Professional Documents
Culture Documents
Volume 8, Number 12
Authors
Joshua M. Kosowsky, MD
Clinical Director, Department of Emergency
Medicine, Brigham & Womens Hospital, Assistant
Professor Harvard Medical School, MA
You start your shift. An elderly woman with shortness of breath has congestive
heart failure written all over her and her chart. She takes beta-blockers, an ACE
inhibitor, and Lasix. She looks and sounds wet. She receives oxygen,
furosemide, morphine, and nitrate therapy. When you return 20 minutes later, she
looks and feels much better. As you reach for the phone to speak with the admitting physician, you ask yourself, Do I need to get cardiac enzymes? She really
looks so good nowdoes she even need to be admitted?
In the next room, you see an obese woman with shortness of breath, COPD,
CAD, but no known history of CHF, and she does not take Lasix. Her lungs
sound wheezy and you hear crackles. Her legs are edematous and she describes
orthopnea. Does she have a COPD exacerbation or new onset CHF? Should you
send a BNP level? Will her obesity affect this test?
The next evening you see a patient with severe CHF and an ejection fraction of 20%. Her family describes recent fatigue and progressive mild confusion.
She is not edematous and her lungs are clear. Her creatinine has increased from
2.5 to 3.2 g/dl. Is this a CHF exacerbation? What are your treatment options?
Are ionotropes indicated?
Editor-in-Chief
Andy Jagoda, MD, FACEP, Professor
and Vice-Chair of Academic Affairs,
Department of Emergency Medicine;
Mount Sinai School of Medicine;
Medical Director, Mount Sinai Hospital,
New York, NY.
Associate Editor
HSC/Jacksonville, FL.
Gregory L Henry, MD, FACEP, CEO,
Medical Practice Risk Assessment,
Inc; Clinical Professor of Emergency
Medicine, University of Michigan, Ann
Arbor.
Keith A Marill, MD, Instructor,
Department of Emergency Medicine,
Massachusetts General Hospital,
Harvard Medical School, Boston, MA.
International Editors
Valerio Gai, MD, Senior Editor,
Professor and Chair, Dept of EM,
University of Turin, Italy.
Peter Cameron, MD, Chair, Emergency
Medicine, Monash University; Alfred
Hospital, Melbourne, Australia.
Amin Antoine Kazzi, MD, FAAEM,
Associate Professor and Vice Chair,
Department of Emergency Medicine,
University of California, Irvine;
American University, Beirut, Lebanon.
Research Editors
Nicholas Genes, MD, PhD, Mount
Sinai Emergency Medicine Residency.
reflecting at least in part its heterogeneous pathophysiology and presentation. Some experts describe
decompensated heart failure as a syndrome whereby; a patient with an established diagnosis of heart
failure develops increasing signs and symptoms of
the disease after a period of relative stability,17 while
others define acute heart failure syndrome as, [the]
gradual or rapid change in heart failure signs and
symptoms resulting in the need for urgent therapy.
Additional terms used by physicians for this syndrome are CHF exacerbation and acute CHF. The
common theme among these definitions is an abrupt
Epidemiology
As a result of the aging of the United States population and improved survival following myocardial
infarction, the overall prevalence of heart failure is
rising.9,10 At the same time, advances in outpatient
medical therapy are allowing patients with chronic
heart failure to live longer. Over 5 million
Americans with heart failure are alive today, and by
2037, an estimated 10 million people in the United
States will have a diagnosis of heart failure.1,11 Heart
failure now accounts for over one million in-patient
admissions annually, and is the number one reason
for hospitalization among the growing elderly population.1 In 2006, the estimated cost of direct hospital
management for heart failure will be $15.4 billion
dollars.13 According to data from ADHERE, 80% of
patients hospitalized for ADHF will initially present
to the emergency department.14 One retrospective
analysis of 2 million ED visits over an eleven-year
period revealed approximately 1.1% of visits to have
a primary diagnosis of heart failure or pulmonary
edema.15
The Euro Heart Failure survey and the Acute
Decompensated Heart Failure National Registry
(ADHERE) add to the current knowledge on the epidemiology of heart failure. The mean age of patients
with ADHF is between 71-75 years with an equal
ratio of men to women.4, 16 New studies have shown
that almost half of all patients presenting with ADHF
have preserved systolic function, coronary artery disease, hypertension and diabetes.4
Definitions, Etiology
There is no universally accepted definition of ADHF,
EBMedicine.net December 2006
clinical change from baseline affecting the cardiopulmonary system that requires emergent or urgent
intervention. Regardless of terminology, this article
will refer to this acute clinical presentation as
Acutely Decompensated Heart Failure or ADHF.
Chronic heart failure is itself a complex syndrome, and is characterized by inadequate cardiac
output at physiologic filling pressures. The etiologies of chronic heart failure are numerous and
diverse (Table 2). In the United States, the vast
majority of heart failure arises as a consequence of
coronary artery disease and/or long-standing hypertension. Table 3 describes the American Heart
Association classification and the commonly used
New York Heart Association (NYHA) classification
system. Understanding the differences in both classification systems can be helpful in evaluating and
managing individual patients when they present
with ADHF.
In the ED, heart failure can present de novo as
an acute process or as an acute decompensation of
chronic heart failure. For example, acute myocardial
infarction (MI) with or without valvular dysfunction
can cause acute heart failure. More commonly,
patients seen in the ED have chronic heart failure
that has decompensated as the result of one or more
precipitating factors.
Pathophysiology
Regardless of etiology, inadequate cardiac function
Moderate limitation
Severe limitation
Symptoms
Asymptomatic during usual daily activities
Mild symptoms (dyspnea, fatigue, or chest pain) with
ordinary daily activities
Symptoms noted with minimal activity
Symptoms at rest
Sources: Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart
Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with
the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart
Rhythm Society. Circulation 2005; 112:e154-235.
sets in motion a common set of compensatory mechanisms, brought about by neurohormonal activation
and characterized by elevated sympathetic tone,
fluid and salt retention, and ventricular remodeling.
These adaptations can allow heart failure to remain
stable (or compensated) for a period of time, but
also provide the final common pathway for decompensationa downward spiral that can accelerate
dramatically in response to a particular precipitant
or stress. High circulating levels of aldosterone, vasopressin, epinephrine, and norepinephrine are ultimately maladaptive, as tachycardia and vasoconstriction compromise the intrinsic performance of the
left ventricle (LV) and simultaneously worsen
myocardial oxygen balance. Deterioration of left
ventricular function results in further neurohormonal activation and self-perpetuation of this adverse
cycle (Figure 1). An acute decompensation can
develop over a period of minutes, hours, or days and
can range in severity from mild symptoms of volume
overload or decreased cardiac output to frank pulmonary edema or cardiogenic shock.
ADHF can be viewed as three overlapping syn-
Prehospital Care
Even before patients reach the hospital, ADHF is
associated with significant morbidity and mortality
including malignant arrhythmias and prehospital
cardiac arrest.28 All patients should have continuous
cardiac monitoring and intravenous access established if possible (See also Clinical Pathway:
Prehospital Therapy For Acutely Decompensated
Heart Failure). Because successful management
depends on reversal of hypoxia, pulse oximetry and
supplemental oxygen should be utilized routinely in
the prehospital care of patients with ADHF.
Prehospital personnel should alert ED staff of any
Differential Diagnosis
Acutely decompensated heart failure can coexist
with or closely mimic a number of other cardiac, respiratory, and systemic illnesses (Table 6). In fact,
when patients present to the ED with undifferentiated dyspnea, the diagnosis of heart failure is often
overlooked.18 Patients who present with mild or
non-specific symptoms pose a particular diagnostic
challenge. Symptoms such as weakness, lethargy,
fatigue, anorexia, or lightheadedness may actually be
a manifestation of decreased cardiac output and low
output ADHF. Older patients frequently lack typical
signs and symptoms of heart failure.20 These features
may be obscured by the aging process itself or by the
presence of coexisting medical conditions.
Patients presenting with acute exacerbations of
either cardiac dysfunction or COPD may have
wheezing on pulmonary auscultation with signs of
chronic right-sided heart failure and non-diagnostic
chest radiographs. In heart failure patients, pulmonary embolism may be clinically indistinguishable from ADHF.21
Precipitating factors for decompensation
should be sought in a careful and deliberate fashion
(Table 4). Myocardial ischemia or infarction and
non-compliance with medications or dietary indiscrition are the most common causes of clinical decompensation.22-27 Often, the cause-effect relationship of
ADHF is difficult to determine due to the co-prevalence of diseases such as coronary artery disease,
hypertension, and atrial fibrillation.14 The exact
Emergency Medicine Practice
patient presenting with symptoms suggestive of pulmonary edema or cardiogenic shock, and receive online medical advice when appropriate. Prehospital
staff trained to interpret electrocardiograms should
obtain a 12-lead electrocardiogram and, if ACS is
identified, ED staff or medical control should be
immediately informed.
The decision to treat a patient in the relatively
uncontrolled prehospital environment carries some
risks that must be weighed against expected benefits.
With few exceptions, the safety and efficacy of prehospital medications have been poorly studied.29
Prehospital therapy for ADHF should be undertaken
with particular caution in light of the relatively high
number of inaccurate diagnoses made in the field.
As many as 50% of patients with assumed cardiac
associated respiratory distress are diagnosed with a
different condition once they arrive at the hospital.28,30,31
Despite these concerns, evidence suggests that prehospital therapy for presumed ADHF can prevent
serious complications and improve survival, particularly for critically ill patients.28,30,31 In a large retrospective case series of 493 patients, there was a
decrease in mortality among critical and non critical
patients who received treatment (nitroglycerin,
Lasix and/or morphine) compared to no pharmacologic intervention.30 In European countries, where
physicians commonly staff ambulances, intensive
prehospital treatment of patients with severe heart
failure confers short-term benefits.32-34 A retrospective
review of 640 patients that presented in the prehospital setting with acute pulmonary edema (APE)
revealed that the use of nitrates were associated with
a trend toward decreased mortality.32
Sublingual nitroglycerin appears to be the safest
and most effective of the prehospital medications
used for presumed pulmonary edema.31 A prospective, randomized, double blind study of 57 patients
comparing morphine, nitroglygerin, and furosemide
found nitroglycerin to be the safest and most effective intervention in the prehospital management of
ADHF.31 Prehospital intravenous (IV) nitrates also
yield positive short-term results. The role of other
medications for heart failure in the prehospital setting is less clear. Early administration of furosemide
appears to have very little benefit, and may result in
short-term complications.31,35 The prehospital use of
morphine sulfate for presumed pulmonary edema is
associated with an increased rate of endotracheal
intubation, particularly among patients who turn out
to have been misdiagnosed in the field.31,36 A
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prospective, randomized study of 57 patients administered four different drug regimens found that the
administration of morphine and Lasix showed little
improvement.31
Physical
Vital signs provide a sense of the severity of illness
and can suggest etiologic factors for decompensation. Hyperthermia or hypothermia may indicate
sepsis or thyroid disease. In the absence of rate-controlling pharmacologic agents, tachycardia is nearly
universal in ADHF. Bradycardia should raise concern for high-degree AV block, hyperkalemia, drug
toxicity (digoxin, calcium channel, beta blocker), or
severe hypoxia. Hypertension is commonly seen in
both systemic volume overload and acute diastolic
dysfunction syndromes of ADHF. Hypotension can
be baseline for patients with end-stage cardiomyopathy or low output heart failure, but otherwise should
raise concern for sepsis, massive pulmonary
embolism, or cardiogenic shock.
Signs of congestion may be detected by careful
attention to heart and lung sounds, jugular venous
distention (JVD), hepatomegaly, and peripheral
edema. Elevated central venous pressure (CVP) is
present when the top of the external or internal jugular veins is more than 3 cm of vertical distance above
the sternal angle.43 The diagnostic utility of this physical exam finding is well documented for chronic heart
failure, but less so for ADHF in the ED setting.44, 45
JVD, abdominojugular reflux, and an audible 3rd
heart sound are very specific. Patients who present
with these exam findings are at least five times more
likely to have ADHF37 (Table 8). A new cardiac murmur in the proper context must be presumed to signal acute valvular or papillary muscle dysfunction.
Diagnostic Studies
Laboratory tests
The majority of patients who present with complaints suggestive of ADHF will need basic laboratory testing. A complete blood count (CBC) is useful
for ruling out anemia as a cause for decompensation.
Some believe that an elevated white blood count
may suggest the presence of an infectious process,
especially if bands are present. However, this is not
well studied in the patient who presents with dyspnea. Serum chemistries help assess renal function
and overall fluid and electrolyte balance.
Cardiac Markers
The question as to which patients with ADHF
require screening for cardiac enzymes is not well
studied. Additional information from the history
(e.g., chest discomfort, new-onset heart failure, or
significant risk factors for coronary artery disease)
should heighten the suspicion of associated cardiac
ischemia. Although not always clear, a high level of
suspicion for acute coronary syndrome (ACS) should
be considered in patients presenting with ADHF.
Several studies have shown that elevated cardiac troponins are found in up to one-third of patients with
severe heart failure and help to identify those with
worse short-term prognosis.46, 47 According to one
review of 151 patients with a discharge diagnosis of
heart failure, 70% of patients did not report chest
pain.47 Therefore, the ED physician should strongly
consider screening for cardiac enzymes in any
patient who presents with ADHF, regardless of the
presence or absence of chest pain.
cardiac conditions (i.e., age, renal insufficiency, pulmonary embolism, and cor pulmonale).58, 64-67 Since
BNP and NT-proBNP levels increase with age, cutpoints for diagnosing ADHF are elevated among the
elderly and have discriminatory value.58,65,67 Data
from the Breathing Not Properly Multinational Study
indicate that BNP is a better indicator at younger
ages.65 In a prospective, observational study of elderly patients greater than 65 years of age with acute
dyspnea, a higher BNP level of 250 pg/ml has a
specificity of 90% in diagnosing ADHF.58
The role of BNP in patients with severe renal
failure is less studied. Patients with severe renal failure have reduced ability to clear metabolites and volume overload resulting in higher levels of circulating
BNP. These proposed elevated cut-points have discriminatory value, but actual cut points are yet to be
determined.59
Obese patients with elevated filling pressures
may have less myocardial stretch which lowers
measured BNP and NT-proBNP levels. This may be
due to increased extracardiac pressure associated
with an elevated BMI. The sensitivity of BNP and
NT-proBNP at existing cut points for obese patients
may be lower than expected and a true cut-point in
this setting is unclear.68 The Breathing Not Properly
Multinational Study found an inverse relationship
between BMI and BNP.69 For overweight and obese
patients, BNP is 80% sensitive at a cut point of 100
pg/ml. In addition, 20% of these patients with
ADHF had BNP levels less than the standard cut
off.68 NT-proBNP may also lose discriminatory value
among obese patients. The ProBNP Investigation of
Dyspnea in the Emergency Department (PRIDE)
study identified significantly lower ProBNP and
BNP levels in overweight and obese patients presenting with ADHF.68
For patients with classic signs of ADHF (i.e.
prior episodes of ADHF, volume overload, dyspnea,
and orthopnea) or those with shortness of breath
consistent with other etiologies (i.e. asthma, COPD),
BNP is not likely to assist in the diagnostic workup.
Checking BNP levels in indeterminate cases may aid
in diagnosing or excluding ADHF, but results may
leave the EP with additional questions.
A provocative single-center study used BNP to
diagnose ADHF and showed beneficial effects on
patient outcomes. In the B-Type Natriuretic Peptide
for Acute Shortness of Breath Evaluation (BASEL)
study, patients presenting to the ED with acute dyspnea were randomized to standard clinical evaluation
Emergency Medicine Practice
Recent studies have shown that a normal chest radiograph alone cannot exclude ADHF. According to a
recent ADHERE study, one in five patients without
radiographic findings of interstitial edema, pulmonary edema, or vascular congestion received a
final diagnosis of ADHF.73
Cardiac Echocardiography
Echocardiography is invaluable and is, in some
sense, considered the gold standard for assessing
the status of left ventricular function, distinguishing
between systolic and diastolic failure, and identifying regional wall motion abnormalities.
Echocardiography can also assist in diagnosing or
excluding potentially reversible etiologies of an acute
decompensation such as pericardial tamponade,
massive pulmonary embolus, ruptured chordae
tendineae, or ruptured ventricular septum (see
Special Circumstances).
Echocardiography is probably not indicated in all
instances of ADHF, particularly if a patient has had a
recent echocardiogram and a clear precipitant for
decompensation. ACC/AHA guidelines recommend
transthoracic echocardiography as soon as possible
after initial stabilization for any patient who presents
with acute pulmonary edema, unless there are obvious precipitating factors and the patients cardiac status has been adequately evaluated previously.74
Guidelines for establishing an effective system for
emergency echocardiography have been published.75
Experience with emergency physicians performing
bedside echocardiography has generally been limited
to ruling out pericardial effusion / tamponade.76-78
Treatment
As with any ill patient, the initial focus of treatment
will be on airway and breathing (see Clinical
Pathway: Treatment For Acutely Decompensated
Heart Failure). Although many patients can be managed with oxygen, with or without non-invasive
ventilatory support, the presence of agonal respirations or profoundly depressed mental status will
mandate emergent intubation with the caveat that
the respiratory symptoms that accompany ADHF
reflect cardiovascular rather than pulmonary pathology and are therefore often rapidly reversible with
aggressive medical therapy (see Respiratory
Therapy).
Sitting the patient upright may reduce pulmonary
congestion and improve respiratory dynamics.
Studies in patients with chronic heart failure show a
large rise in airflow resistance after lying supine for
five minutes, a condition that is reversed by sitting
erect.82 Practice guidelines recommend early use of
pulse oximetry, noninvasive blood pressure monitoring, and continuous cardiac monitoring as these can
provide early warnings of decompensation.3
Pharmacologic Therapy
The main objectives of pharmacologic therapy for
ADHF are relief of pulmonary congestion and
improvement in systemic tissue perfusion. The goal
of therapy is to reduce preload and enhance left ventricular function, while maintaining or improving
myocardial oxygen balance. While the basic
approach to treating ADHF has not changed over the
past two decades, there has been increasing emphasis on afterload reduction and other means of counteracting the adverse cycle of neurohormonal activa11
Nitrates
Nitrates are recommended as initial therapy for
ADHF of both ischemic and non-ischemic origin, par-
12
The European Society of Cardiology (ESC) recommends sodium nitroprusside for patients with
marked systemic hypertension, severe mitral or aortic valvular regurgitation, or pulmonary edema not
responsive to standard nitrate therapy.3
Nitroprusside directly dilates resistance vessels,
rapidly reducing blood pressure and afterload.83
Typically, nitroprusside is started at a dose of 0.1 to
0.3 mcg/kg/min and advanced as needed to
improve clinical and hemodynamic status, maintaining a SBP greater than 90 or mean arterial pressure
greater than 65 mm Hg. In patients with renal failure, long-term use of nitroprusside carries the potential for cyanide toxicity as metabolites accumulate.
Diuretics
Diuretics are the mainstay of therapy for patients
with systemic volume overload.2,3 Although this
practice is recommended by societies and is a commonly accepted approach, there have not been multiple randomized, controlled trials or meta-analysis to
support it use. On the other hand, it is important to
recognize that patients who present with ADHF are
not always volume overloaded. Patients with acute
diastolic dysfunction may benefit more from redistribution of circulating volume by using vasodilators.
The indiscriminate use of diuretics carries the risk of
overdiuresis and detrimental effects on renal function, particularly among elderly patients. Even without overdiuresis, there is growing evidence that
the higher doses of diuretics required to treat
advanced heart failure correlate to worsening renal
function, which has been tied to both longer hospitalizations and increased mortality after discharge.
This adds strength to the argument that the focus
should be on changing loading conditions with
vasodilators rather than diuresis as the stand alone
therapy it often is.
Evidence from a large number of in vitro and in
vivo experiments suggest that direct vascular actions
also contribute to the clinical effects of furosemide.94-97
These actions are not necessarily advantageous, in
that their net effect may promote further activation
of the sympathetic and renin-angiotensin systems
characterized by reflex vasoconstriction, worsening
of cardiac loading conditions, and a decline in cardiac output.98,99 Studies comparing the acute effects
of diuretics and nitrates have emphasized the more
favorable overall hemodynamic effects of the latter
group, as described earlier.
(continued on page 18)
13
14
15
16
17
ACE Inhibitors
Angiotensin converting enzyme inhibitors (ACE
inhibitors) represent a logical extension of vasodilator therapy. The beneficial hemodynamic effects of
ACE inhibitors in acute heart failure have been
appreciated for two decades.115 Acutely, ACE
inhibitors reduce both preload and afterload,
improve renal hemodynamics, impair sodium retention, attenuate sympathetic stimulation, and maintain or enhance left ventricular function.116-118
Although not currently recommended by the
European Society of Cardiology or the Heart Failure
Society of America in the setting of acute heart failure, drug regimens that include an ACE inhibitor
appear to have hemodynamic advantages over those
based upon other vasodilators.119-121
For acutely decompensated heart failure, ACE
inhibitors can be administered intravenously (e.g.,
enalaprilat), orally (e.g., captopril) or sublingually
(e.g., emptied captopril capsules contents).
Nesiritide
Nesiritide (recombinant BNP) is FDA approved for
the treatment of ADHF symptoms. BNP has
vasodilatory as well as mild diuretic and natriuretic
properties. When administered in supraphysiologic
doses, it exerts favorable hemodynamic, natriuretic,
and neurohormonal effects.106-109 Nesiritide can be
administered intravenously with a 2 mcg/kg bolus
Emergency Medicine Practice
18
Morphine
Morphine is one of the oldest drugs still in use for
the treatment of acute heart failure and remains an
adjunct for treating the anxiety and discomfort associated with pulmonary edema. With high doses of
morphine, direct vasodilation may result from histamine release, but the predominant hemodynamic
effects of morphine appear to be mediated through
the central nervous system.129 Morphine can be
administered safely to most patients. However,
because of its sedative properties and potential to
depress respirations, caution should be exercised
when administering morphine in the setting of
chronic pulmonary insufficiency or suspected acidosis. One retrospective study found that ED administration of morphine to patients with pulmonary
edema was associated with an increased rate of
endotracheal intubation and CCU admission.125
Inotropes
Short-term therapy with ionotropes may benefit
patients presenting with low output failure, which
are considered acceptable treatment modalities,
although with notable risks.2,3 Classically, inotropic
agents have been reserved for the treatment of cardiogenic shock. However, short-term inotropic support may also be seen as beneficial for patients with
low output failure who fail to respond to conventional therapy. While short-term inotropic therapy
clearly improves hemodynamic performance, the
impact on clinical outcomes is less sanguine.
Inotropic therapy has deleterious effects upon
patients with preserved or moderately depressed
ventricular function and congestion. The Outcomes
of a Prospective Trial of Intravenous Milrinone for
Exacerbations of Chronic Heart Failure, a randomized, controlled trial, showed no increased benefit
over standard therapy with the use of milrinone.126,127
ADHERE also supports this finding indicating an
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Respiratory Therapy
The majority of patients with respiratory distress
respond to supplemental oxygen and standard pharmacologic therapy, but patients with persistent
hypoxemia or progressive fatigue will require at least
temporary respiratory support (see also the July
2001 issue of Emergency Medicine Practice,
Noninvasive Airway Management Techniques:
How And When To Use Them).
Continuous positive airway pressure (CPAP)
improves lung mechanics by recruiting atelectatic
alveoli, improving pulmonary compliance, and
19
Caveats: Levels of BNP or NT-proBNP are affected by their half-lives. BNP levels may also be
elevated in eldery patients and patients with
renal insufficiency and lower in obese patients.
20
Special Circumstances
Cardiogenic Shock
Cardiogenic shock in the setting of heart failure is
most often seen in the setting of acute ST-segment
elevation MI and acute valvular diseases. Mortality
rates for patients with frank cardiogenic shock
remain alarmingly high, ranging from 50 to 80%165
Stat echocardiograms play a pivotal role in diagnostics and treatment, as many etiologies of cardiogenic
shock will require surgical management. In the context of acute MI, emergent cardiac catheterization
and revascularization have been shown to be of benefit.3,166,167
Other potentially reversible causes of cardiogenic
shock, such as acute valvular dysfunction, ventricular septal wall rupture, and pericardial tamponade,
need to be excluded or addressed promptly. Acute
valvular dysfunction can occur in the setting of ACS
(ischemic papillary muscle dysfunction/rupture) or
independently in acute mitral/aortic insufficiency,
aortic dissection, or prosthetic valve thrombosis
causing cardiogenic shock. Free wall rupture and
ventricular septal wall rupture are uncommon complications of AMI that require rapid recognition.
Once the diagnosis is made, surgical management
provides an opportunity for survival. Again, the etiology of these types of cardiogenic shock should be
promptly identified with emergent echocardiography.2 Once acute surgical causes of cardiogenic
shock are ruled out, non-cardiac etiologies of shock,
such as hypovolemia, sepsis, poisoning, and massive
pulmonary embolism must also be entertained.
Aside from addressing reversible causes of car21
ICG has been investigated in a variety of clinical settings and has been found to compare moderately
well with other modalities for assessing hemodynamics (e.g., echocardiography, Swan-Ganz catheterization).179,180 Because the technique is non-invasive,
portable, and capable of providing beat-to-beat information, potential applications in the ED are numerous. ICG is less accurate in patients with underlying
heart disease; however, serial measurements may
still provide useful information, such as monitoring
response to therapy. In a small study of 38 patients
with undifferentiated dyspnea, incorporation of ICG
data increased diagnostic accuracy of patients with
cardiac causes of dyspnea.181 In the Emergency
Department Impedance Cardiographyaided
Assessment Changes Therapy (ED-IMPACT) trial,
the use of ICG affected treatment plans for 24% of
patients with acute dyspnea.182 However, more studies are necessary to determine the overall utility of
this diagnostic tool and its effects on morbidity, mortality, cost, and length of stay.
Beta-blockers
Large, randomized, controlled trials have demonstrated clear morbidity and mortality benefits of
long-term beta-blocker therapy in patients with systolic heart failure.183-185 In contrast, short-term administration of beta-blockers to patients with severe systolic dysfunction can cause life-threatening clinical
deterioration.186 There has been no study that specifically addresses the potential benefits of beta-blocker
therapy in the setting of ADHF. Therefore, beta-blockers are not routinely recommended by the ESC for treatment of acutely decompensated heart failure and caution is
advised during its use.3 In the setting of an acute
decompensation, chronic beta-blocker therapy
should either be temporarily discontinued or administered cautiously at a reduced dose, according to the
ESC. On the other hand, in the context of ongoing
ischemia, tachycardia, and severe hypertension betablockers may be considered.3
Less is known specifically about the safety and
efficacy of beta-blocker therapy for patients with
acute diastolic dysfunction. In theory, the value of
reducing hypertension and tachycardia would outweigh any concern about negative inotropy in these
patients. Further studies are needed to clarify the
role of beta-blockers in this context.
Calcium Sensitizers
Calcium sensitizers are a novel class of agents that
23
Vasopressin Antagonists
Elevated vasopressin levels are found in patients
with ADHF, and vasopressin antagonists have been
proposed as a means to improve diuresis in patients
with ADHF. In a hemodynamic trial, conivaptan, a
V1a and V2 receptor antagonist, decreased PCWP
and right atrial pressures.191 In a randomized controlled trial among patients with ADHF in the setting
of systolic dysfunction, tolvaptan, a V2 receptor
antagonist, has been shown to decrease body weight
with no changes in worsening heart failure at 60
days.192
Endothelin Antagonists
Endothelin one (ET-1), a potent vasoconstrictor and
modulator of the renin-angiotensin-aldosterone system, are elevated in patients with ADHF. In hemodynamic studies, tezosentan, an ET-1 receptor antagonist, reduced preload and afterload, delayed
myocyte hypertrophy, and increased myocardial contractility.193 A randomized, controlled trial comparing
tezosentan with placebo among patients with low
output ADHF showed improved hemodynamics
with the use of tezosentan without significant
changes in dyspnea compared to standard therapies.194 Future studies will clarify tezosentans role
in the treatment of ADHF.
Disposition
Even in this era of cost containment, the vast majority of patients who present with ADHF are admitted
to the hospital.195 According to ADHERE, the
majority of patients with ADHF are admitted to
telemetry and step-down units while 14% of patients
are admitted to the ICU during their hospital stay.14
Meanwhile, hospital costs for in-patient care of
ADHF are continuing to rise. In-hospital mortality
remains approximately 2.3 to 7%,14,126,196 with major
adverse events occurring in up to 18% of patients.197,198
In patients with NYHA class III or IV heart failure
who are admitted for ADHF, there is a 9.6% mortality
rate at 60 days and a 30% combined rate of rehospitalization and/or death.6 However, while the realities
of modern healthcare economics may not favor routine hospitalization, premature release of inadequately treated patients are likely to result in increased
short-term morbidity and mortality.199
In general, clinicians have great difficulty judging the prognosis of patients with exacerbations of
heart failure.200 Acutely decompensated heart failure
24
25
26
1. She was just weak and dizzy. How was I supposed to know she had heart failure?
You found out when she went into acute pulmonary edema after the aggressive fluid bolus.
Non-specific symptoms such as weakness, lethargy, fatigue, anorexia, or lightheadedness may be a
manifestation of low output acutely decompensated heart failure. Older patients can be particularly difficult to evaluate because they often lack
typical signs and symptoms of heart failure.
6. She was clearly wet and needed to be aggressively diuresed. Is it my fault her creatinine
doubled by the next day?
Maybe. This elderly woman with acute diastolic
dysfunction was not suffering from volume overload. Her pulmonary congestion may have
responded better to vasodilator therapy than to
aggressive diuresis which ended up impairing her
renal function and prolonging her hospital stay.
7. I always thought sublingual nitroglycerin was
harmless. I didnt expect his systolic BP to drop
to single digits.
Nitrates are fast, effective, and relatively safe;
however, patients with preload-dependent conditions (e.g., valvular stenosis) do not tolerate them
well.
27
any ischemic ECG changes, but you changed her disposition to a step-down unit for closer monitoring.
You decided to send a BNP test on the obese
woman in the next room since it was unclear
whether she was presenting with a COPD exacerbation or ADHF. The BNP returned at 1100 pg/dl confirming a diagnosis of ADHF. You informed her of
your clinical diagnosis and she improved after
administration of nitroglycerin and furosemide. She
called you back into the room later to tell you that
she remembers taking a water pill in the past for
similar symptoms but was not restarted on this medication when she moved to your town. This further
confirmed your clinical diagnosis.
Remembering that less is more for patients
with low output failure, you immediately called the
cardiologist of the woman with recent fatigue, confusion, and an ejection fraction of 20%. You discussed
the role of inotropes with her cardiologist and agreed
to hold off on inotropes in the ED, but immediate
admission to the ICU for monitoring was necessary.
Prior to her disposition, you confirmed that her urinalysis and chest x-ray did not show signs of infection to account for her fatigue and mild confusion.
At the end of your busy shift, you reflected upon
the diverse presentation of patients with ADHF and
the importance of tailoring therapy to a specific syndrome.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
References
13.
2.
14.
15.
16.
17.
18.
20.
21.
28
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
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(7085):936-40. (Cross-sectional, prospective; 71
patients)
Le Conte P, Coutant V, Nguyen JM, et al. Prognostic factors in
acute cardiogenic pulmonary edema. Am J Emerg Med
1999;17(4):329-32. (Prospective, cohort; 186 patients)
Goldberger J, Peled H, Stroh J, et al. Prognostic factors in
acute pulmonary edema. Arch Intern Med 1986;146(3):489-93.
(Chart review; 94 patients)
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(9):2013-6.
(Prospective; 101 patients)
Chin MH, Goldman L. Factors contributing to the hospitalization of patients with congestive heart failure. Am J Pub Health
1997;87(4):643-8. (Cross-sectional chart review; 435 patients)
Bennett SJ, Huster GA, Baker SL, et al. Characterization of the
precipitants of hospitalization for heart failure decompensation. Am J Crit Care 1998;7(3):168-74. (Chart review; 691
patients)
Tsuyuki RT, McKelvie RS, Arnold MO, et al. Acute precipitants of congestive heart failure exacerbations. Arch Intern
Med 2001;161(19):2337-42. (Prospective; 768 patients)
Tresch DD, Dabrowski RC, Fioretti GP, et al. Out-of-hospital
pulmonary edema: diagnosis and treatment. Ann Emerg Med
1983;12(9):533-7. (Chart review; 62 patients)
Brazier H, Murphy AW, Lynch C. Searching for the evidence
in pre-hospital care: a review of randomized controlled trials.
J Accid Emerg Med 1999;16(1):18-23. (Review)
Wuerz RC, Meador SA. Effects of prehospital medications on
mortality and length of stay in congestive heart failure. Ann
Emerg Med 1992;21(6):669-74. (Retrospective case series; 493
patients)
Hoffman JR, Reynolds S. Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital
pulmonary edema. Chest 1987; 92(4):586-93.
Bertini G, Giglioli C, Biggeri A, et al. Intravenous nitrates in
the prehospital management of acute pulmonary edema. Ann
Emerg Med 1997;30(4):493-499. (Chart review; 64 patients)
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(1):15-24. (Retrospective; 316 patients)
Kallio T, Kuisma M, Alaspaa A, et al. The use of prehospital
continuous positive airway pressure treatment in presumed
acute severe pulmonary edema. Prehosp Emerg Care
2003;7(2):209-13. (Retrospective, cohort; 121 patients)
Sporer KA, Tabas JA, Tam RK, et al. Do medications affect
vital signs in the prehospital treatment of acute decompensated heart failure? Prehosp Emerg Care 2006;10(1):41-5. (Chart
review; 319 patients)
Chambers JA, Baggoley CJ. Pulmonary oedemaprehospital
treatment. Caution with morphine dosage. Med J Aust
1992;157(5):326-8. (Case series; 3 patients)
Wang CS, FitzGerald JM, Schulzer M, et al. Does this dyspneic patient in the emergency department have congestive heart
failure? JAMA 2005;294(15):1944-56. (Meta-analysis)
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):110-6. (491 patients)
Michalsen A, Konig G, Thimme W. Preventable causative factors leading to hospital admission with decompensated heart
failure. Heart 1998;80(5):437-41. (Prospective; 179 patients)
Opasich C, Febo O, Riccardi PG, et al. Concomitant factors of
decompensation in chronic heart failure. Am J Cardiol
29
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
30
renal and endocrine effects of atrial natriuretic peptide infusion in severe heart failure. J Am Coll Cardiol 1988;12(1):175-86.
(Controlled, prospective; 12 patients)
107. 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)
108. 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(12):3184-9. (Double-blind, placebo-controlled, randomized, crossover; 27 patients)
109. Abraham WT, Lowes BD, Ferguson DA, et al. Systemic hemodynamic, neurohormonal, and renal effects of a steady-state
infusion of human brain natriuretic peptide in patients with
hemodynamically decompensated heart failure. J Card Failure
1998;4(1):37-44. (Double-blind, placebo-controlled, randomized; 16 patients)
110. Abraham WT, Cheng ML, Smoluk G. Clinical and hemodynamic effects of nesiritide (B-type natriuretic peptide) in
patients with decompensated heart failure receiving beta
blockers. Congest Heart Fail 2005;11(2):59-64. (Retrospective,
489 patients)
111. Mills RM, LeJemtel TH, Horton DP, et al. Sustained hemodynamic effects of an infusion of nesiritide (human b-type natriuretic peptide) in heart failure: a randomized, double-blind,
placebo-controlled clinical trial. Natrecor Study Group. J Am
Coll Cardiol 1999;34(1):155-62. (Randomized, double-blind,
placebo controlled; 103 patients)
112. Colucci WS, Elkayam U, Horton DP, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated
congestive heart failure. Nesiritide Study Group. N Engl J Med
2000;343(4):246-53. (Efficacy comparative trial; 127,305
patients)
113. Sackner-Bernstein JD, Kowalski M, Fox M, et al. Short-term
risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled
trials. JAMA 2005;293(15):1900-5. (Meta-analysis)
114. Sackner-Bernstein JD, Skopicki HA, Aaronson KD. Risk of
worsening renal function with nesiritide in patients with
acutely decompensated heart failure. Circulation
2005;111(12):1487-91. (Meta-analysis)
115. 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(5):369-373.
(Prospective; 8 patients)
116. Barnett JC, Zink KM, Touchon RC. Sublingual captopril in the
treatment of acute heart failure. Curr Ther Res 1991;49:274-81.
(Two-part observational study; 7 and 12 subjects)
117. 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(4):523-7.
(Prospective; 10 patients)
118. 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(6):1316-24. (Double-blind, placebo-controlled, randomized; 20 patients)
119. 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(3):351-9.
(Controlled, randomized, cross-over; 24 patients)
120. Verma SP, Silke B, Reynolds GW,et al. Vasodilator therapy for
acute heart failure: hemodynamic comparison of
hydralazine/isosorbide, alpha-adrenergic blockade, and
angiotensin-converting enzyme inhibition. J Cardiovasc
31
32
cardiogenic circulatory collapse. Am Heart J 1982;103(6):9951000. (Controlled, randomized, cross-over study; 13 patients)
169. Weinfeld MS, Chertow GM, Stevenson LW. Aggravated renal
dysfunction during intensive therapy for advanced chronic
heart failure. Am Heart J 1999;138(2 Pt 1):285-90.
(Retrospective; 48 patients)
170. Hillege HL, Girbes AR, de Kam PJ, et al. Renal function, neurohormonal activation, and survival in patients with chronic
heart failure. Circulation 2000;102(2):203-10. (Retrospective,
sub-group analysis; 372 patients)
171. Krumholz HM, Chen YT, Vaccarino V, et al. Correlates and
impact on outcomes of worsening renal function in patients >
or =65 years of age with heart failure. Am J Cardiol
2000;85(9):1110-3. (Retrospective; 1681 patients)
172. Harnett JD, Foley RN, Kent GM, et al. Congestive heart failure in dialysis patient: prevalence, incidence, prognosis, and
risk factors. Kidney Int 1995;47(3):884-90. (Prospective, multicenter cohort; 432 patients)
173. Sacchetti A, Harris R, Patel K, et al. Emergency department
presentation of renal dialysis patients: indications for EMS
transport directly to dialysis centers. J Emerg Med
1991;9(3):141-4. (Prospective; 100 patients)
174. Schmieder RE, Messerli FH, deCarvalho JG, et al. Immediate
hemodynamic response to furosemide in patients undergoing
chronic hemodialysis. Am J Kidney Dis 1987;9(1):55-9.
(Prospective; 10 patients)
175. Crijns HJ, Van den Berg MP, Van Gelder IC, et al.
Management of atrial fibrillation in the setting of heart failure.
Eur Heart J 1997;18 Suppl C:C45-9.
176. 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(6):1262-77. (Practice guideline)
177. 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(8):614-32. (Review)
178. 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(6):1149-53.
(Randomized, controlled, prospective; 60 patients)
179. 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(3):450-5. (Prospective, observational; 24 patients)
180. Raaijmakers E, Faes TJ, Scholten RJ, et al. A meta-analysis of
three decades of validating thoracic impedance cardiography.
Crit Care Med 1999;27(6):1203-13. (Meta-analysis)
181. Springfield CL, Sebat F, Johnson D, et al. Utility of impedance
cardiography to determine cardiac vs. noncardiac cause of
dyspnea in the emergency department. Congest Heart Fail
2004;10(2 Suppl 2):14-6. (Retrospective; 38 patients)
182. Peacock WF, Summers RL, Vogel J, et al. Impact of impedance
cardiography on diagnosis and therapy of emergent dyspnea:
the ED-IMPACT trial. Acad Emerg Med 2006;13(4):365-71.
(Convenience sample; 89 patients)
183. 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(21):1349-55. (Double-blind, placebo-controlled;
1094 patients)
184. 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(9169):20017. (Doubleblind, controlled, randomized; 3991 patients)
185. CIBIS-II. The cardiac insufficiency bisoprolol study II (CIBISII): a randomized trial. Lancet 1999;353(9146):9-13. (Doubleblind, placebocontrolled, randomized, multi-center; 2647
33
patients)
186. Felix SB, Stangl V, Kieback A, et al. Acute hemodynamic
effects of beta-blockers in patients with severe congestive
heart failure; comparison of celiprolol and esmolol. J
Cardiovasc Pharmacol 2001;38(5):666-71
186b. Follath F, Cleland JG, Just H, et al. Efficacy and safety of
intravenous levosimendan compared with dobutamine in
severe low-output heart failure (the LIDO study): a randomised double-blind trial. Lancet 2002;360(9328):196-202.
(Randomized, double-blind; 103 patients)
187. 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(6):1903-12. (Double-blind, placebo-controlled, randomized, multi-center; 151 patients)
188. Zairis MN, Apostolatos C, Anastasiadis P, et al. The Effect of a
Calcium Sensitizer or an Inotrope or None in Chronic Low
Output Decompensated Heart Failure: Results From the
Calcium Sensitizer or Inotrope or None in Low Output Heart
Failure Study (CASINO). Program and abstracts from the
American College of Cardiology Annual Scientific Sessions
2004; March 7-10, 2004; New Orleans, Louisiana. Abstract 8356. (Abstract)
189. Lubsen J, Just H, Hjalmarsson AC, et al. Effect of pimobendan
on exercise capacity in patients with heart failure: main
results from the Pimobendan in Congestive Heart Failure
(PICO) trial. Heart 1996;76(3):223-31. (Randomized, doubleblind, controlled; 317 patients)
190. Suwa M, Seino Y, Nomachi Y, et al. Multicenter prospective
investigation on efficacy and safety of carperitide for acute
heart failure in the real world of therapy. Circ J
2005;69(3):283-90. (Prospective; 3777 patients)
191. Udelson JE, Smith WB, Hendrix GH, et al. Acute hemodynamic effects of conivaptan, a dual V(1A) and V(2) vasopressin receptor antagonist, in patients with advanced heart
failure. Circulation 2001;104(20):2417-23. (Randomized, double-blind; 142 patients)
192. Gheorghiade M, Gattis WA, OConnor CM, et al. Effects of
tolvaptan, a vasopressin antagonist, in patients hospitalized
with worsening heart failure: a randomized controlled trial.
JAMA 2004;291(16):1963-71. (Randomized, controlled; 319
patients)
193. Duchman SM, Thohan V, Kalra D, et al. Endothelin-1: a new
target of therapeutic intervention for the treatment of heart
failure. Curr Opin Cardiol 2000;15(3):136-40. (Review)
194. Torre-Amione G, Young JB, Colucci WS, et al. Hemodynamic
and clinical effects of tezosentan, an intravenous dual
endothelin receptor antagonist, in patients hospitalized for
acute decompensated heart failure. J Am Coll Cardiol
2003;42(1):140-7. (Prospective, double-blind; 292 patients)
195. Graff L, Orledge J, Radford MJ, et al. Correlation of the
Agency for Health Care Policy and Research congestive heart
failure admission guideline with mortality: peer review
organization voluntary hospital association initiative to
decrease events (PROVIDE) for congestive heart failure. Ann
Emerg Med 1999;34(4 Pt 1):429-37. (Review)
196. Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure
syndromes: current state and framework for future research.
Circulation 2005;112(25):3958-68. (Review)
197. 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(24):3617-24.
(Retrospective, cohort; 5888 patients)
198. 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(10):10819. (Prospective, cohort, multi-center; 1390 patients)
34
CME Questions
92. An ideal drug (or drug combination) for the treatment of acutely decompensated heart failure would
do which of the following?
a. Reduce preload
b. Enhance left ventricular function
c. Maintain or improve myocardial oxygen balance
d. All of the above
35
Accreditation: This activity has been planned and implemented in accordance with
the Essentials and Standards of the Accreditation Council for Continuing Medical
Education (ACCME) through the joint sponsorship of Mount Sinai School of
Medicine and Emergency Medicine Practice. The Mount Sinai School of Medicine
is accredited by the ACCME to provide continuing medical education for physicians.
Credit Designation: The Mount Sinai School of Medicine designates this educational activity for a maximum of 48 AMA PRA Category 1 Credit(s)TM per year.
Physicians should only claim credit commensurate with the extent of their participation in the activity. Credit may be obtained by reading each issue and completing the printed post-tests administered in December and June or online singleissue post-tests administered at EBMedicine.net.
Target Audience: This enduring material is designed for emergency medicine physicians.
Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of
prior activities for emergency physicians.
Date of Original Release: This issue of Emergency Medicine Practice was published December 1, 2006. This activity is eligible for CME credit through
December 1, 2009. The latest review of this material was November 20, 2006.
Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that is
outside Food and Drug Administration approved labeling. Information presented as
part of this activity is intended solely as continuing medical education and is not
intended to promote off-label use of any pharmaceutical product. Disclosure of OffLabel Usage: This article discusses the administration of calcium sensitizers,
vasopressin antagonists, endothelin antagonists, and novel natriuretic peptide
agents for the treatment of acutely decompensated heart failure. However, it is not
the intention of this article to promote the off-label use of these agents for the
treatment of acute decompensated heart failure outside the context of an
approved clinical trial.
levels of evidence
Case series, animal studies, consensus panels
Occasionally positive results
In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for
this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Kosowsky, Dr. Chan, Dr. Toscano, and Dr. Hermann
report no significant financial interest or other relationship with the manufacturer(s)
of any commercial product(s) discussed in this educational presentation.
Indeterminate
Continuing area of research
No recommendations until further
research
For further information, please see The Mount Sinai School of Medicine website at
www.mssm.edu/cme.
ACEP Accreditation: Emergency Medicine Practice is approved by the American
College of Emergency Physicians for 48 hours of ACEP Category 1 credits per
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Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent, contradictory
Results not compelling
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