LWW/AENJ AENJ-D-08-00024R1 January 21, 2009 15:32 Char Count= 0

Advanced Emergency Nursing Journal

Vol. 31, No. 1, pp. 36–43
Copyright 
c 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins

Management of Acute Cardiogenic

Pulmonary Edema
A Literature Review
Jeremy M. Johnson, MS, RN, CEN, CCRN

Abstract
Acute cardiogenic pulmonary edema (CPE) is a pathology frequently seen in patients presenting to
emergency departments (EDs) and can usually be attributed to preexisting cardiovascular disease.
Heart failure alone accounts for more than 1 million hospital admissions annually and has one of
the highest ED morbidity and mortality to date (Hunt et al., 2005). Historically, CPE has been man-
aged by the treating clinician in a manner that is based largely on anecdotal evidence. Furosemide
(Lasix), morphine, and nitroglycerin have historically been the baseline standard for drug therapy
in CPE management. A lack of drastic improvement in the patient’s condition over the course of
the ED visit may reflect a management style that results in higher morbidity and mortality for CPE
patients. Several recent articles provide evidence-based outcomes that suggest changing standard
therapy along with the adjunctive use of other medications. These articles also describe treatment
modalities that result in a marked improvement in the management of patients with CPE along with
decreases in adverse outcomes and hospital length of stay. The goal of this article is to present a
summary of the evidence regarding the management of CPE and discuss the implications for current
practice. Key words: cardiogenic pulmonary edema, furosemide (Lasix), heart failure, morphine,
nitroglycerin

A S MANY AS 4.5 million people cur-
rently live with heart failure and more
than 500,000 new cases are diagnosed
each year (Abbas, Fausto, & Kumar, 2005).
The disease has a higher incidence in the el-
derly, affecting 1% of persons over the age of
65. Although this number may appear lower
than expected, approximately 50% of pa-
tients with untreated heart failure die within
5 years of initial diagnosis, a statistic that
has increased threefold in the last 25 years
From the Adult Emergency Department, University of
Mississippi Medical Center, Jackson.
Corresponding author: Jeremy M. Johnson, MS, RN,
CEN, CCRN, Adult Emergency Department, University of
Mississippi Medical Center, 2500 North State St, Jackson,
MS 39216 (e-mail: jmjohnson2@nursing.umsmed.edu).
(Abbas et al., 2005). Over the years, cardio-
genic pulmonary edema (CPE) has become
one of the leading disease processes pre-
senting to the emergency department (ED).
More than 250,000 people are affected by
CPE each year, and this number continues to
grow at an alarming rate. Despite its many
causes, management of CPE has been his-
torically approached by utilizing the same
generally accepted therapies and strategies.
However, in patients with respiratory failure,
standard treatment, including diuretics, ni-
troglycerin, morphine, and oxygen, may not
be sufficient to reduce respiratory distress.
Recent literature has shown many subtle
changes in the management of CPE patients,
which may, in turn, improve the quality of
care provided to these patients as well as
decrease morbidity, mortality, and hospital

36
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January–March 2009 r Vol. 31, No. 1
stay within each ED. Unfortunately, much of
the literature documented is not readily avail-
able to ED nurses, nurse practitioners, or
other advanced clinicians. The goal of this ar-
ticle is to present a comprehensive literature
review of the more recent evidence-based re-
search concerning the management of these
patients and illustrate the subtle changes that
could be made in our common everyday treat-
ment practices.
LABORATORY DATA
Pro-BNP
Pro-brain natriuretic peptide (Pro-BNP) is a
hormone released by the myocardium in re-
sponse to ventricular stretch caused by in-
creased end-diastolic pressure and volume
(Silvers, Howell, Kosowsky, Rokos, & Jagoda,
2007). This Pro-BNP is cleaved into an ac-
tive BNP and inactive N-terminal pro-brain
natriuretic peptide (NT-proBNP) and it is
this active form that promotes diuresis, na-
truresis, and general vasodilatation, in both
venous and arterial vasculature (Scios Inc.,
2003). Most recently, a recombinant form of
BNP has been engineered from strains of Es-
cherichia Coli and synthetically duplicated to
be used therapeutically in the form of nesir-
itide (see below for discussion) (Scios Inc.,
2003).
BNP levels can be quantitatively measured
by most laboratories, providing the clinician
with a more accurate direction in diagnos-
ing CPE. A single BNP measurement (BNP
level >500 pg/dL or NT-proBNP level >
1,000 pg/dL) can help support a clinician’s
index of suspicion for CPE and increase speci-
ficity for a more accurate diagnosis (Hunt
et al., 2005; Silvers et al., 2007). However,
the American Heart Association (AHA) warns
clinicians that BNP levels can be falsely ele-
vated in the setting of pulmonary embolism
and/or pulmonary disease (Hunt et al., 2005).
In addition, the course of treatment and sub-
tle changes in the patient’s clinical status may
also be incorrectly correlated with trending
BNP measurements as evidenced by recent
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Management of Acute Cardiogenic Pulmonary Edema 37
animal studies, suggesting that BNP levels
can lag behind the patient’s clinical picture
by up to 1 hr (Silvers et al., 2007). Mattu
(2006) notes the importance of remembering
that stressed myocardium (i.e., in the setting
of decompensating heart failure) may not be
able to produce adequate amounts of BNP to
facilitate appropriate amounts of diuresis, and
thus yield a false-negative serum result. BNP
measurements vary among different patient
populations, and baseline measurements
may be skewed because of age, body mass,
and renal function (Hunt et al., 2005; Silvers
et al., 2007). However, despite greater than
normal body mass index (BMI) in the obese
population, increasing BNP measurements
predict worsening prognosis, hemodynam-
ics, and mortality for all body types (Horwich,
Hamilton, & Fonarow, 2006).
Despite the many adversities BNP use
has had in the clinical setting, studies have
shown that when coupled with an accurate
and timely clinical assessment, BNP measure-
ments can reduce in-hospital stay and treat-
ment cost for patients with CPE (Mueller
et al., 2004). NT-proBNP measurement ac-
curacy has not been studied as thoroughly,
however, and the American College of Emer-
gency Physicians (ACEP) Clinical Policies Sub-
committee on Acute Heart Failure Syndromes
found it to be as statistically accurate as BNP
data (Silvers et al., 2007). Silvers et al. (2007)
also suggested that the same factors that
skewed BNP measurements could be applica-
ble to NT-proBNP measurements.
Cardiac Troponin
Quite frequently, troponin I is obtained as part
of a standard set of labs when pulmonary
edema is suspected to have a cardiac origin.
Even though the use of serum troponin may
be intuitively obvious in the setting of possi-
ble myocardial damage, it is worth mention-
ing here in our discussion of common labora-
tory markers useful in the diagnosis of heart
failure.
The Acute Decompensated Heart Fail-
ure National Registry (ADHERE) investigators
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38 Advanced Emergency Nursing Journal

conducted a 4-year analysis of patients with Noninvasive Mask Ventilation

acutely decompensated heart failure and
Both CPAP and BiPAP deliver positive pres-
found that a troponin level greater than
sure oxygen noninvasively via a mask and
1 mcg/L was associated with higher in-
may provide the needed FiO2 while avoiding
hospital mortality, independent of other pre-
intubation (DeBlieux & Broderick, 2008;
dictive laboratory values (Peacock et al.,
Mattu, 2006). Although CPAP and BiPAP
2008; You, Austin, Alter, Ko, & Tu, 2007).
use different mechanisms to deliver positive
However, an Italian study demonstrated that
pressure oxygen, both have been shown to
cardiac troponin I is detectable in only 25%–
decrease the work of breathing, improve
30% of patients with severe heart failure, and
oxygenation, decrease preload and afterload
therefore, although a positive troponin result
(thus increasing cardiac output), reduce the
is helpful in making a diagnosis, a negative tro-
need for endotracheal intubation, and reduce
ponin result does not rule out the diagnosis of
intensive care unit stays (Mattu, 2006). The
CPE (La Vecchia et al., 2000).
ACEP subcommittee states that under moder-
ate clinical certainty, 5–10 cm H2 O of CPAP
can be used for the patient with CPE in the
OXYGENATION
absence of hypotension or the need for other
Oxygen airway interventions (Silvers et al., 2007).
Moritz et al. (2007) found that CPAP through
Oxygen is undeniably the most essential tool
a Boussignac device and BiPAP were both
the ED clinician has against CPE. Unfortu-
effective in reducing respiratory distress. Fur-
nately, it seems to be the most overlooked
thermore, they found that there was no clini-
medication available to the clinician. Oxygen
cally significant difference between CPAP and
is a potent pulmonary vasodilator and en-
BiPAP (Moritz et al., 2007). When adminis-
hances oxygenation in an already tachypneic,
tered appropriately and in a timely fashion,
dyspneic, and often hypoxic patient. It
these noninvasive forms of ventilation may
should be one of the first treatments admin-
allow time for other medical therapies to take
istered, yet clinicians rarely see oxygen as a
effect and consequently avoid invasive ven-
medication. Short of invasive ventilation (i.e.,
tilatory techniques (DeBlieux & Broderick,
endotracheal intubation), nasal cannulas, sim-
2008).
ple face masks, and nonrebreathing masks are
Contrary to older publications, the current
the mainstay of supplemental oxygen ther-
literature indicates that CPAP and more par-
apy. Quite often, the decompensating patient
ticularly BiPAP do not correlate with an in-
with CPE requires oxygen at an FiO2 of 1 yet
creased risk of myocardial infarction in pa-
lacks the strength to satisfy the great oxygen
tients with pulmonary edema, although many
demand and overcome the impediment to
clinicians are uncertain and would appreciate
gas exchange created by pulmonary edema.
further study of this issue (Cross, Cameron,
Unfortunately, providing supplemental oxy-
Kierce, Ragg, & Kelly, 2003; Levitt, 2001;
gen without positive pressure, when coupled
Mehta et al., 1997; Silvers et al., 2007). De-
with intravenous medications such as nitro-
spite the recent trends, the literature clearly
glycerin, morphine, and diuretics, may not
demonstrates that noninvasive oxygenation
reduce respiratory distress. Nonrebreathing
techniques must be used early in the treat-
masks deliver 65%–75% oxygen and then only
ment course of patients with CPE for maxi-
when the mask is tightly fitted to the patient’s
mum effectiveness (Mattu, 2006).
face (Barker & Schneider, 2008). Nonin-
vasive mask ventilation with continuous
Bronchodilator Therapy
positive airway pressure (CPAP) or bilevel
positive airway pressure (BiPAP) may be Some patients in respiratory distress need
more effective and help prevent the need for emergent intervention before a definitive
intubation. diagnosis is established. Frequently, patients
LWW/AENJ AENJ-D-08-00024R1 January 21, 2009
January–March 2009 r Vol. 31, No. 1
in respiratory distress, especially those found
to be wheezing, receive bronchodilator ther-
apy in the form of a β-agonist. Although this
may prove helpful to patients with asthma
or other forms of restrictive lung disease,
it may prove detrimental to patients with
CPE (Singer et al., 2008). Although β-agonists
cause bronchodilation, a result of β 2 recep-
tor stimulation, cross-reacting β-agonists also
stimulate the β 1 receptors found in the heart
and cause tachycardia. This can be delete-
rious because the weakened myocardium is
forced to work harder and it may also result
in heart rates too fast to allow for adequate
diastole and further reduction in cardiac out-
put. Singer et al. (2008) found that inhaled
bronchodilators, when administered to the
patient with CPE in the absence of confound-
ing chronic obstructive pulmonary disorders,
were more likely to ultimately lead to more
aggressive airway intervention. Although this
makes intuitive sense, it is important to re-
member that wheezing, tachypnea, and dys-
pnea are not always associated with a pul-
monary etiology and other pathologies should
be considered prior to bronchodilator ther-
apy. The study of Singer et al. (2008) amplifies
the importance of determining the etiology of
respiratory distress prior to the administration
of bronchodilator therapy.
PRELOAD REDUCTION
Preload is defined as the “the load imposed
on resting muscle that stretches the mus-
cle to a new length” (Marino, 2007, p. 4)
and is clinically appreciated by left ventricu-
lar end-diastolic pressure and central venous
pressure. Preload reduction can be accom-
plished via a variety of mechanisms; how-
ever, current literature seems to focus on the
three main pharmacologic agents: nitroglyc-
erin, furosemide, and morphine sulfate.
Nitroglycerin
Nitroglycerin effectively dilates the inferior
vena cava (and other veins), thus directly re-
ducing myocardial fiber stretch (i.e., preload)
and also reducing myocardial oxygen de-
mand. At higher doses, nitroglycerin di-
15:32 Char Count= 0
Management of Acute Cardiogenic Pulmonary Edema 39
lates arterial blood vessels including the
coronary arteries, allowing for better my-
ocardial blood flow. There have been mul-
tiple studies demonstrating the superior-
ity of nitroglycerin over the effectiveness
of furosemide and morphine (Levy et al.,
2007; Mattu, 2006). However, nitroglycerin
can be used alone or in combination with
other drugs targeted at restoring appropriate
cardiac output (Mattu, 2006). Mattu (2006)
argues that nitroglycerin should be the first-
line agent of choice, and when used at ap-
propriate doses, it may effectively lower af-
terload as well as preload. Mattu (2006) also
states that because of nitroglycerin’s variety of
administration routes, it can be used quickly
and safely in the patient with CPE. Nitroglyc-
erin has been shown to be safer than mor-
phine when compared with furosemide and
allows a greater range of aggressive admin-
istration with more limited adverse effects
(Mattu, 2006). Nitroglycerin infusions are eas-
ily titratable with predictable outcomes and
can be infused up to 600 mcg/min if nec-
essary (Hunt et al., 2005). There is insuffi-
cient evidence to support the use of nitroglyc-
erin paste, especially in obese patients (Vakil,
2008).
Furthermore, Levy et al. (2007) found that
high-dose nitroglycerin (titrated in 20 mcg in-
crements up to 400 mcg/min using a concen-
trated infusate of 1 mg/mL) was associated
with decreased requirement for respiratory
intervention beyond the use of a nonrebreath-
ing mask. Patients receiving a mean total dose
of 6.5 mg of nitroglycerin along with other
AHA-approved treatments had fewer cardiac
complications and less hemodynamic instabil-
ity (Levy et al., 2007). In addition, the ACEP
subcommittee also identified that many stud-
ies have shown that the use of high-dose ni-
trates (i.e., 3-mg isosorbide dinitrate IV ev-
ery 5 min) coupled with low-dose furosemide
was more effective than monotherapy alone
(Silvers et al., 2007).
Furosemide
Furosemide is a loop Na-Cl-K symport in-
hibitor and accomplishes preload reduction
by direct removal of total body water via
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40
renal diuresis (Mattu, 2006). Historically,
furosemide has been used aggressively to treat
CPE. However, Mattu (2006) identified no
evidence demonstrating an immediate effect
of furosemide in the setting of CPE, and in
fact, the evidence shows a delayed diuretic ef-
fect with onset of action in 30–120 min. The
ACEP subcommittee states that aggressive di-
uretic therapy, when used alone, does not de-
crease the likelihood of endotracheal intuba-
tion when compared with the use of nitrate
monotherapy. Moreover, the aggressive use
of diuretics may, in fact, worsen renal func-
tion and increase long-term mortality (Silvers
et al., 2007).
Mattu (2006) found several studies that
demonstrated an initial adverse effect of
furosemide on the hemodynamic profile as
evidenced by an initial increase in heart rate
and stroke volume resistance and decreases
in stroke volume and cardiac output. Several
studies compared groups of patients receiving
either high-dose furosemide therapy or high-
dose nitrate therapy and concluded that the
incidence of myocardial infarction, endotra-
cheal intubation, and hospital mortality was
significantly decreased in patients with CPE
receiving high-dose nitrate therapy (Silvers
et al., 2007).
Silvers et al. (2007) noted that the best
dose of furosemide is likely to vary from
patient to patient and that it requires care-
ful titration in patients with acute heart fail-
ure to provide effective diuresis and avoid
worsening renal function. When other ther-
apies are used appropriately, furosemide
may be used in smaller doses. Clinicians
should also consider systolic versus dias-
tolic dysfunction as the cause of CPE be-
cause some patients may be volume depleted
and not require furosemide at all. Although
furosemide remains a part of the standard
treatment regimen, it should be used with
caution.
Morphine Sulfate
Morphine sulfate is a narcotic that binds
to μ-opiate pain receptors. Historically used
for pain relief, morphine is used as an ad-
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Advanced Emergency Nursing Journal
junct therapy in the treatment of CPE. It
has been suggested that morphine-induced
histamine release may decrease preload and
the anxiolytic effect may decrease the cate-
cholamine load that exacerbates cardiac af-
terload (Mattu, 2006; Vakil, 2008). However,
Mattu (2006) also described disadvantages to
the use of morphine in patients with CPE.
The anxiolytic effects of morphine usually re-
quire high doses, and thus the already dysp-
neic patients may experience more respira-
tory or myocardial depression (Mattu, 2006).
Sacchetti, Ramoska, Moakes, McDermott,
and Moyer (1999) found that patients suf-
fering from CPE were 5 times more likely
to need intubation when they received mor-
phine. Furthermore, morphine-induced his-
tamine release could actually increase cat-
echolamine synthesis, if sensitive patients
experienced rash, urticaria, nausea, or vom-
iting (Mattu, 2006). Mattu (2006) suggests
the use of benzodiazepines for anxiolysis
due to the lessened concern of allergic re-
sponses and cardiovascular and/or respiratory
depression.
AFTERLOAD REDUCTION
Afterload is defined as “the total load that
must be moved by a muscle when it con-
tracts and can be measured clinically by not-
ing the pulmonary and systemic vascular resis-
tances (PVR and SVR, respectively)” (Marino,
2007, p. 8). Afterload reduction may arguably
be the most critical element of cardiac out-
put that affects the patient with CPE, espe-
cially those with poor systolic function (Vakil,
2008). Reduction in afterload aids in break-
ing the cycle of heart failure, thus reliev-
ing CPE and helping restore adequate blood
flow to critical tissues. Many medications
aid in reducing afterload; however, Mattu
(2006) argues that angiotensin-converting en-
zyme (ACE) inhibitors should become the
gold standard in care of these patients. Con-
currently, other medications (e.g., nitroglyc-
erin) used to reduce preload may also reduce
afterload when used in high doses (Mattu,
2006).
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January–March 2009 r Vol. 31, No. 1
Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme inhibitors
help down regulate the rennin–angiotensin–
aldosterone system (RAAS) and improve
left ventricular function (Mattu, 2006). AHA
guidelines suggest the use of ACE inhibitors
could be beneficial for patients with hyper-
tension and left ventricular hypertrophy,
even when the symptoms of heart failure are
absent or minimally appreciated (Hunt et al.,
2005). Vakil (2008) noted that the perindopril
for elderly people with chronic heart failure
(PEP-CHF trial) investigators found that ACE
inhibitors were correlated with a significant
reduction in mortality and hospitalization in
a study of more than 800 patients with CPE
secondary to heart failure. When used as a
second-line agent, ACE inhibitors also offer
rapid reduction in preload as well as in after-
load, so much so that objective and subjective
improvement in a patient’s hemodynamic
profile can be seen within 12 min (Mattu,
2006). Most often, captopril is administered
orally and/or via sublingual/buccal routes.
When captopril is chewed or nitroglycerin is
placed directly on the oral mucosa, the med-
ication is directly absorbed into the buccal
or sublingual vascular bed and avoids first
pass metabolism by the liver, thus lowering
afterload quickly even when intravenous
access is not readily available (Page, Curtis,
Walker, & Hoffman, 2006). There is moderate
evidence that although ACE inhibitors may
be used in the initial management of CPE, the
clinician should be aware of adverse effects
such as first-dose hypotension (Silvers et al.,
2007). Southall, Bissell, and Burton (2004)
found that the administration of sublingual
ACE inhibitors, throughout the course of
treatment, demonstrated no increased in-
cidence of hypotension and no increased
need of vasopressor therapy. When used in
conjunction with nitroglycerin, captopril
works more efficiently than either drug used
alone (Mattu, 2006). However, when there
is concern about the use of nitroglycerin
in patients with hypotension, mitral regur-
gitation, or aortic stenosis, or in patients
currently taking other vasodilators such as
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Management of Acute Cardiogenic Pulmonary Edema 41
phosphodiesterase inhibitors like sildenafil,
Mattu (2006) notes that ACE inhibitors are an
effective treatment choice when used alone,
without nitroglycerine. ACE inhibitors have
been shown to decrease the likelihood of
intubation of patients with CPE (Sacchetti
et al., 1999).
Angiotensin Receptor Blockers
There is conflicting evidence whether
monotherapy or combination therapy, using
ACE inhibitors and angiotensin receptor
blockers (ARB), is useful in combating the
effects of the renin–angiotensin–aldosterone
system in the setting of heart failure. Weir
(2007) concluded that combining ACE
inhibitors and ARB may increase the proba-
bility of end-organ protection; however, their
use should be judicious in the borderline
hypotensive patient.
NESIRITIDE
Nesiritide (Natrecor) is a recombinant form of
BNP that is a vasodilator, diuretic, and natri-
uretic agent. It increases stroke volume and
cardiac output without increasing heart rate.
It functions to decrease sodium and water re-
tention without causing a reflexive tachycar-
dia (Vakil, 2008). However, there is no evi-
dence that nesiritide is superior to nitrates
(Marino, 2007). Muller et al. (2004) found no
difference in the efficacy of nesiritide when
compared with the standard therapy in pa-
tients with CPE.
There are also potential detrimental ef-
fects associated with nesiritide. In a retrospec-
tive evaluation of 84 patients, Chow, Peng,
Okamoto, and Heywood (2007) found that
patients who received nesiritide infusions for
greater than 24 hr demonstrated greater evi-
dence of worsening renal function through el-
evated blood urea nitrogen (BUN) and serum
creatinine levels than did patients who re-
ceived nesiritide infusions for less than 24 hr.
Excessive diuresis is a concern when com-
bining nesiritide and other diuretics when
treating volume overload in heart failure pa-
tients. However, some studies have found no
increase in mortality or worsening of renal
LWW/AENJ AENJ-D-08-00024R1 January 21, 2009 15:32
42
function when nesiritide is used in combi-
nation with furosemide or inotropic agents
(Kurien, Warfield, Wood, & Miller, 2006).
In the face of limited evidence demonstrat-
ing superior outcomes and potential negative
effects, clinicians should be hesitant to admin-
ister nesiritide as a first-line drug for CPE un-
til more clinical trials are conducted (Mattu,
2006; Silvers et al., 2008).
SUMMARY POINTS
Brain natriuretic peptide measurement may
be a useful diagnostic test in the acutely dys-
pneic patient. However, BNP levels should be
evaluated concomitantly with a clinical assess-
ment and an elevated index of suspicion in
a patient with CPE. Several factors may di-
rectly or indirectly cause false-negative and
false-positive BNP levels and these should be
considered when assigning a diagnosis to a pa-
tient. There appears to be no statistical differ-
ence in diagnostic accuracy when using BNP,
Pro-BNP, or NT-proBNP measurements.
Cardiac troponin I is an invaluable tool in
diagnosing myocardial disease/injury and may
further support a cardiac etiology in the pa-
tient with CPE. Expedient consultation and
treatment is needed because of the high cor-
relation of troponin level and mortality.
Supplemental oxygen administration is es-
sential, and for patients with respiratory dis-
tress, noninvasive techniques such as Bi-PAP
or CPAP should be considered. Studies show
that early intervention with noninvasive mask
ventilation significantly decreases the need
for intubation as well as morbidity and
mortality.
Nitroglycerin is considered a first-line treat-
ment of CPE and should be used aggressively
for preload and afterload reduction. Infusions
are easily titratable with generally predictable
effects on hemodynamics. Similar to oxygen
therapy, nitroglycerin should be administered
early and at appropriate doses, thus reducing
the incidence of adverse outcomes and the
need for aggressive use of other therapies.
Furosemide, used in lower doses, has been
proven to decrease mortality and reduce dev-
astating effects on renal function. The clini-
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Advanced Emergency Nursing Journal
cal status of the patient with CPE and specific
cardiac etiologies should be investigated prior
to furosemide use. The clinician should exer-
cise caution when administering furosemide
to patients who seem fluid overloaded but
who may actually have right ventricular dys-
function. Low-dose furosemide (e.g., 40 mg)
may be used cautiously in conjunction with
other therapies.
Morphine sulfate, when used in the CPE pa-
tient, should never be given in doses that may
mask ischemic chest pain or other pertinent
subjective data, because the misdiagnosis of
evolving chest pain could be deleterious for
the patient. Furthermore, the doses needed
to achieve anxiolysis may cause histamine re-
lease, hypotension, and myocardial and res-
piratory depression. Benzodiazepines may be
more appropriate if anxiolysis is still indicated
after other therapies have been initiated.
ACE inhibitors are effective afterload reduc-
ers; however, they may cause hypotension
and should be administered cautiously to pa-
tients with marginal blood pressure. The com-
bination of ACE inhibitors with ARBs shows
great potential; however, this may not be in-
dicated in the ED setting. Although used with
special patient populations (i.e., patients al-
lergic to ACE inhibitors), ARBs have shown
no significant improvement in mortality when
used as monotherapy.
Nesiritide is a vasodilator that does not
cause tachycardia and has diuretic and natri-
uretic properties. However, there is no evi-
dence that it is clinically superior to nitrates.
Caution should be used when combining ne-
siritide with other diuretics. Extended admin-
istration may result in renal damage.
In conclusion, subtle differences in treat-
ment strategies can affect the outcome of pa-
tients with CPE. It is imperative to remain
abreast of current research and modify prac-
tice with evidence-based information in the
interest of our patients.
REFERENCES
Abbas, A. K., Fausto, N., & Kumar, V. (2005). Pathologic
basis of disease (7th ed.). Philadelphia: Saunders.
Barker, R. D., & Schneider, R. E. (2008). Supplemental
oxygenation and bag-mask ventilation. In R. M. Walls
LWW/AENJ AENJ-D-08-00024R1 January 21, 2009 15:32
January–March 2009 r Vol. 31, No. 1
& M. F. Murphy (Eds.), Manual of emergency air-
way management (3rd ed., pp. 47–61) Philadelphia:
Lippincott Williams & Wilkins.
Chow, S. l., Peng, J. T., Okamoto, M. P., & Heywood,
J. T. (2007). Effect of nesiritide infusion duration on
renal function in acutely decompensated heart failure
patients [Abstract]. Annals of Pharmacotherapeutics,
41(4), 556–561.
Cross, A. M., Cameron, P., Kierce, M., Ragg, M., & Kelly,
A. M. (2003). Non-invasive ventilation in acute respira-
tory failure: A randomized comparison of continuous
positive airway pressure and bi-level positive airway
pressure. Emergency Medicine, 20(6), 531–534.
DeBlieux, P. M. C., & Broderick, K. B. (2008). Noninva-
sive mechanical ventilation. In R. M. Walls & M.F. Mur-
phy (Eds.), Manual of emergency airway manage-
ment (3rd ed., pp. 422–427). Philadelphia: Lippincott
Williams & Wilkins.
Horwich, T. B., Hamilton, M. A., & Fonarow, G. C. (2006).
B-Type natriuretic peptide levels in obese patients
with advanced heart failure [Abstract]. Journal of the
American College of Cardiology, 47(1), 85–90.
Hunt, S. A., Abraham, W. T., Chin, M. H., Feldman, A. M.,
Francis, G. S., Ganiaats, T. G., et al. (2005). ACC/AHA
2005 guideline update for the diagnosis and manage-
ment of chronic heart failure in the adult. Circulation,
112 (12), 1825–1852.
Kurien, S., Warfield, K. T., Wood, C. M., & Miller, W. L.
(2006). Effects of standard heart failure therapy and
concomitant treatment with intravenous furosemide
or inotropes (dobutamine, dopamine, and/or milri-
none) on renal function and mortality in patients
treated with nesiritide [Abstract]. American Journal
of Cardiology, 98(12), 1627–1630.
La Vecchia, L., Mezzena, G., Zanolla, L., Paccanaro, M.,
Varotto, L., Bonanno, C., et al. (2000). Cardiac tro-
ponin I as diagnostic and prognostic marker in severe
heart failure [Abstract]. Journal of Heart and Lung
Transplantation, 19(7), 644–652.
Levitt, M. A. (2001). A prospective, randomized trial of
BiPAP in severe acute congestive heart failure. Journal
of Emergency Medicine, 21(4), 363–369.
Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A.,
Penugonda, N., et al. (2007). Treatment of severe de-
compensated heart failure with high-dose intravenous
nitroglycerin: A feasibility and outcome analysis. An-
nals of Emergency Medicine, 50(2), 144–152.
Marino, P. L. (2007). The ICU book. Philadelphia: Lippin-
cott Williams & Wilkins.
Mattu, A. (2006, Aug). Winning at failure: Modern
management of cardiogenic pulmonary edema. Pa-
per presented at the American College of Emergency
Physicians conference, Boston, MA.
Mehta, S., Jay, G. D., Woolard, R. H., Hipona, R. A.,
Connolly, E. M., Cimini, D. M., et al. (1997). Random-
Char Count= 0
Management of Acute Cardiogenic Pulmonary Edema 43
ized, prospective trial of bilevel versus continuous
positive airway pressure in acute pulmonary edema.
Critical Care Medicine, 25(4), 620–628.
Moritz, F., Brousee, B., Gellee, B., Chajara, A., L’Her, E.,
Hellot, M. F., et al. (2007). Continuous positive air-
way pressure versus bilevel noninvasive ventilation in
acute cardiogenic pulmonary edema: A randomized
multicenter trial. Annals of Emergency Medicine, 50,
666–675.
Mueller, C., Scholer, A., Laule-Kilian, K., Martina, B.,
Schindler, C., Buser, P., et al. (2004). Use of B-type na-
triuretic peptide in the evaluation and management
of acute dyspnea. New England Journal of Medicine,
350(7), 647–654.
Page, C., Curtis, M., Walker, M., & Hoffman, B. (2006).
Integrated pharmacology (3rd ed.). Philadelphia:
Elsevier-Mosby.
Peacock, W. F., IV , De Marco, T., Fonarow, G. C., Diercks,
D., Wynne, J., Apple, F. S., et al. (2008). Cardiac tro-
ponin and outcome in acute heart failure. New Eng-
land Journal of Medicine, 358(20), 2117–2126.
Sacchetti, A., Ramoska, E., Moakes, M. E., McDermott, P.,
& Moyer, V. (1999). Effect of ED management on ICU
use in acute pulmonary edema. American Journal of
Emergency Medicine, 17(6), 571–574.
Scios, Inc. (2003). Intravenous B-type natriuretic pep-
tide: Natrecor (Nesiritide) [package insert]. Raritan,
NJ: Author.
Silvers, S. M., Howell, J. M., Kosowsky, J. M., Rokos,
I. C., & Jagoda, A. S., American College of Emer-
gency Physicians Clinical Policies Subcommitte on
Acute Heart Failure Syndromes. (2007). Clinical pol-
icy: Critical issues in the evaluation and management
of adult patients presenting to the emergency depart-
ment with acute heart failure syndromes. Annals of
Emergency Medicine, 49(5), 627–669.
Singer, A. J., Emerman, C., Char, D. M., Heywood, J. T.,
Kirk, J. D., Hollander, J. E., et al. (2008). Bronchodilator
therapy in acute decompensated heart failure patients
without a history of chronic obstructive pulmonary
disease. Annals of Emergency Medicine, 51(1), 25–
34.
Southall, J. C., Bissell, D. M., Burton J. H. (2004). ACE
inhibitors in acutely decompensated congestive heart
failure. Academic Emergency Medicine, 11, 503.
Vakil, M. (2008, May 22). CHF. Lecture presented at ED
Grand Rounds at the University of Mississippi Medical
Center, Jackson.
Weir, M. R. (2007). Effects of renin-angiotensin system in-
hibition on end-organ protection: Can we do better?
[Abstract]. Clinical Therapeutics, 29(9), 1803–1824.
You, J. J., Austin, R. C., Alter, D. A., Ko, D. T., & Tu, J. V.
(2007). Relation between cardiac troponin I and mor-
tality in acute decompensated heart failure. American
Heart Journal, 153(4), 462–470.