Академический Документы
Профессиональный Документы
Культура Документы
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
Womens 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 nowdoes she even need to
be admitted?
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
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
Womens 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.
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 decompensationa 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.
February 2002
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
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
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.
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.
symptomatic
decompensation
cardiac ischemia
decreased left ventricle function
February 2002
Prehospital Care
Pulmonary
COPD
Pulmonary thromboembolism
Multilobar pneumonia
Acute respiratory distress syndrome (ARDS)
Other
Pure volume overload
Renal failure
Iatrogenic (e.g., post-transfusion)
Sepsis
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
February 2002
ED Evaluation
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
February 2002
Physical Examination
The patients 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 pressureprovides 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-
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.
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
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 patients 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 (18031882), U.S. essayist, poet,
philosopher. Circles, in Essays, First Series (1841, repr. 1847).29
February 2002
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.)
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
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.
February 2002
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
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 0.30.5 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
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
10
February 2002
(continued)
Inotropes
February 2002
11
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
But his flawed heart / (Alack, too weak the conflict to support!) /
Twixt two extremes of passion, joy and grief, / Burst smilingly.
William Shakespeare (15641616),
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
Pulmonary edema?
Chest pain?
Arrhythmia?
ASA (Class I)
SL TNG/Nitro-Spray (Class II)
IV morphine (Class II)
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
patients 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
Yes
Yes
Endotracheal
intubation (Class I)
Cardiogenic shock?
Yes
No
No
No
Consider CPAP
(Class II)
Yes
No
Unstable tachycardia?
ASA (Class I)
percutaneous transluminal coronary angioplasty (PTCA)
(Class I)
Thrombolytics (Class I-II for ST-elevation MI)
Yes
No
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patients 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
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
Consider morphine sulfate (2-3 mg boluses) for anxiety as needed (Class II-III)
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)
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
patients 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
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
Valve/septal rupture?
Pericardial tamponade?
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
patients 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
Yes
Yes
Dialysis (Class I)
IV nitroglycerin (Class II)
IV nitroprusside (Class II)
IV/PO ACE inhibitor (Class II)
IV furosemide (Class II)
Yes
Yes
Antibiotics (Class I)
Pressors (Class I-II)
Fluids (Class II)
No
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
patients 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
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.
18
February 2002
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 conditione.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 patients 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
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 betablockersfor example, in the management of hypertensive
criseshas 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,
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
20
February 2002
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.*
7.
February 2002
8.
9.
10.
11.
12.
21
22
February 2002
72.
February 2002
23
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
24
February 2002
February 2002
25
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, DAgostino 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
23. Some patients presenting to the ED with decompensated heart failure have sustained an acute MI.
a. True
b. False
February 2002
27
28
February 2002