must be weighed against the known
benefits of beta-blockade.176-178
Less is known about the safety and efficacy of betablocker 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. Anecdotal experience with betablockers—for example, in the management of hypertensive
crises—has been positive. Further studies are needed to
clarify the role of beta-blockers in the treatment of acute
diastolic dysfunction.
Disposition
Even in this era of cost containment, the vast majority of
patients who present with decompensated heart failure are
admitted to the hospital.18 Meanwhile, hospital costs for
inpatient care of decompensated heart failure are continuing
to rise. In 1996, an average of over $5000 was paid on behalf
of Medicare beneficiaries per hospital discharge for heart
failure.2 However, while the realities of modern healthcare
economics may not favor routine hospitalization, premature
release of inadequately treated patients is likely to increase
short-term morbidity and mortality.187 Alarmingly, a recent
outcome study of 112 patients discharged from the ED with
a primary diagnosis of CHF showed that within three
months of the initial visit, more than 60% experienced a
recurrent ED visit, hospitalization, or death.13
In general, clinicians have great difficulty judging the
prognosis of patients with exacerbations of heart failure.188
Acutely decompensated heart failure is a dynamic entity,
and the ED physician is with the patient for only a short
time. Some patients are dramatically ill at presentation but
respond rapidly to treatment, while others deteriorate after
a period of relative stability.
Previous studies have found that certain patient
characteristics predict in-hospital morbidity and mortality.
Multivariate analyses have found several independent
correlates of major complications or death during hospitalization.6,9,189,190 These include hypotension, tachypnea,
jugular venous distention, electrocardiographic abnormalities, hyponatremia, and poor initial diuresis.
A number of other characteristics have also been
correlated with in-hospital mortality.6,8-11,15,189,191-195 (See Table
6.) Disturbingly, even patients without any independent risk
B-Natriuretic Peptide
As a naturally occurring counter-regulatory hormone, BNP
also has therapeutic potential. Like the other natriuretic
peptides in its class, BNP exerts favorable hemodynamic,
Table 6. 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
Digoxin use
Advanced renal dysfunction
Poor response to initial therapy
Emergency Medicine Practice
20
February 2002
factors appear to have substantial rates (6%) of in-hospital
morbidity and mortality.6
The AHCPR has established criteria for hospitalization
of patients with heart failure.17 (See Table 7.) However, in
one study, these criteria failed to identify up to one-third of
the patients who die within 30 days.18 In this same study, the
ED physician’s clinical judgment appeared to be a better
predictor of 30-day mortality. ACC/AHA guidelines state
that in the absence of specific criteria (e.g., recent MI, symptomatic arrhythmias, marked hypokalemia), patients with “mild-tomoderate symptoms” are generally at low risk and do not require
hospital admission. Using ACC/AHA definitions, over half of
the patients admitted for heart failure may be “low risk,” yet
up to 5% of these “low-risk” admissions are associated with
an adverse cardiovascular event.196 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 decisionmaking process.
ACC/AHA guidelines explicitly allow for an observation period prior to determining a patient’s disposition.16
During this period of time, patients can be monitored for
their response to therapy and for the development of any
potentially serious adverse events. Theoretically, an EDbased observation unit or other subacute care setting can
accomplish this at substantial cost savings. Observation
units have been advanced as a safe and effective means of
reducing hospital admissions in general and heart failure
admissions in particular.197,198 Appropriate patient selection
is critical for the functioning of such units. (See Table 8.)
For patients who are ultimately discharged home,
consultation with the patient’s primary care physician and/
or cardiologist is imperative. 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.13 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.199,200 Referral to an
outpatient heart failure program where available can reduce
the frequency of ED visits and hospitalizations.201 Sample
discharge instructions are shown on page 18. ▲
Table 7. AHCPR Criteria For Hospital Admission.
3.
•
•
•
•
•
•
•
•
References
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. In addition, the most informative references cited
in the paper, as determined by the authors, will be noted by
an asterisk (*) next to the number of the reference.
1.*
2.
Myocardial ischemia
Pulmonary edema/severe respiratory distress
Hypoxia (oxyhemoglobin saturation < 90%)
Anasarca
Severe complicating medical disease
Symptomatic hypotension or syncope
Heart failure refractory to outpatient management
Inadequate social support for safe outpatient
management
4.
5.
6.*
Table 8. Observation Unit Heart Failure Protocol—
Exclusion Criteria.
7.
• Alternative diagnosis primarily responsible for acute
symptoms (e.g., chronic obstructive pulmonary disease,
pneumonia, arrhythmia)
• Acute myocardial infarction or persistent anginal
chest pain
• New persistent oxygen requirement
• Requirement for mechanical ventilation (including
noninvasive ventilatory support)
• Requirement for vasopressor/inotropic agents to support
hypotension
• Requirement for nitroprusside to control hypertension
• Requirement for emergent hemodialysis
• Severe complicating medical disease
• Inadequate social support for expected disposition to
safe outpatient management
February 2002
8.
9.
10.
11.
12.
21
Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart
J 1991;121:951-7. (Review)
American Heart Association. 2000 Heart and Stroke Statistical
Update. Washington, DC: American Heart Association; 2000.
(Review)
McCaig LF, Burt CW. National Hospital Ambulatory Medical Care
Survey (NHAMCS): 1999 Emergency Department Summary. Adv
Data 2001;320:1-36. (Epidemiologic survey)
Allegra JR. Monthly, weekly, and daily patterns in the incidence of
congestive heart failure. Acad Emerg Med 2001;8:682-685.
(Retrospective chart review; 26,224 patients)
Daley J, Jencks S, Draper D, et al. Predicting hospital-associated
mortality for Medicare patients. A method for patients with
stroke, pneumonia, acute myocardial infarction, and congestive
heart failure. JAMA 1988;260:3617-3624. (Retrospective, cohort;
5888 patients)
Chin MH, Goldman L. Correlates of major complications or death
in patients admitted to the hospital with congestive heart failure.
Arch Intern Med 1996;156:1814-1820. (Prospective, cohort;
435 patients)
Jaagosild P, Dawson NV, Thomas C, et al. Outcomes of acute
exacerbation of severe congestive heart failure: quality of life,
resource use, and survival. Arch Intern Med 1998;158:1081-1089.
(Prospective, cohort, multi-center; 1390 patients)
Plotnick GD, Kelemen MH, Garrett RB, et al. Acute cardiogenic
pulmonary edema in the elderly: factors predicting in-hospital
and one-year mortality. South Med J 1982;75:565-569. (Prospective,
observational; 55 patients)
Katz MH, Nicholson BW, Singer DE, et al. The triage decision in
pulmonary edema. J Gen Intern Med 1988;3:533-539. (Prospective,
observational; 216 patients)
Le Conte P, Coutant V, Nguyen JM, et al. Prognostic factors in
acute cardiogenic pulmonary edema. Am J Emerg Med 1999;17:329332. (Prospective, cohort; 186 patients)
Edoute Y, Roguin A, Behar D, et al. Prospective evaluation of
pulmonary edema. Crit Care Med 2000;28:330-335. (Prospective,
observational; 150 patients)
Barron HV, Every NR, Parsons LS, et al. Investigators in the
National Registry of Myocardial Infarction 2. Am Heart J 2001
Emergency Medicine Practice
Emerg Med 1999;16:18-23. (Review)
33.* Hoffman JR, Reynolds S. Comparison of nitroglycerin, morphine
and furosemide in treatment of presumed pre-hospital pulmonary
edema. Chest 1987;92:586-93. (Prospective; 57 patients)
34. Wuerz RC, Meador SA. Effects of prehospital medications on
mortality and length of stay in congestive heart failure. Ann Emerg
Med 1992;21:669-674. (Retrospective case series; 493 patients)
35. Bertini G, Giglioli C, Biggeri A, et al. Intravenous nitrates in the
prehospital management of acute pulmonary edema. Ann Emerg
Med 1997;30:493-499. (Chart review; 64 patients)
36. Gardtman M, Waagstein L, Karlsson T, et al. Has an intensified
treatment in the ambulance of patients with acute severe left heart
failure improved the outcome? Eur J Emerg Med 2000;7:15-24.
(Retrospective; 316 patients)
37. Chambers JA, Baggoley CJ. Pulmonary oedema—prehospital
treatment. Caution with morphine dosage. Med J Aust
1992;157:326-328. (Case series; 3 patients)
38. Craven RA, Singletary N, Bosken L, et al. Use of bilevel positive
airway pressure in out-of-hospital patients. Acad Emerg Med
2000;7:1065-1068. (Prospective; 62 patients)
39. Middlekauff HR, Stevenson WG, Stevenson LW, et al. Syncope in
advanced heart failure: high risk of sudden death regardless of
origin of syncope. J Am Coll Cardiol 1993 Jan;21(1):110-116. (491
patients)
40. Cheitlin MD, Hutter AD, Brindis RG, et al. Use of sildenafil
(Viagra) in patients with cardiovascular disease. Circulation
1999;99:168-177. (Consensus statement)
41. Stevenson LW, Perloff JK. The limited reliability of physical signs
for estimating hemodynamics in chronic heart failure. JAMA
1989;261:884-888. (Prospective; 50 patients)
42. Butman SM, Ewy GA, Standen JR, et al. Bedside cardiovascular
examination in patients with severe chronic heart failure:
importance of rest or inducible jugular venous distention. J Am
Coll Cardiol 1993;22:968-974. (Prospective, observational; 52
patients)
43.* Badgett RG, Lucey CR, Mulrow CD. Can the clinical examination
diagnose left-sided heart failure in adults. JAMA 1997;277:17121719. (Meta-analysis)
44. Gadsboll N, Hoilund-Carlsen PF, Nielsen GG, et al. Symptoms
and signs of heart failure in patients with myocardial infarction:
reproducibility and relationship to x-ray, radionuclide ventriculography and right heart catheterization. Eur Heart J 1989;10:10171028. (Prospective; 40 patients)
45. Lok CE, Morgan CD, Ranganathan N. The accuracy and
interobserver agreement in detecting the “gallop sounds” by
cardiac auscultation. Chest 1998;114:1283-1288. (Blinded,
prospective; 46 patients)
46. McGee SR. Physical examination of venous pressure: a critical
review. Am Heart J 1998 Jul;136(1):10-18. (Review; 78 references)
47. Wiese J. The abdominojugular reflux sign. Am J Med 2000
Jul;109(1):59-61. (Review; 20 references)
48. Patel R, Bushnell DL, Sobotka PA. Implications of an audible third
heart sound in evaluating cardiac function. West J Med 1993
Jun;158(6):606-609. (Prospective; 49 men)
49. Logeart D, Beyne P, Cusson C, et al. Evidence of cardiac myolysis
in severe nonischemic heart failure and the potential role of
increased wall strain. Am Heart J 2001 Feb;141(2):247-253.
(Comparative; 95 patients)
50. La Vecchia L, Mezzena G, Zanolla L, et al. Cardiac troponin I as
diagnostic and prognostic marker in severe heart failure. J Heart
Lung Transplant 2000 Jul;19(7):644-652. (Comparative; 34 patients)
51. Haug C, Metzele A, Kochs M, et al. Plasma brain natriuretic
peptide and atrial natriuretic peptide concentrations correlate
with left ventricular end-diastolic pressure. Clin Cardiol 1993;16:
553-557. (Comparative; 85 patients)
52. Darbar D, Davidson NC, Gillespie N, et al. Diagnostic value of Btype natriuretic peptide concentrations in patients with acute
myocardial infarction. Am J Cardiol 1996;78:284-287. (Observational; 75 patients)
53. Omland T, Aakvaag A, Bonarjee VVS, et al. Plasma brain
natriuretic peptide as an indicator of left ventricular systolic
function and long-term survival after acute myocardial infarction.
Comparison with plasma atrial natriuretic peptide and N-terminal
Jun;141(6):933-939. (Retrospective, cohort; 23,180 patients)
13.* Rame JE, Sheffield MA, Dries DL, et al. Outcomes after emergency
department discharge with a primary diagnosis of heart failure.
Am Heart J 2001;142:714-719. (Retrospective chart review; 112
patients)
14. Loh E. Maximizing management of patients with decompensated
heart failure. Clin Cardiol 2000;23 (Suppl. III):III-1-5. (Review)
15. Goldberger J, Peled H, Stroh J, et al. Prognostic factors in acute
pulmonary edema. Arch Intern Med 1986;146:489-493. (Chart
review; 94 patients)
16.* Williams JF, Bristow MR, Fowler MB, et al. Guidelines for the
evaluation and management of heart failure. Report of the
American College of Cardiology/American Heart Association
Task Force on Practice Guidelines (Committee on Evaluation and
Management of Heart Failure). Circulation 1995;92:2764-2784.
(Practice guideline)
17.* Konstam M, Dracup K, Baker D, et al. Heart Failure: Evaluation and
Care of Patients With Left-Ventricular Systolic Dysfunction. Clinical
Practice Guideline No. 11. AHCPR Publication No. 94-0612.
Rockville, MD: Agency for Health Care Policy and Research,
Public Hearth Service, U.S. Department of Health and Human
Services; June 1994. (Practice guideline)
18.* Graff L, Orledge J, Radford MJ, et al. Correlation of the Agency for
Health Care Policy and Research congestive heart failure
admission guideline with mortality: peer review organization
voluntary hospital association initiative to decrease events
(PROVIDE) for congestive heart failure. Ann Emerg Med
1999;34:429-37. (Review)
19.* Marantz PR, Kaplan MC, Alderman MH. Clinical diagnosis of
congestive heart failure in patients with acute dyspnea. Chest
1990;97:776-781. (Review and prospective study; 51 patients)
20. Ander DS, Jaggi M, Rivers E, et al. Undetected cardiogenic shock
in patients with congestive heart failure presenting to the
emergency department. Am J Cardiol 1998;82:888-891. (Prospective; 44 patients)
21. Tresch DD. The clinical diagnosis of heart failure in older patients.
J Am Geriatr Soc 1997;45:1128-1133. (Review)
22. McNamara RM, Cionni DJ. Utility of the peak expiratory flow rate
in the differentiation of acute dyspnea. Cardiac vs pulmonary
origin. Chest 1992;101:129-132. (Comparative study; 56 patients)
23. Brown LH, Gough JE, Seim RH. Can quantitative capnometry
differentiate between cardiac and obstructive causes of respiratory
distress? Chest 1998 Feb;113(2):323-326. (Prospective, observational; 42 patients)
24.* Gillespie ND, McNeill G, Pringle T, et al. Cross sectional study of
contribution of clinical assessment and simple cardiac investigations to diagnosis of left ventricular systolic dysfunction in
patients admitted with acute dyspnoea. BMJ 1997;314:936-940.
(Cross-sectional, prospective; 71 patients)
25. Ghali JK, Kadakia S, Cooper R, et al. Precipitating factors leading
to decompensation of heart failure: traits among urban blacks.
Arch Intern Med 1988;148:2013-2016. (Prospective; 101 patients)
26. Chin MH, Goldman L. Factors contributing to the hospitalization
of patients with congestive heart failure. Am J Pub Health
1997;87:643-648. (Cross-sectional chart review; 435 patients)
27. Bennett SJ, Huster GA, Baker SL, et al. Characterization of the
precipitants of hospitalization for heart failure decompensation.
Am J Crit Care 1998;7:168-174. (Chart review; 691 patients)
28. Tsuyuki RT, McKelvie RS, Arnold MO, et al. Acute precipitants of
congestive heart failure exacerbations. Arch Intern Med
2001;161:2337-2342. (Prospective; 768 patients)
29. The Columbia World of Quotations. Andrews R, Biggs M, Seidel M,
eds. New York: Columbia University Press, 1996. Also New York:
bartleby.com; 2001.
30. Tresch DD, Dabrowski RC, Fioretti GP, et al. Out-of-hospital
pulmonary edema: diagnosis and treatment. Ann Emerg Med
1983;12:533-537. (Chart review; 62 patients)
31. Mak S, Azevedo ER, Liu PP, et al. Effect of hyperoxia on left
ventricular function and filling pressures in patients with and
without congestive heart failure. Chest 2001;120:467-473.
(Controlled, prospective; 28 patients)
32.* Brazier H, Murphy AW, Lynch C. Searching for the evidence in
pre-hospital care: a review of randomized controlled trials. J Accid
Emergency Medicine Practice
22
February 2002
72.
Li J, Murphy-Lavoie H, Bugas C, et al. Complications of
emergency intubation with and without paralysis. Am J Emerg
Med 1999;17:141-143. (Prospective, comparative; 233 patients)
73. Sivilotti ML, Ducharme J. Randomized, double-blind study on
sedatives and hemodynamics during rapid-sequence intubation
in the emergency department: the SHRED Study. Ann Emerg Med
1999;33:125-126. (Double-blind, randomized study; 86 patients)
74. Smith DC, Bergen JM, Smithline H, et al. A trial of etomidate for
rapid sequence intubation in the emergency department. J Emerg
Med 2000;18:13-16. (Prospective; 34 patients)
75. Grace MP, Greenbaum DM. Cardiac performance in response to
PEEP in patients with cardiac dysfunction. Crit Care Med
1982;10:358-360. (Prospective; 21 patients)
76. Schuster S, Erbel R, Weilemann LS, et al. Hemodynamics during
PEEP ventilation in patients with severe left ventricular failure
studied by transesophageal echocardiography. Chest 1990;97:11811189. (Prospective; 5 patients)
77. Fellahi JL, Valtier B, Beauchet A, et al. Does positive endexpiratory pressure ventilation improve left ventricular function?
A comparative study by transesophageal echocardiography in
cardiac and non-cardiac patients. Chest 1998;114:556-562.
(Prospective; 12 patients)
78. Yap JC, Moore DM, Cleland JG, et al. Effect of supine posture on
respiratory mechanics in chronic left ventricular failure. Am J
Respir Crit Care Med 2000 Oct;162(4 Pt 1):1285-1291. (10 patients)
79. Paterna S, Di Pasquale P, Parrinello G, et al. Effects of high-dose
furosemide and small-volume hypertonic saline solution infusion
in comparison with a high dose of furosemide as a bolus, in
refractory congestive heart failure. Eur J Heart Fail 2000
Sep;2(3):305-313. (Randomized, controlled trial; 60 patients)
80. Leier CV, Bambach D, Thompson MJ, et al. Central and regional
hemodynamic effects of intravenous isosorbide dinitrate,
nitroglycerin, and nitroprusside in patients with congestive heart
failure. Am J Cardiol 1981;48:1115-1123. (Randomized, controlled,
crossover; 10 patients)
81. Rabinowitz B, Katz A, Shotan A, et al. Haemodynamic effects of
intravenous isosorbide-5-mononitrate in acute and chronic left
heart failure of ischaemic etiology. Eur Heart J 1988;9 Suppl A:175180. (Prospective; 19 patients)
82. Imhof PR, Ott B, Frankhauser P, et al. Differences in nitroglycerin
dose response in the venous and arterial beds. Eur J Clin Pharmacol
1980;18:455-460. (Prospective; 12 patients)
83. Haber HL, Simek CL, Bergin JD, et al. Bolus intravenous
nitroglycerin predominantly reduces afterload in patients with
severe congestive heart failure. J Am Coll Cardiol 1993;22:251-257.
(Prospective; 27 patients)
84. Franciosa JA, Silverstein SR. Hemodynamic effects of nitroprusside and furosemide in left ventricular failure. Clin Pharmacol Ther
1982;32:62-69. (Prospective, observational; 13 patients)
85. Nelson GI, Silke B, Ahuja RC, et al: Haemodynamic advantages of
isosorbide dinitrate over furosemide in acute heart-failure
following myocardial infarction. Lancet 1983;1:730-733. (Controlled, randomized, prospective; 28 patients)
86. Verma SP, Silke B, Hussain M, et al. First-line treatment of left
ventricular failure complicating acute myocardial infarction: a
randomised evaluation of immediate effects of diuretic,
venodilator, arteriodilator, and positive inotropic drugs on left
ventricular function. J Cardiovasc Pharmacol 1987;10:38-46.
(Controlled, randomized, prospective; 48 patients)
87.* Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of highdose isosorbide dinitrate plus low-dose furosemide versus highdose furosemide plus low-dose isosorbide dinitrate in severe
pulmonary edema. Lancet 1998;351:389-393. (Controlled,
randomized, multi-center; 110 patients)
88. Bussmann WD, Kaltenbach M. Sublingual nitroglycerin in the
treatment of left ventricular failure and pulmonary edema. Eur J
Cardiol 1976;4:327-333. (Prospective; 15 patients)
89. Bussmann WD, Schupp D. Effect of sublingual nitroglycerin in
emergency treatment of severe pulmonary edema. Am J Cardiol
1978;41:931-936. (Prospective; 22 patients)
90. Edwards JD, Grant PT, Plunkett P, et al. The haemodynamic
effects of sublingual nitroglycerin spray in severe left ventricular
failure. Intensive Care Med 1989;15:247-249. (Review)
proatrial natriuretic peptide. Circulation 1996;93:1963-1969.
(Observational; 131 patients)
54. Valli N, Gobinet A, Bordenave L. Review of 10 years of the clinical
use of brain natriuretic peptide in cardiology. J Lab Clin Med
1999;134:437-444. (Review)
55. Maeda K, Tsutamoto T, Wada A, et al. High levels of plasma brain
natriuretic peptide and interleukin-6 after optimized treatment for
heart failure are independent risk factors for morbidity and
mortality with congestive heart failure. J Am Coll Cardiol
2000;36:1587-1593. (Prospective, observational; 112 patients)
56. Davis M, Espiner E, Richards G, et al. Plasma brain natriuretic
peptide in assessment of acute dyspnoea. Lancet 1994;343:440-444.
(Comparative; 52 patients)
57. Fleischer D, Espiner EA, Yandle TG, et al. Rapid assay of plasma
brain natriuretic peptide in the assessment of acute dyspnea. NZ
Med J 1997;110:71-74. (Prospective; 123 patients)
58.* Morrison LK, Harrison A, Krishnaswamy P, et al. Utility of a rapid
B-natriuretic peptide assay in differentiating congestive heart
failure from lung disease in patients presenting with dyspnea. J
Am Coll Cardiol 2002;39:202-209. (321 patients)
59. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type
natriuretic peptide in the diagnosis of congestive heart failure in
an urgent-care setting. J Am Coll Cardiol 2001;37:379-385.
(Retrospective, comparative; 250 patients)
60. Troughton RW, Frampton CM, Yandle TG, et al. Treatment of heart
failure guided by plasma aminoterminal brain natriuretic peptide
(N-BNP) concentrations. Lancet 2000;355:1126-1130. (Prospective,
double-blind, randomized; 69 patients)
61. Kawai K, Hata K, Takaoka H, et al. Plasma brain natriuretic
peptide as a novel therapeutic indicator in idiopathic dilated
cardiomyopathy during beta-blocker therapy: A potential of
hormone-guided treatment. Am Heart J 2001;141:925-932.
(Prospective, observational; 30 patients)
62. Rywik SL, Wagrowska H, Broda G, et al. Heart failure in patients
seeking medical help at outpatients clinics. Part I. General
characteristics. Eur J Heart Fail 2000 Dec;2(4):413-421. (Crosssectional; 19,877 patients)
63. Rihal CS, Davis KB, Kennedy JW, et al. The utility of clinical,
electrocardiographic, and roentgenographic variables in the
prediction of left ventricular function. Am J Cardiol 1995;75:220223. (Secondary data analysis; 14,507 patients)
64. Chen JT. Radiographic diagnosis of heart failure. Heart Dis Stroke
1992;1:58-63. (Review)
65. Trippi JA, Lee KS, Kopp G, et al. Emergency echocardiography
telemedicine: an efficient method to provide 24-hour consultative
echocardiography. J Am Coll Cardiol 1996;27:1748-1752. (Prospective; 187 patients)
66.* Stewart WJ, Douglas PS, Sagar K, et al. Echocardiography in
emergency medicine: a policy statement by the American Society
of Echocardiography and the American College of Cardiology.
Task Force on Echocardiography in Emergency Medicine of the
American Society of Echocardiography and the Echocardiography
and Technology and Practice Executive Committees of the
American College of Cardiology. J Am Coll Cardiol 1999;13:586-588.
(Practice guideline)
67. Lanoix R, Leak LV, Gaeta T, Gernsheimer JR. A preliminary
evaluation of emergency ultrasound in the setting of an
emergency medicine training program. Am J Emerg Med
2000;18:41-45. (Prospective, observational; 456 examinations [73
cardiac])
68. Kimura BJ, Bocchicchio M, Willis KL, et al. Screening cardiac
ultrasonographic examination in patients with suspected cardiac
disease in the emergency department. Am Heart J 2001;142:324330. (Prospective; 124 patients)
69. Mandavia DP, Hoffner RJ, Mahaney K, et al. Bedside
echocardiography by emergency physicians. Ann Emerg Med
2001;38:377-382. (Prospective; 515 patients)
70. Dalen JE, Bone RC. Is it time to pull the pulmonary artery
catheter? JAMA 1996 Sep 18;276(11):916-918. (Letter, editorial)
71. Connors AF Jr, Speroff T, Dawson NV, et al. The effectiveness of
right heart catheterization in the initial care of critically ill
patients. SUPPORT Investigators. JAMA 1996 Sep 18;276(11):889897. (Prospective, cohort; 5735 patients)
February 2002
23
Emergency Medicine Practice
91.
92.
93.
94.
95.*
96.
97.
98.
99.
100.
101.
102.
103.
104.
105.
106.
107.
108.
109.
110.
111.
112. Barnett JC, Zink KM, Touchon RC: Sublingual captopril in the
treatment of acute heart failure. Curr Ther Res 1991;49:274-281.
(Two-part observational study; 7 and 12 subjects)
113. Tohmo H, Karanko M, Korpilahti K. Haemodynamic effects of
enalaprilat and preload in acute severe heart failure complicating
myocardial infarction. Eur Heart J 1994;15:523-527. (Prospective;
10 patients)
114. Annane D, Bellissant E, Pussard E, et al: Placebo-controlled,
randomized double-blind study of enalaprilat efficacy and safety
in acute cardiogenic pulmonary edema. Circulation 1996;94:13161324. (Double-blind, placebo-controlled, randomized; 20
patients)
115. Haude M, Steffen W, Erbel R, et al: Sublingual administration of
captopril versus nitroglycerin in patients with severe congestive
heart failure. Int J Cardiol 1990;27:351-359. (Controlled, randomized, cross-over; 24 patients)
116. Verma SP, Silke B, Reynolds GW, Kelly JG, et al. Vasodilator
therapy for acute heart failure: hemodynamic comparison of
hydralazine/isosorbide, alpha-adrenergic blockade, and
angiotensin-converting enzyme inhibition. J Cardiovasc Pharmacol
1992;20:274-281. (Prospective; 36 patients)
117. Adigun AQ, Ajayi OE, Sofowora GG, et al. Vasodilator therapy of
hypertensive acute left ventricular failure: comparison of
captopril-prazosin with hydralazine-isosorbide dinitrate. Int J
Cardiol 1998;67:81-86. (Prospective, single-blind, randomized; 17
patients)
118. Podbregar M, Voga G, Horvat M, et al. Bolus versus continuous
low dose of enalaprilat in congestive heart failure with acute
refractory decompensation. Cardiology 1999;91:41-49. (Controlled,
randomized, comparative; 20 patients)
119.* Hamilton RJ, Carter WA, Gallagher EJ: Rapid improvement of
acute pulmonary edema with sublingual captopril. Acad Emerg
Med 1996;3:205-212. (Double-blind, placebo-controlled,
randomized; 48 patients)
120.* Sacchetti A, Ramoska E, Moakes ME, et al. Effect of ED management on ICU use in acute pulmonary edema. Am J Emerg Med
1999;17:571-574. (Chart review; 181 patients)
121. Flapan AD, Davies E, Waugh C, et al. Acute administration of
captopril lowers the natriuretic and diuretic response to a loop
diuretic in patients with chronic cardiac failure. Eur Heart J 1991
Aug;12(8):924-927. (Comparative; 12 patients)
122. McLay JS, McMurray JJ, Bridges AB, et al. Acute effects of
captopril on the renal actions of furosemide in patients with
chronic heart failure. Am Heart J 1993 Oct;126(4):879-886.
(Randomized, controlled trial; 25 patients)
123. Goldstein RA, Passamani ER, Roberts R. A comparison of digoxin
and dobutamine in patients with acute infarction and cardiac
failure. N Engl J Med 1980; 303:846-50. (Comparative; 6 patients)
124. Tanaka K, Takano T, Seino Y. Effects of intravenous amrinone on
heart failure complicated by acute myocardial infarction:
comparative study with dopamine and dobutamine. Jpn Circ J
1986;50:652-658. (Prospective, comparative; 40 patients)
125. Caldicott LD, Hawley K, Heppell R, et al. Intravenous enoximone
or dobutamine for severe heart failure after acute myocardial
infarction: a randomized double-blind trial. Eur Heart J
1993;14:696-700. (Double-blind, randomized; 18 patients)
126. Asanoi H, Sasayama S, Sakurai T, et al. Intravenous dopexamine
in the treatment of acute congestive heart failure: results of a
multi-center, double-blind, placebo-controlled withdrawal study.
Cardiovasc Drugs Ther 1995;9:791-796. (Double-blind, placebocontrolled, multi-center; 20 patients)
127. Seino Y, Momomura S, Takano T, et al. Multicenter, double-blind
study of intravenous milrinone for patients with acute heart
failure in Japan. Japan Intravenous Milrinone Investigators. Crit
Care Med 1996;24:1490-1497. (Double-blind, placebo-controlled,
multi-center; 52 patients)
128. Verma SP, Silke B, Nelson GI, et al. Haemodynamic advantages of
a combined inotropic/venodilator regimen over inotropic
monotherapy in acute heart failure. J Cardiovasc Pharmacol
1985:7:943-947. (Prospective; 10 patients)
129. Verma SP, Silke B, Reynolds GW, Richmond A, et al. Modulation
of inotropic therapy by venodilation in acute heart failure: a
randomised comparison of four inotropic agents, alone and
Harf C, Welter R. Emergency treatment of severe cardiogenic
pulmonary edema with intravenous isosorbide-5-mononitrate.
Am J Cardiol 1988;61:22E-27E. (Prospective; 24 patients)
Nashed AH, Allegra JR. Intravenous nitroglycerin boluses in
treating patients with cardiogenic pulmonary edema. Am J Emerg
Med 1995;13:612-3. (Letter)
Melandri G, Semprini F, Branzi, et al. Comparative effects of
transdermal vs intravenous nitroglycerin in acute myocardial
infarction with elevated pulmonary artery wedge pressure. Eur
Heart J 1990;11:649-655. (Comparative; 16 patients)
Magrini F, Niarchos AP. Ineffectiveness of sublingual nitroglycerin
in acute left ventricular failure in the presence of massive
peripheral edema. Am J Cardiol 1980;45:841-847. (Prospective; 15
patients)
Sacchetti A, McCabe J, Torres M, et al. ED management of acute
congestive heart failure in renal dialysis patients. Am J Emerg Med
1993;11:644-647. (Prospective case series; 46 patients)
Grosskopf I. Combination of furosemide and metolazone in the
treatment of severe congestive heart failure. Isr J Med Sci
1986;22:787-790. (Prospective; 10 patients)
Murray MD, Deer MM, Ferguson JA, et al. Open-label randomized trial of torsemide compared with furosemide therapy for
patients with heart failure. Am J Med 2001;111:513-520. (Prospective; 234 patients)
Howard PA, Dunn MI. Aggressive diuresis for severe heart failure
in the elderly. Chest 2001;119:807-810. (Case series; 17 patients)
Lahav M, Regev A, Ra’anani P, et al. Intermittent administration
of furosemide vs continuous infusion preceded by a loading dose
for congestive heart failure. Chest 1992 Sep;102(3):725-731.
(Randomized, controlled trial; 9 patients)
Pivac N, Rumboldt Z, Sardelic S, et al. Diuretic effects of
furosemide infusion versus bolus injection in congestive heart
failure. Int J Clin Pharmacol Res 1998;18(3):121-128. (Randomized,
controlled trial; 20 patients)
Dormans TP, van Meyel JJ, Gerlag PG, et al. Diuretic efficacy of
high dose furosemide in severe heart failure: bolus injection
versus continuous infusion. J Am Coll Cardiol 1996 Aug;28(2):376382. (Randomized, controlled trial)
Salvador DRK, Rey, NR, Ramos GC, et al. Cochrane Heart Group.
Continuous infusion versus bolus injection of loop diuretics in
congestive heart failure. Cochrane Database of Systematic Reviews.
Issue 4, 2001. (Protocol)
Dikshit K, Vyden JK, Forrester JS, et al. Renal and extrarenal
hemodynamic effects of furosemide in congestive heart failure
after acute myocardial infarction. N Engl J Med 1973;288:1087-1090.
(Prospective; 21 patients)
Biddle TL, Yu PN. Effect of furosemide on hemodynamics and
lung water in acute pulmonary edema secondary to myocardial
infarction. Am J Cardiol 1979;43:86-90. (Controlled, prospective; 19
patients)
Baltopoulos G, Zakynthinos S, Dimopoulos A, et al. Effects of
furosemide on pulmonary shunts. Chest 1989;96:494-498.
(Prospective; 20 patients)
Dormans TP, Pickkers P, Russel FG, et al. Vascular effects of loop
diuretics. Cardiovasc Res 1996;32:988-997. (Review)
Pickers P, Dormans TP, Russel FG, et al. Direct vascular effects of
furosemide in humans. Circulation 1997;96:1847-1852. (Prospective; 60 patients)
Francis GS, Siegel RM, Goldsmith SR, et al. Acute vasoconstrictor
response to intravenous furosemide in patients with chronic
congestive heart failure: activation of the neurohumoral axis. Ann
Intern Med 1985;103:1-6. (Prospective; 15 patients)
Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990;98:124-128. (Prospective; 33 patients)
Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on
morbidity and mortality in patients with severe heart failure.
Randomized Aldactone Evaluation Study Investigators. N Engl J
Med 1999 Sep 2;341(10):709-717. (Randomized, controlled trial;
1663 patients)
Brivet F, Delfraissy JF, Giudicelli JF, et al: Immediate effects of
captopril in acute left ventricular heart failure secondary to
myocardial infarction. Eur J Clin Invest 1981;11:369-373. (Prospective; 8 patients)
Emergency Medicine Practice
24
February 2002
trial of bilevel vs continuous positive airway pressure in acute
pulmonary edema. Crit Care Med 1997;25:620-628. (Double-blind,
controlled, randomized; 27 patients)
149. Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous
isosorbide-dinitrate is safer and better than B-PAP ventilation
combined with conventional treatment for severe pulmonary
edema. J Am Coll Cardiol 2000;36:832-837. (Prospective, comparative; 40 patients)
150.* Kosowsky JM, Storrow AB, Carleton SC. Continuous and bi-level
positive airway pressure in the treatment of acute cardiogenic
pulmonary edema. Am J Emerg Med 2000;18:91-95. (Review)
151. Kosowsky JM, Stephanides SL, Branson RD, et al. Prehospital use
of continuous positive airway pressure (CPAP) for presumed
pulmonary edema: a preliminary case series. Prehosp Emerg Care
2001;5:190-196. (Case series; 19 patients)
152. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann
Intern Med 1999;131:47-59. (Review)
153. Holmes DR Jr, Berger PB, Hochman JS, et al. Cardiogenic shock in
patients with acute ischemic syndromes with and without STsegment elevation. Circulation 1999;100:2067-2073. (Randomized,
controlled trial; 12,084 patients)
154.* Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization
in acute myocardial infarction complicated by cardiogenic shock.
SHOCK Investigators. Should we emergently revascularize
occluded coronaries for cardiogenic shock. N Engl J Med
1999;341:625-634. (Controlled, randomized, multi-center; 302
patients)
155. Sanborn TA, Sleeper LA, Bates ER, et al. Impact of thrombolysis,
intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial
infarction: a report from the SHOCK Trial Registry. SHould we
emergently revascularize Occluded Coronaries for cardiogenic
shocK? J Am Coll Cardiol 2000 Sep;36(3 Suppl A):1123-1129.
(Randomized, controlled trial; 1190 patients)
156. Siniorakis EE, Nikolaou NI, Sarantopoulos CD, et al. Volume
loading in predominant right ventricular infarction: bedside
haemodynamics using rapid response thermistors. Eur Heart J
1994 Oct;15(10):1340-1347. (Prospective; 11 patients)
157. Ferrario M, Poli A, Previtali M, et al. Hemodynamics of volume
loading compared with dobutamine in severe right ventricular
infarction. Am J Cardiol 1994 Aug 15;74(4):329-333. (Randomized,
controlled trial; 11 patients)
158. 124. Francis GS, Sharma B, Hodges, M. Comparative hemodynamic effects of dopamine and dobutamine in patients with acute
cardiogenic circulatory collapse. Am Heart J 1982;103:995-1000.
(Controlled, randomized, cross-over study; 13 patients)
159. Lane AS, Woodward AC, Goldman MR. Massive propranolol
overdose poorly responsive to pharmacologic therapy: use of the
intra-aortic balloon pump. Ann Emerg Med 1987;16:1381-1383.
(Case report; 1 patient)
160. Harnett JD, Foley RN, Kent GM, et al. Congestive heart failure in
dialysis patient: prevalence, incidence, prognosis, and risk factors.
Kidney Int 1995;47:884-890. (Prospective, multi-center cohort; 432
patients)
161. Sacchetti A, Harris R, Patel K, et al R. Emergency department
presentation of renal dialysis patients: indications for EMS
transport directly to dialysis centers. J Emerg Med 1991; 9:141-144.
(Prospective; 100 patients)
162. Schmieder RE, Messerli FH, deCarvalho JG, et al. Immediate
hemodynamic response to furosemide in patients undergoing
chronic hemodialysis. Am J Kidney Dis 1987;19:55-59. (Prospective;
10 patients)
163. Anderson CC, Shahvari MB, Zimmerman JE. The treatment of
pulmonary edema in the absence of renal function. A role for
sorbitol and furosemide. JAMA 1979 Mar 9;241(10):1008-1010.
(Case report; 2 patients)
164. Murdoch DR, McDonagh TA, Byrne J, et al. Titration of vasodilator therapy in chronic heart failure according to plasma brain
natriuretic peptide concentration: Randomized comparison of the
hemodynamic and neuroendocrine effects of tailored versus
empirical therapy. Am Heart J 1999;138:1126-1132. (Single-blind,
randomized, comparative; 30 patients)
165. Graff L, Orledge J, Radford MJ, et al. Correlation of the Agency for
combined with isosorbide dinitrate. J Cardiovasc Pharmacol
1992;19:24-33. (Controlled, randomized, prospective; 48 patients)
130. Karlsberg RP, DeWood MA, DeMaria AN, et al. Comparative
efficacy of short-term intravenous infusions of milrinone and
dobutamine in acute congestive heart failure following acute
myocardial infarction. Milrinone-Dobutamine Study Group. Clin
Cardiol 1996;19:21-30. (Randomized, controlled, comparative; 33
patients)
131. Mager G, Klocke RK, Kux A, et al. Phosphodiesterase III
inhibition or adrenoreceptor stimulation: milrinone as an
alternative to dobutamine in the treatment of severe heart failure.
Am Heart J 1991 Jun;121(6 Pt 2):1974-1983. (Comparative,
controlled; 20 patients)
132. Lowes BD, Simon MA, Tsvetkova TO, et al. Inotropes in the betablocker era. Clin Cardiol 2000;23 (Suppl. III):III-11-16. (Review)
133. Timmis AD, Rothman MT, Henderson MA, et al: Haemodynamic
effects of intravenous morphine in patients with acute myocardial
infarction complicated by severe left ventricular failure. BMJ
1980;280:980-982. (Prospective; 10 patients)
134.* Rasanen J, Heikkila J, Downs J, et al. Continuous positive airway
pressure by face mask in acute cardiogenic pulmonary edema. Am
J Cardiol 1985;55:296-300. (Controlled, randomized, prospective;
40 patients)
135.* Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe
cardiogenic pulmonary edema with continuous positive airway
pressure delivered by face mask. N Engl J Med 1991;325:1825-1830.
(Controlled, randomized; 39 patients)
136.* Lin M, Yang YF, Chiang HT, et al. Reappraisal of continuous
positive airway pressure therapy in acute cardiogenic pulmonary
edema. Short-term results and long-term follow up. Chest
1995;107:1379-1386. (Controlled, comparative; 100 patients)
137.* Pang D, Keenan SP, Cook DJ, et al. The effect of positive pressure
airway support on mortality and the need for intubation in
cardiogenic pulmonary edema: a systematic review. Chest
1998;114:1185-1192. (Review)
138. Katz JA, Marks JD. Inspiratory work with and without continuous
positive airway pressure in patients with acute respiratory failure.
Anesthesiology 1985;63:598-607. (Comparative; 16 patients)
139. Baratz DM, Westbrook PR, Shah PK, et al. Effect of nasal
continuous positive airway pressure on cardiac output and
oxygen delivery in patients with congestive heart failure. Chest
1992;102:1397-1401. (Prospective; 13 patients)
140. Bradley TD, Holloway RM, McLaughlin PR, et al. Cardiac output
response to continuous positive airway pressure in congestive
heart failure. Am Rev Respir Dis 1992;145:377-382. (Controlled,
prospective; 22 patients)
141. Montner PK, Greene ER, Murata GH, et al. Hemodynamic effects
of nasal and face mask continuous positive airway pressure. Am J
Respir Crit Care Med 1994;149:1614-1618. (Comparative; 6 patients)
142. Naughton MT, Rahman MA, Hara K, et al. Effects of continuous
positive airway pressure on intrathoracic and left ventricular
transmural pressures in patients with congestive heart failure.
Circulation 1995;91:1725-1731. (Prospective; 24 patients)
143. Sacchetti AD, Harris RH, Paston C, et al: Bi-level positive airway
pressure support system use in acute congestive heart failure:
preliminary case series. Acad Emerg Med 1995;2:714-718. (Case
series)
144. Hoffmann B, Welte T. The use of non-invasive pressure support
ventilation for severe respiratory insufficiency due to pulmonary
edema. Intensive Care Med 1999;25:15-20. (Prospective; 29 patients)
145. Rusterholtz T, Kempf J, Berton C, et al. Non-invasive pressure
support ventilation (NIPSV) with face mask in patients with acute
cardiogenic pulmonary edema (ACPE). Intensive Care Med
1999;25:212-8. (Prospective; 26 patients)
146.* Masip J, Betbese AJ, Paez J, et al. Non-invasive pressure support
ventilation versus conventional oxygen therapy in acute
cardiogenic pulmonary edema: a randomized trial. Lancet
2000;356:2126-2132. (Controlled, randomized; 40 patients)
147. Wigder HN, Hoffman P, Mazolini D, et al. Pressure support noninvasive positive pressure ventilation treatment of acute
cardiogenic pulmonary edema. Am J Emerg Med 2001;19:179-181.
(Prospective; 20 patients)
148.* Mehta S, Jay GD, Woolard RH, et al: Randomized, prospective
February 2002
25
Emergency Medicine Practice
Health Care Policy and Research congestive heart failure
admission guideline with mortality: peer review organization
voluntary hospital association initiative to decrease events
(PROVIDE) for congestive heart failure. Ann Emerg Med
1999;34:429-37. (Review)
166. Prystowsky EN, Benson DW, Fuster V, et al. Management of
patients with atrial fibrillation: A statement for healthcare
professionals from the subcommittee on electrocardiography and
electrophysiology, American Heart Association. Circulation
1996;93:1262-1277. (Practice guideline)
167. Khand AU, Rankin AC, Kaye GC, et al. Systematic review of the
management of atrial fibrillation in patients with heart failure. Eur
Heart J 2000;21:614-632. (Review)
168. Delle Karth G, Geppert A, Neunteufl T, et al. Amiodarone versus
diltiazem for rate control in critically ill patients with atrial
tachyarrhythmias. Crit Care Med 2001;29:1149-1153. (Randomized,
controlled, prospective; 60 patients)
169. Woltjer HH, Bogaard HJ, Bronzwaer JG, et al. Prediction of
pulmonary capillary wedge pressure and assessment of stroke
volume by noninvasive impedance cardiography. Am Heart J
1997;134:450-455. (Prospective, observational; 24 patients)
170. Raaijmakers E, Faes TJ, Scholten RJ, et al. A meta-analysis of three
decades of validating thoracic impedance cardiography. Crit Care
Med 1999;27:1203-1213. (Meta-analysis)
171. Summers RL, Kolb JC, Woodward LH, et al. Differentiating
systolic from diastolic heart failure using impedance cardiography. Acad Emerg Med 1999;6:693-699. (Prospective; 42 patients)
172.* Packer M, Bristow MR, Cohn JN, et al. The effect of cavedilol on
morbidity and mortality in patients with chronic heart failure.
U.S. Carvedilol Heart Failure Study Group. N Engl J Med
1996;334:1349-1355. (Double-blind, placebo-controlled; 1094
patients)
173.* MERIT-HF. Effect of metoprolol CR/XL in chronic heart failure:
Metoprolol CR/XL randomized intervention trial in congestive
heart failure (MERIT-HF). Lancet 1999;353:2001-2007. (Doubleblind, controlled, randomized; 3991 patients)
174. CIBIS-II. The cardiac insufficiency bisoprolol study II (CIBIS-II): a
randomized trial. Lancet 1999;353:9-13. (Double-blind, placebocontrolled, randomized, multi-center; 2647 patients)
175. Braunwald E. Expanding indications for beta-blockers in heart
failure. N Engl J Med 2001;344:1711-1712. (Review)
176.* Ryan TJ, Antman EM, Brooks NH, et al. 1999 update: ACC/AHA
Guidelines for the Management of Patients With Acute Myocardial Infarction: Executive Summary and Recommendations: A
report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (Committee on
Management of Acute Myocardial Infarction). Circulation
1999;100:1016-1030. (Practice guideline)
177.* Braunwald E, Antman EM, Beasley JW et al. ACC/AHA
guidelines for the management of patients with unstable angina
and non-ST-segment elevation myocardial infarction. J Am Coll
Cardiol 2000;36:970-1062 (Practice guidelines)
178. Pollack CV, Gibler WB. 2000 ACC/AHA guidelines for the
management of patients with unstable angina and non-STsegment elevation myocardial infarction: a practical summary for
emergency physicians. Ann Emerg Med 2001;38:229-240. (Review)
179. Molina CR, Fowler MB, McCrory S, et al. Hemodynamic, renal
and endocrine effects of atrial natriuretic peptide infusion in
severe heart failure. J Am Coll Cardiol 1988;12:175-186. (Controlled,
prospective; 12 patients)
180. Hobbs RE, Miller LW, Bott-Silverman C, et al. Hemodynamic
effects of a single intravenous injection of synthetic human brain
natriuretic peptide in patients with heart failure secondary to
ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol
1996;78:896-901. (Double-blind, placebo-controlled, randomized;
27 patients)
181. Marcus LS, Hart D, Packer M, et al. Hemodynamic and renal
excretory effects of human brain natriuretic peptide infusion in
patients with congestive heart failure. Circulation 1996;94:31843189. (Double-blind, placebo-controlled, randomized, crossover; 27 patients)
182. Abraham WT, Lowes BD, Ferguson DA, et al. Systemic hemodynamic, neurohormonal, and renal effects of a steady-state infusion
Emergency Medicine Practice
183.
184.
185.
186.
187.
188.
189.
190.
191.
192.
193.
194.
195.
196.
197.
198.
199.
200.
201.
26
of human brain natriuretic peptide in patients with hemodynamically decompensated heart failure. J Card Failure 1998;4:37-44.
(Double-blind, placebo-controlled, randomized; 16 patients)
Colucci WS, Elkayam U, Horton DP, et al. for the Nesiritide Study
Group. Intravenous nesiritide, a natriuretic peptide, in the
treatment of decompensated congestive heart failure. N Engl J Med
2000;343:246-253. (Combined efficacy study, 127 patients;
comparative study, 305 patients)
Nieminen MS, Akkila J, Hasenfuss G, et al. Hemodynamic and
neurohumoral effects of continuous infusion of levosimendan in
patients with congestive heart failure. J Am Coll Cardiol
2000;36:1903-1912. (Double-blind, placebo-controlled, randomized, multi-center; 151 patients)
Ishiki R, Ishihara H, Izawa H, et al. Acute effects of a single low
oral dose of pimobendan on left ventricular systolic and diastolic
function in patients with congestive heart failure. J Cardiovasc
Pharm 2000;35:897-905. (Case series; 10 patients)
Slawsky MT, Colucci WS, Gottlieb SS, et al. Acute hemodynamic
and clinical effects of levosimendan in patients with severe heart
failure. Circulation 2000;102:2222-2227. (Double-blind, placebocontrolled, randomized, multi-center; 146 patients)
Kosecoff J, Kahn KL, Rogers WH, et al. Prospective payment
system and the impairment at discharge: the “quicker and sicker”
story revisited. JAMA 1990;264:1980-1983. (Epidemiologic survey)
Poses RM, Smith WR, McClish DK, et al. Physicians’ survival
predictions for patients with acute congestive heart failure. Arch
Intern Med 1997;157:1001-1007. (Prospective, multi-center, cohort;
1173 patients)
Brophy JM, Deslauriers G, Boucher B, et al. The hospital course
and short term prognosis of patients presenting to the emergency
room with decompensated congestive heart failure. Can J Cardiol
1993;9:219-224. (Prospective, observational; 153 patients)
Philbin EF, Rocco TA, Lynch LJ, et al. Predictors and determinants
of hospital length of stay in congestive heart failure in ten
community hospitals. J Heart Lung Transplant 1997;16:548-555.
(Chart review; 1402 patients)
Mohan P, Hii JTY, Wuttke RD, et al. Acute heart failure: determinants of outcome. Int J Cardiol 1991;32:365-376. (Prospective,
observational; 69 patients)
Esdaile JM, Horwitz RI, Levington C, et al. Response to initial
therapy and new onset as predictors of prognosis in patients
hospitalized with congestive heart failure. Clin Invest Med
1992;15:122-131. (Retrospective; 191 patients)
Weingarten SR, Riedinger MS, Shinbane J, et al. Triage practice
guideline for patients hospitalized with congestive heart failure:
improving the effectiveness of the coronary care unit. Am J Med
1993;94:483-490. (Retrospective; 384 patients)
Selker HP, Griffith JL, D’Agostino RB. A time-insensitive
instrument for acute hospital mortality due to congestive heart
failure: development, testing, and use for comparing hospitals: a
multicenter study. Med Care 1994;32:1040-1052. (Multi-center;
5773 patients)
Philbin EF, Cotto M, Rocco TA, et al. Association between diuretic
use, clinical response, and death in acute heart failure. Am J
Cardiol 1997;80:519-522. (Observational; 1150 patients)
Butler J, Hanumanthu S, Chomsky D, et al. Frequency of low-risk
hospital admissions for heart failure. Am J Cardiol 1998;81:41-44.
(Chart review; 120 patients)
Graff LG. Principles of observation medicine. In: Graff LG, ed.
Observation Medicine. Newton, MA: Butterworth-Heinemann,
1993. (Textbook)
Graff LG, Krivenko C, Maag R, et al. Emergency Department
Evaluation of Congestive Heart Failure: The Appropriate Evaluation and
Treatment of DRG 127. Farmington, Conn: VHA of Southern New
England; 1995. (Review)
Chapman DB, Torpy J. Development of a heart failure center; a
medical center and cardiology practice join forces to improve care
and reduce costs. Am J Manag Care 1997;3:431-437.
West JA, Miller NH, Parker KM, et al. A comprehensive
management system for heart failure improves clinical outcomes
and reduces medical resource utilization. Am J Cardiol 1997;79:5863. (Prospective; 51 patients)
Krumholz HM, Baker DW, Ashton CM, et al. Evaluating quality of
February 2002
care for patients with heart failure. Circulation 2000;101:e122.
(Review)
202. Peacock WF 4th, Albert NM. Observation unit management of
heart failure. Emerg Med Clin North Am 2001 Feb;19(1):209-232.
(Review, tutorial)
203. Albert NM, Peacock WF: Patient outcome and costs after
implementation of an acute heart failure management program in
an emergency department observation unit. J Internat Soc Heart
Lung Transplant 1999;18:92.
24. Which medication improves congestive symptoms
of heart failure most rapidly?
a. Nitrates
b. Beta-blockers
c. Diuretics
d. Amiodarone
25. An ideal drug (or drug combination) for the
treatment of acutely decompensated heart
failure would:
a. reduce preload.
b. enhance left ventricular function.
c. maintain or improve myocardial oxygen balance.
d. all of the above.
Physician CME Questions
17. Diastolic failure primarily involves impairment of:
a. myocardial contractility.
b. ventricular filling.
c. atrioventricular conduction.
d. systemic vascular resistance.
26. ACE inhibitors are contraindicated in heart failure
patients with which of the following conditions?
a. Peanut allergy
b. Hyperkalemia
c. Hypokalemia
d. Current menses
18. Progressive severe respiratory distress in the
prehospital setting should be addressed with:
a. prone positioning.
b. continuous high-dose furosemide infusion.
c. CPAP with ambient air.
d. endotracheal intubation.
27. Which of the following excludes a patient from a
trial of CPAP?
a. Diaphoresis
b. Renal failure
c. Left ventricular hypertrophy on ECG
d. Severe agitation
19. Which of the following tests is unlikely to be
helpful in patients presenting with decompensated
heart failure?
a. Cardiac enzymes
b. BUN/creatinine
c. Amylase
d. CBC
28. Which of the following indicators has been
shown to correlate with left ventricular overload,
severity of clinical heart failure, and both shortand long-term cardiovascular mortality in heart
failure patients?
a. ESR
b. CRP
c. BNP
d. d-dimer ELISA
20. The most common cause of cardiogenic shock is:
a. acute ST-elevation MI.
b. ventricular septal rupture.
c. pericardial tamponade.
d. mitral valve chordae rupture.
21. A patient with new cardiac murmur and acute onset
of heart failure needs to have which of the following studies performed emergently?
a. Gated myocardial scan
b. Cardiac MRI
c. Blood cultures
d. Transthoracic echocardiography
29. Which of the following is true?
a. A normal ECG rules out left ventricular diastolic
dysfunction.
b. Acute ST-segment elevation in a patient with
decompensated heart failure is a contraindication for thrombolytic therapy.
c. Clinical findings usually lag behind chest x-ray
findings in heart failure patients.
d. Heart size may be normal in acute heart failure.
22. What percentage of “low-risk” heart failure
admissions have an adverse cardiovascular event
during their in-hospital stay?
a. 45%
b. 33%
c. 5%
d. < 2%
30. Cardiac enzymes:
a. are not necessary if the ECG is normal.
b. are always positive in the case of MI by the
time the patient is symptomatic.
c. should be drawn on all patients with
heart failure.
d. are indicated when the patient has
anginal-type pain or has unexplained
sudden-onset heart failure.
23. Some patients presenting to the ED with decompensated heart failure have sustained an acute MI.
a. True
b. False
February 2002
27
Emergency Medicine Practice
Physician CME Information
31. Which of the following statements regarding heart
failure is true?
a. Morphine’s main effect is through its direct
effect on cardiac contractility.
b. Morphine may cause respiratory depression and
increase the incidence of intubation.
c. Diuretics are more important than nitrates in
managing acute respiratory distress.
d. Furosemide has no vasodilating properties.
This CME enduring material is sponsored by Mount Sinai School of
Medicine and has been planned and implemented in accordance with
the Essentials and Standards of the Accreditation Council for Continuing
Medical Education. Credit may be obtained by reading each issue and
completing the post-tests administered in December and June.
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 February 1, 2002. This activity is eligible for
CME credit through February 1, 2005. The latest review of this material
was January 18, 2002.
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 Off-Label Usage: This issue of Emergency Medicine Practice
discusses no off-label use of any pharmaceutical product.
32. Which of the following is true about ACE inhibitors?
a. They reduce both preload and afterload.
b. They promote sodium retention.
c. They increase sympathetic stimulation.
d. They decrease left ventricular function.
Class Of Evidence Definitions
Each action in the clinical pathways section of Emergency
Medicine Practice receives an alpha-numerical 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
case-control 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
Faculty Disclosure: 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. Kobayashi, Dr. Fesmire, and Dr. Rosko report no
significant financial interest or other relationship with the
manufacturer(s) of any commercial product(s) discussed in this
educational presentation.
Accreditation: Mount Sinai School of Medicine is accredited by the
Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credit Designation: Mount Sinai School of Medicine designates this
educational activity for up to 4 hours of Category 1 credit toward the
AMA Physician’s Recognition Award. Each physician should claim only
those hours of credit actually spent in the educational activity.
Emergency Medicine Practice is approved by the American College of
Emergency Physicians for 48 hours of ACEP Category 1 credit (per
annual subscription).
Earning Credit: Physicians with current and valid licenses in the United
States, who read all CME articles during each Emergency Medicine
Practice six-month testing period, complete the CME post-test and
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 mailed to each participant
scoring higher than 70% at the end of the six-month testing period.
• Case series, animal studies,
consensus panels
• Occasionally positive results
Indeterminate
• Continuing area of research
• No recommendations until
further research
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent,
contradictory
• Results not compelling
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.
Publisher: Robert Williford. Vice President/General Manager: Connie Austin.
Executive Editor: Heidi Frost.
Direct all editorial or subscription-related questions to EB Practice, LLC:
1-800-249-5770
Fax: 678-366-7934
EB Practice, LLC
305 Windlake Court
Alpharetta, GA 30022
E-mail: [email protected]
Web Site: http://www.ebpractice.com
Emergency Medicine Practice (ISSN 1524-1971) 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 are not intended to establish policy,
procedure, or standard of care. Emergency Medicine Practice is a trademark of EB
Practice, LLC. Copyright 2002 EB Practice, LLC. All rights reserved. No part of this
publication may be reproduced in any format without written consent of EB Practice,
LLC. Subscription price: $249, U.S. funds. (Call for international shipping prices.)
Emergency Medicine Practice is not affiliated
with any pharmaceutical firm
or medical device manufacturer.
Emergency Medicine Practice
28
February 2002