C o n g e s t i v e H e a r t F a i l u re

a,b a,
Michael C. Scott, MD , Michael E. Winters, MD *

KEYWORDS
 Congestive heart failure  Acute decompensated heart failure
 Noninvasive positive pressure ventilation  Nitrates
 Angiotensin converting enzyme inhibitors  Diuretics  Inotropes

KEY POINTS
 Many patients with acute decompensated heart failure do not have intravascular volume
overload.
 The foundation of emergency department management of acute decompensated heart
failure is the use of noninvasive positive pressure ventilation and nitrate medications.
 Diuretics should not be used until optimal preload and afterload reduction has been
achieved.
 Morphine, nesiritide, b-blockers, and intraaortic balloon pump should not routinely be
used in the management of patients with acute heart failure in the emergency department.

INTRODUCTION

Congestive heart failure (CHF) remains the most common reason for hospitalization in
the United States for people aged 65 years and older, with more than 1 million patients
admitted for this condition each year.1,2 Despite improvements in diagnosis and treat-
ment, approximately 300,000 deaths each year can be attributed to CHF. Further-
more, the in-hospital mortality rate can be as high as 12% for patients admitted
with an acute exacerbation of CHF.2 Patients with acute decompensated heart failure
(ADHF) frequently present to the emergency department (ED) for evaluation; many of

Disclosure: The authors have no relevant financial relationships to disclose.

The article was copyedited by L.J. Kesselring, MS, ELS, the technical writer/editor in the Depart-
ment of Emergency Medicine at the University of Maryland School of Medicine.
a
Emergency Medicine/Internal Medicine/Critical Care Program, Department of Emergency
Medicine, University of Maryland Medical Center, 110 South Paca Street, 6th Floor, Suite 200,
Baltimore, MD 21201, USA; b Department of Medicine, University of Maryland Medical Center,
22 South Greene Street, Baltimore, MD 21201, USA
* Corresponding author. Department of Emergency Medicine, University of Maryland Medical
Center, 110 South Paca Street, 6th Floor, Suite 200, Baltimore, MD 21201.
E-mail address: [email protected]

Emerg Med Clin N Am 33 (2015) 553–562

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554 Scott & Winters

them are critically ill, requiring immediate treatment. In 2007, CHF accounted for 6.3%
of ED patients requiring hospital admission.3 It is imperative that the emergency phy-
sician be expert in the rapid assessment and treatment of patients with ADHF. The
article focuses on the management of the ED patient with ADHF, with attention to
therapies that improve patient symptoms, morbidity, and mortality.

PATHOPHYSIOLOGY

Recent reports have improved our understanding of the pathophysiology of ADHF.

Although some patients present with the textbook description of preexisting systolic
dysfunction and progressive volume overload, most ED patients with ADHF have pre-
served systolic function and are not overloaded in terms of total body volume. In fact,
most acutely ill ED patients with ADHF harbor processes much more complex than an
excess of intravascular volume. These processes can be divided into 2 categories:
cardiac failure and vascular failure.4,5
Patients with cardiac failure represent the textbook description of ADHF, that is, a
patient with chronic heart failure who develops intravascular volume overload through
a variety of mechanisms (eg, medication noncompliance, dietary noncompliance,
acute kidney injury). Quite simply, their damaged heart cannot tolerate increases in
intravascular volume, so edema develops in the lungs and peripheral tissues. In
general, symptoms develop gradually in the patient with this type of ADHF.
Patients with vascular failure have an abrupt increase in vasoconstriction and
afterload, resulting in acute decompensation. This sharp increase in afterload is
believed to occur through neurohumoral pathways involving the sympathetic and
renin–angiotensin–aldosterone axes.4,5 Patients with vascular failure typically pre-
sent with an acute onset of symptoms, often lack the classic signs of peripheral
edema, and generally have preserved cardiac function. In addition, these patients
are frequently hypertensive upon ED presentation and can be either euvolemic or
hypovolemic.

CLASSIFICATION

The European Society of Cardiology has classified acute heart failure into distinct
clinical syndromes (Box 1).6,7 Some patients present with overlapping features, but
their appropriate classification is important, because each requires a specific thera-
peutic approach.

Box 1
Classification of acute heart failure

 Acute decompensated heart failure

 Hypertensive acute heart failure
 Pulmonary edema
 Cardiogenic shock
 Right heart failure
 Acute coronary syndrome complicated by acute heart failure

Adapted from Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC guidelines for the diagnosis
and treatment of acute heart failure 2008. Eur J Heart Fail 2008;10:968.

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 Congestive Heart Failure 555

CAUSES

Common precipitants of ADHF are listed in Box 2.

SYMPTOMS AND SIGNS

Regardless of the underlying pathophysiology, the most common complaint of ED pa-

tients with ADHF is dyspnea. Additional symptoms can include orthopnea, parox-
ysmal nocturnal dyspnea, decreased exercise tolerance, peripheral edema,
weakness, and fatigue. Depending on the classification and cause, patients with
ADHF can present with either hypertension or hypotension. Although most patients
are tachycardic, bradycardia can be seen in the setting of medication toxicity (eg,
b-blocker, digoxin) or high-degree atrioventricular block. Physical examination find-
ings in patients with ADHF include pulmonary edema, peripheral edema, jugular
venous distention, hepatomegaly, hepatojugular reflux, and a third heart sound.

DIAGNOSTIC TESTING

The diagnostic evaluation of the patient with suspected ADHF generally includes elec-
trocardiogram, chest radiography (CXR), bedside echocardiogram, and laboratory
analysis.
Electrocardiogram
After an evaluation and stabilization of airway, breathing, and circulation, it is crucial
that an electrocardiogram be obtained as soon as possible in patients with suspected
ADHF to evaluate for signs of acute myocardial ischemia or infarction. For patients
with electrocardiographic signs of acute myocardial ischemia or infarction, emergent
cardiac catheterization should be performed, because restoring perfusion by percuta-
neous coronary intervention is the most successful therapy for ADHF in this setting.
Additional electrocardiographic findings that might be seen in ADHF include atrial or
ventricular hypertrophy, arrhythmias, or conduction abnormalities.
Chest Radiography
A CXR should also be obtained as soon as possible to evaluate for findings consistent
with ADHF. Typical CXR findings of ADHF include pulmonary edema, hilar fullness,

Box 2
Precipitants of acute decompensated heart failure

 Medication noncompliancea
 Dietary noncompliancea
 Acute coronary syndrome
 Arrhythmias
 Acute valvular dysfunction
 Hypertensive crisis
 Infection
 Anemia
a
Most common causes.
Adapted from Kosowsky JM. Congestive heart failure. In: James GA, editor. Emergency med-
icine: clinical essentials. Philadelphia: Elsevier; 2013. p. 477.

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556 Scott & Winters

increased vascularization, pleural effusions, and cardiomegaly. Fig. 1 illustrates

classic CXR finding of ADHF.

Echocardiography
As with other critical illnesses, the use of bedside ultrasonography and echocardio-
graphy has become a keystone in the diagnosis and management of ADHF in the
ED. The portability and rapidity of ultrasound as a diagnostic modality lends itself quite
well to this setting. The finding of diffuse b-lines (Fig. 2), although not truly specific to
ADHF, helps the emergency physician to refine the differential diagnosis in the setting
of undifferentiated dyspnea. Furthermore, the ability to evaluate ejection fraction,
exclude other causes of dyspnea such as pleural or pericardial effusion, and evaluate
for diastolic or valvular dysfunction makes bedside echocardiography an enormously
valuable tool in the evaluation of the ED patient with ADHF.

Laboratory Testing
In the patient with suspected ADHF, a complete blood count should be obtained to
exclude anemia, along with a basic metabolic panel to evaluate for renal dysfunction.
Cardiac biomarkers (eg, troponin I) are commonly obtained and increased in many pa-
tients with ADHF.8 Although increases in troponin might simply reflect the severity of
heart failure and not myocardial necrosis, elevated values are associated with
increased short-term mortality.8

Fig. 1. Chest x-ray demonstrating vascular prominence typical of pulmonary edema

(arrows).

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 Congestive Heart Failure 557

Fig. 2. Lung ultrasound showing finding of a b-line (arrows). Note the extension fully to the
end of the field. Multiple, diffuse b-lines suggests the presence of fluid in the lung fields, as
in pulmonary edema.

A common laboratory test obtained in the patient with ADHF is the measurement of
B-type natriuretic peptide (BNP) or the N-terminal proBNP (NT-proBNP).9 BNP is
released from cardiac myocytes in response to volume overload and has been used
in the evaluation of ED patients with undifferentiated dyspnea. In general, BNP values
of less than 100 pg/mL indicate that ADHF is an unlikely cause of dyspnea, whereas
values of greater than 400 pg/mL strongly suggest the presence of ADHF.9 Although
NT-proBNP has a different half-life and different cutoff values for ADHF than BNP,
both are degradation products of a common precursor and are clinically interchange-
able. Importantly, ADHF is not the only cause of increases in BNP or NT-proBNP. Any
condition that increases the stretch of the left or right ventricle (eg, pulmonary embo-
lism) can result in elevated BNP and NT-proBNP levels. In addition, elevated BNP and
NT-proBNP levels can also be seen in older patients and those with renal dysfunction.
In contrast, obese patients often have lower values of BNP and NT-proBNP. Optimal
cutoff values for both BNP and NT-proBNP in these patient populations remain
controversial; therefore, values must be interpreted within the clinical context of the
patient’s history, the clinical presentation, and prior BNP or NT-proBNP values.
Regardless of the cause, increases in BNP and NT-proBNP are associated with
increased in-hospital mortality and therefore have prognostic importance.10

EMERGENCY DEPARTMENT TREATMENT

Patients with ADHF often present to the ED in extremis and require rapid treatment.
Similar to other critical conditions, patients with suspected ADHF should be placed
on a cardiac monitor and continuous pulse oximetry and should be given

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558 Scott & Winters

supplemental oxygen. Adequate intravenous access should be obtained and blood

sent for the laboratory studies previously described. Rapid initiation of noninvasive
ventilation and appropriate pharmacologic therapy form the foundation of ED therapy
for patients with ADHF.

Noninvasive Positive-Pressure Ventilation

Noninvasive positive-pressure ventilation (NPPV), whether it is continuous positive
airway pressure (CPAP) or bilevel positive airway pressure (BiPAP), provides
numerous benefits to the patient with ADHF. NPPV reduces afterload by reducing
the transmural pressure across the left ventricle.11 In addition, NPPV increases intra-
thoracic pressure, thereby reducing venous return and preload. Decreases in both
afterload and preload significantly benefit the acutely failing left heart. Through these
mechanisms, NPPV reduces the work of breathing and improves oxygenation. A
recent Cochrane review found that, compared with standard medical therapy alone,
the addition of NPPV resulted in significant reductions in the rates of in-hospital
mortality and endotracheal intubation in patients with ADHF.12 Neither CPAP nor
BiPAP has been shown to be superior. A recent metaanalysis found no difference in
in-hospital mortality, need for intubation and mechanical ventilation, or rate of acute
myocardial infarction between CPAP and BiPAP for patients with ADHF.13 It is more
important to initiate NPPV early in the course of ED treatment than to deliberate
over which modality to use. A typical initial setting for CPAP ranges from 5 to
10 mm Hg, whereas initial settings for BiPAP are an inspiratory positive airway pres-
sure of 10 mm Hg and an expiratory positive airway pressure of 5 mm Hg.

Pharmacologic Therapy
The primary objective of pharmacologic therapy in the patient with ADHF is to
decrease preload and afterload. Decreases in preload decrease myocardial wall ten-
sion and, ultimately, myocardial oxygen demand. Decreases in afterload decrease the
myocardial work of the left ventricle, resulting in increased cardiac output and tissue
perfusion. Common classes of medications used to treat the ED patient with ADHF are
nitrates, angiotensin-converting enzyme (ACE) inhibitors, diuretics, and inotropes.
Nitrates, namely nitroglycerin, are the initial medications of choice for patients with
ADHF. At low doses, nitroglycerin reduces preload primarily through its dilatory effects
on the venous system. At higher doses, nitroglycerin causes arterial dilation, thereby
also reducing afterload.14 Initially, nitroglycerin can be given via the sublingual route
(400 mg every 5 minutes) while adequate intravenous access is being secured. Once
that access is established, a nitroglycerin infusion should be started. The infusion
often begins at 20 mg/min, depending on institutional guidelines. It is critically impor-
tant for the emergency physician to titrate the infusion rapidly to clinical improve-
ment.15 In general, the dose of nitroglycerin can be increased by 40 mg/min every
5 minutes to a maximum of 200 mg/min. Recent studies involving small numbers of
patients demonstrated lower intubation rates, without the adverse effect of hypoten-
sion, when nitroglycerin infusions were started at doses higher than the traditional
20 mg/min.16–18 Larger studies are required to validate the safety and efficacy of this
approach.
For patients unresponsive to nitroglycerin and for those with severe hypertension,
sodium nitroprusside can be considered for additional afterload reduction. Nitroprus-
side is given intravenously at a starting dose of 0.100 to 0.125 mg/kg per minute. The
infusion can be increased by 0.1 mg/kg per minute every 5 minutes until a maximum
dose of 400 mg/min is reached. Importantly, nitroprusside is metabolized to cyanide,
which can accumulate rapidly in patients with renal dysfunction. In addition,

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 Congestive Heart Failure 559

nitroprusside might increase the mortality rate among patients with acute myocardial
infarction.19
ACE inhibitors are effective at reducing afterload and have been used in the ED
treatment of patients with ADHF. Several small studies on ACE inhibitors in patients
with ADHF demonstrated improvement in hemodynamic markers.20,21 In addition, a
single-center study demonstrated reduced rates of intubation and intensive care
unit admission for patients who received sublingual captopril as a component of their
ED treatment.22 Importantly, current guidelines from the American College of Emer-
gency Physicians include ACE inhibitors in the treatment options for ED patients
with ADHF.23 The most commonly used ACE inhibitors in studies of patients with
ADHF are enalaprilat and captopril. Enalaprilat can be given intravenously at a dose
of 1.25 mg over 5 minutes, whereas captopril can be administered via intravenous
or sublingual routes.
Traditionally, diuretic medications have been considered the mainstay of pharma-
cologic therapy for patients with ADHF. Because the majority of acutely ill ED patients
with ADHF are not volume overloaded, indiscriminate administration of diuretics could
be harmful.5 Adequate renal perfusion is necessary for these medications to be effec-
tive. As a result, the role of diuretics in the ED management of patients with ADHF is
limited.19 The administration of a diuretic should not supersede known effective ther-
apies, namely NPPV and nitrates. When a diuretic is deemed appropriate, furosemide
is used most commonly. For patients not routinely taking furosemide as an outpatient,
an initial dose of 20 to 40 mg can be given. For patients already prescribed furose-
mide, an initial intravenous dose equivalent to their oral outpatient dose can be given.
Studies comparing high- and low-dose diuretic therapy, as well as those comparing
intermittent bolus dosing with continuous infusions, have not demonstrated superior
outcomes with any dose or method.
Inotropic medications should be considered in patients with ADHF who manifest
signs of cardiogenic shock. Bedside echocardiography performed by the emergency
physician can be immensely helpful in identifying patients who might benefit from
inotropic support. Current guidelines generally recommend initiating inotropic medica-
tions after optimizing administration of nitrates and diuretics.24,25 Dobutamine and mil-
rinone are the most common inotropic medications used in these patients. A
dobutamine infusion can be initiated at 2.5 mg/kg per minutes and titrated by 2.5 mg/
kg per minute every 10 minutes to a maximum dose of 20 mg/kg per minute. These 2
agents have important differences in mechanism and duration of action. Although
dobutamine stimulates adrenergic receptors, resulting in increased contractility and
reduced afterload milrinone inhibits phosphodiesterase, the resultant increase in
cyclic adenosine monophosphate causes increased contractility and diastolic relaxa-
tion, as well as vasodilation and, therefore, decreased afterload. Because it does not
rely on sympathetic receptors, it may be preferred in patients on chronic b-blocker
therapy. Furthermore, milrinone has more potent vasodilatory effects, making it
more attractive than dobutamine in patients with severe pulmonary hypertension.
Finally, it is important to note that milrinone’s half-life is 2 to 4 hours, whereas dobut-
amine has a half-life of just 2 minutes.26 If the patient’s blood pressure remains inad-
equate despite inotropic therapy, a vasopressor medication (ie, norepinephrine,
epinephrine) can be initiated. It is important to recall that inotropic medications can
have the significant adverse effects of hypotension and tachydysrhythmias. As a result,
they should not be used routinely for all patients with ADHF. In fact, several studies
suggested an increase in mortality rate when these agents were used liberally.27,28
The use of morphine in the treatment of ADHF has long been considered standard
care, even though no well-designed, randomized trials have established its efficacy for

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560 Scott & Winters

these purposes. Over the past 10 to 15 years, evidence has been mounting to suggest
that morphine is actually not helpful in the treatment of ADHF and very likely could
carry significant harm. Sacchetti and colleagues22 reported an increased rate of
mechanical ventilation and admission to the intensive care unit for ADHF patients
treated with morphine and Peacock and associates29 found an increased likelihood
of mortality. These studies are based on retrospective reviews and are, therefore,
subject to the flaws inherent in such research, but they are far from unique in sug-
gesting that morphine might very well worsen the effects of ADHF.30 Given these un-
settling findings, we recommend against the use of morphine in the management of
ED patients with ADHF.
Nesiritide, a recombinant form of BNP with vasodilatory and diuretic properties,
received initial positive reviews as well as approval for use by the US Food and
Drug Administration, but controversy arose when 2 metaanalyses indicated a signifi-
cant increase in kidney injury and a trend toward increased mortality among ADHF pa-
tients receiving this drug.31,32 The ASCEND-HF trial failed to demonstrate a reduction
in the 30-day mortality rate and the rate of rehospitalization for patients with ADHF
receiving nesiritide.33 The same trial also demonstrated significantly higher rates of
hypotension in patients randomized to the nesiritide group compared with patients
in the control group. As a result, nesiritide should not be used commonly in the treat-
ment of ED patients with ADHF.
b-Blocker medications are an integral component of the outpatient management of
patients with chronic heart failure. In general, these medications are not used in
patients with ADHF, because of their negative inotropic effects. For patients who
take these medications routinely, it is common to withhold them during an acute exac-
erbation of chronic heart failure. However, recent guidelines indicate that withholding
b-blocker therapy from patients with chronic heart failure is not beneficial and recom-
mend continuing the medication at its previously prescribed doses during an episode
of ADHF.25 The decision to continue b-blocker therapy for ED patients with ADHF is
best left to the inpatient team in consultation with the patient’s cardiologist.

Mechanical Assistance
Traditionally, placement of an intraaortic balloon pump (IABP) was recommended as a
bridge to surgery for patients with refractory cardiogenic shock that is complicating
acute myocardial infarction. An IABP inflates during diastole, improving coronary
artery perfusion, and deflates during systole, decreasing afterload. The recently
completed IABP-SHOCK II trial failed to demonstrate improvement in the 30-day
mortality rate for patients randomized to receive an IABP compared with patients in
the control group.34 As a result of that trial, routine placement of an IABP can no longer
be recommended.

SUMMARY

Patients with ADHF who come to the ED are usually critically ill and require immediate
treatment. In contrast with traditional teaching, many of them are not volume over-
loaded. The foundation of ED management of patients with ADHF is rapid initiation
of NPPV along with aggressive titration of nitrates. For patients who do not respond
to escalating doses of nitrates, afterload reduction with an ACE inhibitor can be
considered. A diuretic should not be administered before these critical interventions
have been completed, but can be given after optimal preload and afterload reduction
has been achieved. Short-term inotropic therapy can be considered in select patients
with cardiogenic shock and ADHF who fail to respond to standard therapy. Morphine,

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 Congestive Heart Failure 561

nesiritide, b-blockers, and placement of an IABP are not recommended for routine use
in the ED management of patients with ADHF.

REFERENCES

1. Roger VL. Epidemiology of heart failure. Circ Res 2013;113:646–59.

2. Bui AL, Horwich TB, Fonarow GC. Epidemiology and risk profile of heart failure.
Nat Rev Cardiol 2011;8:30–41.
3. Niska R, Bhuiya F, Xu J. National hospital ambulatory medical care survey: 2007
emergency department summary. Natl Health Stat Report 2010;6:1–31.
4. Gheorghiade M, De Luca L, Fonarow GC, et al. Pathophysiologic targets in the
early phase of acute heart failure syndromes. Am J Cardiol 2005;19:11G–7G.
5. Cotter G, Felker GM, Adams KF, et al. The pathophysiology of acute heart failure –
is it all about fluid accumulation? Am Heart J 2008;155:9–18.
6. Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines
on the diagnosis and treatment of acute heart failure: the task force on acute
heart failure of the European society of cardiology. Eur Heart J 2005;26:
384–416.
7. Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC guidelines for the diagnosis
and treatment of acute heart failure 2008: the task force for the diagnosis and
treatment of acute and chronic heart failure 2008 of the European society of
cardiology. Eur J Heart Fail 2008;10:933–89.
8. Peacock WF, De Marco T, Fonarow GC, et al. Cardiac troponin and outcome in
acute heart failure. N Engl J Med 2008;358:2117–26.
9. Maisel A, Mueller C, Adams K Jr, et al. State of the art: using natriuretic peptides
levels in clinical practice. Eur J Heart Fail 2008;10:824–39.
10. Fonarow GC, Peacock WF, Phillips CO, et al. Admission B-type natriuretic
peptide levels and in-hospital mortality in acute decompensated heart failure.
J Am Coll Cardiol 2007;49:1943–50.
11. Bellone A, Barbieri A, Bursi F, et al. Management of acute pulmonary edema in
the emergency department. Curr Heart Fail Rep 2006;3:129–35.
12. Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation
(CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database
Syst Rev 2013;(5):CD005351.
13. Li H, Hu C, Xia J, et al. A comparison of bilevel and continuous positive airway
pressure noninvasive ventilation in acute cardiogenic pulmonary edema. Am J
Emerg Med 2013;31:1322–7.
14. Moazemi K, Chana JS, Willard AM, et al. Intravenous vasodilator therapy in
congestive heart failure. Drugs Aging 2003;20:485–508.
15. Mattu A, Martinez JP, Kelly BS. Modern management of cardiogenic pulmonary
edema. Emerg Med Clin North Am 2005;23:1105–25.
16. Cotter G, Metzkor E, Kaluski E, et al. Randomized trial of high-dose iso-
sorbide dinitrate plus low-dose furosemide versus high-dose furosemide
plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet
1998;351:389–93.
17. Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate is
safer and better than Bi-PAP ventilation combined with conventional treatment for
severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.
18. Levy P, Compton S, Welch R, et al. Treatment of severe decompensated heart
failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis.
Ann Emerg Med 2007;50:144–52.

Downloaded for Anonymous User (n/a) at Pontifical Catholic University of Chile from ClinicalKey.com by Elsevier on March
22, 2022. For personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.
562 Scott & Winters

19. Mebazaa A, Gheorghiade M, Pina IL, et al. Practical recommendations for preho-
spital and early in-hospital management of patients presenting with acute heart
failure syndromes. Crit Care Med 2008;36:S129–39.
20. Varriale P, David W, Chryssos BE. Hemodynamic response to intravenous enalap-
rilat in patients with severe congestive heart failure and mitral regurgitation. Clin
Cardiol 1993;16:235–8.
21. Podbregar M, Voga G, Horvat M, et al. Bolus versus continuous dose of enalap-
rilat in congestive heart failure with acute refractory decompensation. Cardiology
1999;91:41–9.
22. Sacchetti A, Ramoska E, Moakes ME, et al. Effect of ED management on ICU use
in acute pulmonary edema. Am J Emerg Med 1999;17:571–4.
23. Silvers SM, Howell JM, Kosowsky JM, et al. Clinical policy: critical issues in the
evaluation and management of adult patients presenting to the emergency
department with acute heart failure syndromes. Ann Emerg Med 2007;49:627–69.
24. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the man-
agement of heart failure: a report of the American college of cardiology founda-
tion/American heart association task force on practice guidelines. J Am Coll
Cardiol 2013;62:147–239.
25. McMurray JJ, Adamopoulos S, Anker SD, et al. ESC guidelines for the diagnosis
and treatment of acute and chronic heart failure 2012: the Task Force for the
Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the Euro-
pean Society of Cardiology. Developed in collaboration with the heart failure
association (HFA) of the ESC. Eur Heart J 2012;33:1787–847.
26. Overgaard CB, Dzavik V. Inotropes and vasopressors: review of physiology and
clinical use in cardiovascular disease. Circulation 2008;118:1047–56.
27. Abraham WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with
acute decompensated heart failure requiring intravenous vasoactive medica-
tions: an analysis form the acute decompensated heart failure national registry
(ADHERE). J Am Coll Cardiol 2005;46:57–64.
28. Arnold LM, Crouch MA, Carroll NV, et al. Outcomes associated with vasoactive
therapy in patients with acute decompensated heart failure. Pharmacotherapy
2006;26:1078–85.
29. Peacock WF, Hollander JE, Diercks DB, et al. Morphine and outcomes in acute
decompensated heart failure: an ADHERE analysis. Emerg Med J 2008;25:
205–9.
30. Sosnowski MA. Review article: lack of effect of opiates in the treatment of acute
cardiogenic pulmonary oedema. Emerg Med Australas 2008;20:384–90.
31. 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;293:1900–5.
32. Sackner-Bernstein JD, Skopicki HA, Aaronson KD. Risk of worsening renal func-
tion with nesiritide in patients with acutely decompensated heart failure. Circula-
tion 2005;111:1487–91.
33. O’Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with
acute decompensated heart failure. N Engl J Med 2011;365:32–43.
34. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial
infarction with cardiogenic shock. N Engl J Med 2012;367:1287–96.

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