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ACUTE HEART FAILURE
175
causes
52
do not report an increase in MI or mortality
in patients receiving BiPAP.
18
Two additional studies
directly compare CPAP and BiPAP for patients with
acute heart failure syndrome, and neither modality has
an advantage over the other.
53,54
Pharmacologic therapies: preload
and afterload reduction
The fi rst goal in pharmacologic treatment of patients
with AHF and CPE should be preload reduction. By
reducing right heart and pulmonary venous return, and
right-heart fi lling pressures and pulmonary capillary
hydrostatic pressures, patients will have early symptom-
atic improvements in dyspnea.
21
Typical medications uti-
lized for preload reduction are nitroglycerin, morphine
sulfate, and loop diuretics. More recently, a recombinant
form of beta-natriuretic peptide known as nesiritide has
been recommended for preload reduction, but with no
clear advantages over conventional therapy.
21
Utility of nitrates
Nitroglycerin (NTG) is the most effective and
rapidly-acting preload-reducing medication.
7,55–58
Multiple studies demonstrate the superiority of NTG
over furosemide and morphine sulfate for preload
reduction, symptomatic improvement, and patient
safety.
5,9,21,48,51,55,59–61
NTG can be administered in sub-
lingual, intravenous, or transdermal form, although
the transdermal absorption can be erratic.
21
An addi-
tional benefi t of NTG is its short half-life. If the patient
develops a precipitous fall in blood pressure (gener-
ally uncommon in AHF patients), the blood pressure
should return to previous values within 5–10 minutes
of discontinuation of medication.
21
Preload reduction
and subsequent noticeable symptomatic improvements
occur within 5 minutes of sublingual administration of
NTG, and the dose can be repeated every 3–5 minutes
during the fi rst 10–15 minutes of presentation.
21,62,63
Standard anti-anginal dosages of sublingual NTG
(400 µg every 5 minutes) with which most physicians
are comfortable have the bioequivalence of an IV
NTG infusion of 60–80 mg/min.
21
If using IV NTG,
an initial dose of 10–20 mg/min should be titrated
upwards rapidly until a dose of at least 100 mg/min
is achieved.
13
This type of aggressive administration of
NTG also produces afterload reduction.
64,65
Due to concerns for precipitous drops in blood
pressure, nitrates should not be used in patients pre-
senting with hypotension, or patients presently taking
prevent respiratory failure while defi nitive care is
being established; however, patients with signifi cant
mental status changes who are unable to cooperate
with this modality are not candidates for this inter-
vention. Patients who present with pulmonary edema
and concurrent hypotension, along with evidence
of end-organ hypoperfusion (altered mental status,
reduced urine output, poorly perfused extremities),
may require a fl uid challenge and aggressive inotro-
pic therapy. This subset of critically ill patients may
benefi t from right-sided heart catheterization, and
need ICU admission for close monitoring and con-
tinued treatment.
14
BiPaP and CPAP
Noninvasive ventilatory assistance may be provided by
either continuous positive airway pressure or bilevel
positive airway pressure. CPAP provides a constant,
positive, end-expiratory airway pressure, whereas
BiPAP provides the same constant end-expiratory pres-
sure, as well as added positive pressure at the onset
of inspiration to assist ventilation. CPAP and BiPAP
devices typically attach to the patient by a nasal or face
mask.
11
By improving oxygenation, reducing respira-
tory work, and decreasing left-ventricular afterload,
the positive airway pressure provided by these devices
has been thought to improve pulmonary mechanics
and hemodynamics, as well as to reduce the need for
endotracheal intubation, hospital length of stay, and
mortality.
48,49
Initial studies evaluating CPAP by either nasal or
face mask at 5 to 10 mmHg consistently show signifi -
cant improvements in oxygenation, reductions in heart
rate, reductions in respiratory rate, and reductions in
blood pressure compared with standard oxygen ther-
apy. Several of these studies also report statistically
signifi cant improvements in cardiopulmonary indices
(i.e., pulmonary capillary wedge pressure, stroke vol-
ume, cardiac output, or cardiac index), as well as a
reduction in the rate of intubation.
11
In a 1997 Class III study, Mehta, et al.
50
report a
trial comparing BiPAP, CPAP, and conventional oxy-
gen therapy for patients with acute heart failure syn-
drome. BiPAP is no more effi cacious than CPAP, and is
associated with a higher rate of myocardial infarction
as defi ned by elevated cardiac markers.
11
Subsequent
studies comparing BiPAP with mask ventilation in
patients who present with CPE
51
and BiPAP versus
CPAP in acute respiratory failure of heterogeneous
CHAPTER 12
176
diuretics produce a decrease in preload by inhibiting
sodium chloride reabsorption in the ascending loop of
Henle, thereby promoting increases in urine volume
and excretion.
18
Unfortunately, because patients who
develop AHF have elevated systemic vascular resis-
tance (afterload), renal perfusion is markedly dimin-
ished.
67
This causes diuretics to have a signifi cantly
delayed onset of action, often taking 45–120 minutes
to produce effective diuresis.
6–8,52,68
More than half of
the patients who present with CPE have intravascular
euvolemia or hypovolemia, and diuretic administra-
tion in these patients may be associated with adverse
effects, including electrolyte abnormalities and hypoten-
sion caused by overdiuresis.
55,63,69,70
Currently, there are no randomized clinical trials
evaluating the clinical benefi t of furosemide alone in
acute heart failure syndromes.
11
Two clinical studies
conclude that loop diuretic monotherapy does not
improve short-term ED outcomes (i.e., improve hemo-
dynamic status, patient dyspnea, and reduce rate of
endotracheal intubation) among patients presenting
with moderate-to-severe acute pulmonary edema.
53,55
The adverse hemodynamic changes may be blunted in
AHF by administration of preload-reducing (i.e., NTG)
and afterload reducing (i.e., angiotensin-converting
enzyme inhibitors) medications before furosemide.
18,52
Potential safety considerations regarding diuretic
administration are reported in a multicenter study
of 382 patients.
71
Worsening renal function is asso-
ciated with a greater total dose of furosemide in the
preceding 24 hours compared to those patients who
don’t develop worsening renal function (394 mg ver-
sus 262 mg; P 0.05).
63
The possible association of
diuretics with worsening renal function is important,
given that several recent studies report an association
between impaired renal function and increased mor-
tality among acute heart failure syndrome patients.
11
Data from more than 60,000 patients in the ADHERE
registry show that in hospital mortality is greater than
20% among patients with an admission blood urea
nitrogen level greater than 43 mg/dL, a creatinine level
greater than 2.7 mg/dL, and a systolic blood pressure
less than 115 mmHg.
72
In a retrospective study of
1681 patients younger than 65 years of age who were
admitted for AHF syndromes, an increase in the serum
creatinine level of greater than 0.3 mg/dL during the
index hospitalization is associated with a nearly three
times greater risk of inhospital mortality (OR 2.7,
95% CI 1.6 to 4.6).
73
Furthermore, in a prospective
sidenafi l or other similar medications for erectile
dysfunction, Furthermore, nitrates should be used
with extreme caution (if at all) in patients with aor-
tic stenosis or pulmonary hypertension because of
the dependence these conditions place on preload to
maintain adequate perfusion.
21
Utility of morphine
Morphine sulfate (MS) has been administered as a
standard preload-reducing medication in patients with
suspected AHF, especially in the prehospital setting.
However, MS has not been studied in a randomized
fashion in these patients to confi rm hemodynamic ben-
efi ts. MS most likely exerts mild indirect hemodynamic
benefi ts through anxiolysis, resulting in a decrease in
catecholamine production and indirectly causing vaso-
dilatation.
18
While early studies demonstrate some
evidence of vasodilatation and venous pooling in the
peripheral circulation, a consistent central preload-
reducing effect (i.e., reduction in pulmonary capillary
wedge pressures [PCWP]) is not present.
18
In contrast,
multiple studies show that MS may be associated with
adverse hemodynamic effects, including increases in
left and right heart fi lling pressures and reductions in
cardiac index caused by a direct myocardial depres-
sant effect on the already-reduced contractile state of
the ischemic heart.
4,9,50,66
The adverse hemodynamic
effects have clinical drawbacks. In a prehospital study
evaluating the use of various medications in patients
with presumed CPE, 38% of patients receiving MS
have subjective deterioration (e.g., increased dyspnea)
in clinical status, and 46% have objective deteriora-
tion (e.g., increased respiratory rate).
18,55
Morphine sulfate also has an undesirable side effect
profi le, including nausea, emesis, pruritus, and urti-
caria. If a patient requires medications for anxiety,
low-dose benzodiazepines have a better side-effect
profi le and are not associated with signifi cant myo-
cardial or respiratory depression.
18
In conclusion,
based on available evidence regarding the superiority
of NTG over MS to reduce preload and availability of
low-dose benzodiazepines for anxiolysis, the routine
use of MS is not recommended in acute heart failure
(AHF) syndromes.
18
Utility of diuretics
Furosemide (common loop diuretic) has been used
intravenously for years as the cornerstone of treat-
ment in patients who present with CPE. Loop
ACUTE HEART FAILURE
177
Hypotensive patients who may be in or at imme-
diate risk of cardiogenic shock should not initially
receive ACEIs or other afterload reducing agents.
However, afterload-reducing medications can be
administered cautiously after vasopressors therapy is
initiated in hypotensive patients, although titrateable
afterload-reducers (e.g., nitroprusside) are preferred
in this setting. Afterload-reducing agents should also
be used with caution in patients who have severe
aortic stenosis. In patients with chronic renal insuf-
fi ciency with markedly increased serum levels of crea-
tinine (greater than 3 mg/dL), known bilateral renal
artery stenosis, or elevated levels of serum potassium
(greater than 5.5 mmol/liter), repetitive dosing of
ACEIs should be avoided; however, a single dose of
ACEIs for acute afterload reduction even in the pres-
ence of CRI or hyperkalemia should not produce an
acute change in renal function or potassium level.
18
Adverse reactions of ACEIs are generally attribut-
able to the two principal pharmacological actions of
these drugs: those related to angiotensin suppression
(hypotension) and those related to kinin potentiation
(angiodema).
76
Patients should not be given an ACEI
if they have experienced life-threatening adverse reac-
tions (angioedema or anuric renal failure) during pre-
vious exposure to the drug, or if they are pregnant.
Pharmacologic therapies: inotropic support
Inotropic agents can cause tachycardia, dysrhyth-
mias, increased myocardial oxygen demand, myocar-
dial ischemia, and sometimes increased mortality in
patients with AHF.
87,88
These medications should be
reserved for hypotensive AHF patients who are unable
to tolerate the use of fi rst-line preload- and afterload-
reducing medications discussed previously.
18
After
initiation of inotropic agents and suffi cient improve-
ments in blood pressure, IV NTG can then be admin-
istered to obtain the desired preload and afterload
reduction to relieve pulmonary congestion.
89,90
These
critically-ill patients are best managed in the ICU with
pulmonary artery catheterization and invasive moni-
toring to closely track their hemodynamic status and
allow precise titration of the medications.
18
Typical agents fall into two main classifi cations:
catecholamines and phosphodiesterase inhibitors.
The catecholamine inotropes include dobutamine,
dopamine, and norepinephrine. No studies to date
have demonstrated a mortality benefi t of these over
others in the ED setting. From a hemodynamic
cohort study of 412 hospitalized patients with acute
heart failure syndrome, a stepwise increase in 6-month
mortality as serum creatinine increases from greater
than or equal to 0.1 mg/dL to greater than or equal to
0.5 mg/dl above baseline is reported.
74
Utility of ACE inhibitors: afterload reduction
Afterload reduction with vasodilatator medications
produces an increase in cardiac output and reduc-
tion in pulmonary interstitial edema. Another benefi t
is improved renal perfusion, which can lead to sub-
stantial improvements in diuresis even before admin-
istration of diuretics.
75
High-dose IV NTG effectively
reduces afterload, but prolonged infusion can induce
tolerance and limit its effi cacy. Nitroprusside is a
potent afterload-reducing medication used in certain
hypertensive emergency states. However, it can induce
labile fl uctuations in blood pressure, requires intra-
arterial hemodynamic monitoring, and cause refl ex
tachycardia in an already stressed state with AHF.
18
Angiotensin-converting enzyme inhibitors (ACEIs)
interrupt the renin-angiotensin system and lead to
decreased preload and decreased afterload.
11
The
administration of sublingual (captopril) or IV (capto-
pril, enalapril) forms of ACEIs to patients who develop
CPE is associated with reductions in systemic vascu-
lar resistance (afterload) and improvements in PCWP
(preload), stroke volume, cardiac output, and mitral
regurgitation without causing adverse changes in heart
rate or mean arterial pressure.
6,21,76–82
Improvements
of both hemodynamics and subjective dyspnea are
noted within 6–12 minutes. Similar improvements
have been shown when ACEIs are administered to
patients who have already received other “standard”
therapies, including MS, furosemide, and NTG,
83
and
in patients who have hemodialysis-dependent renal
failure.
18,84
The available data suggest that there are
no differences among available ACEIs in their effects
on symptoms or survival.
76
The use of ACEIs in patients with AHF decreases
rates of endotracheal intubation, intensive care unit
(ICU) admission rates, and ICU length of stay.
70,85
These benefi ts of ACE inhibition are seen in patients
with mild, moderate, or severe symptoms, and in
patients with or without coronary artery disease.
86
ACEIs can be used safely in conjunction with NTG
to provide combination preload and afterload reduc-
tion, or they can be used as an effective single agent in
patients who are unable to receive NTG.
18
CHAPTER 12
178
heart failure.
99,101
One randomized double-blind
trial compared 24-hour infusions of this agent with
dobutamine in patients who presented with severe
low-output heart failure.
100
Levosimendan not only
produces more signifi cant improvements in cardiac
output and PCWP, but also is associated with a lower
180-day mortality rate (26% versus 38%) compared
with patients who receive dobutamine. Further trials
are needed to clarify whether levosimendan has a role
in the acute ED management of patients who have
developed CPE.
Utility of nebulizers (if patient is wheezing)
The use of bronchodilators is common among pre-
hospital providers when caring for patients who
have undifferentiated dyspnea.
1
Many patients who
have decompensated CHF can present with wheez-
ing, and bronchodilators are commonly administered
to these patients.
1
A prehospital study suggests that
bronchodilators are safe in all types of patients who
have dyspnea regardless of the fi nal diagnosis, fi nd-
ing no increased mortality in patients receiving these
medications.
101
However, a nonrandomized, retro-
spective study suggests otherwise.
102
Over 10,000
patients from the Acute Decompensated Heart Failure
National Registry Emergency Module who were pro-
vided bronchodilators during acute treatment, in
the prehospital setting or in the ED, were evaluated.
The use of bronchodilators in patients who do not
have a history of COPD is associated with a slightly
greater need for “aggressive interventions,” including
mechanical ventilation. Whether the bronchodilata-
tor use is causing adverse outcomes, or is simply a
marker of sicker patients, is unclear. Nevertheless, the
study does raise concerns regarding the liberal use of
bronchodilatators in the management of prehospital
and ED patients who have undifferentiated dyspnea,
especially if the presumptive diagnosis is decompen-
sated CHF.
1
Disposition of patients with acute heart failure
Unstable and critically Ill patients with AHF
syndromes Patients who require mechanical ventila-
tion, experience acute valvular dysfunction, require
inotropic support, and who present with evidence
of acute cardiac ischemia or infarction (based on
EKG changes or elevated cardiac biomarkers) should
be admitted to an ICU setting after initial attempts
at stabilization.
103,104
Emergent consultation by a
standpoint, dobutamine provides the advantage of
inducing mild reductions in preload and afterload in
addition to inotropic support. Close monitoring is
required as may cause a reduction in blood pressure,
precluding its continued use.
91
If this occurs, dobu-
tamine should be discontinued, and dopamine or
norepinephrine can be administered to support blood
pressure. These medications improve blood pressure
by increasing systemic vascular resistance, but may at
the same time cause a detrimental decrease in cardiac
output. In cases when dopamine and norepinephrine
are given, preload- and afterload-reducing medica-
tions should be added as soon as possible to improve
LV performance and relieve pulmonary congestion.
Several limitations of catecholamine inotropes exist.
Their activity depends on adrenoreceptor sensitivity.
CHF patients have chronically elevated levels of circu-
lating catecholamines that produce adrenoreceptor tol-
erance, thereby requiring higher inotropic dosages than
normal. Additionally, many patients who experience
CHF are now treated chronically with beta-adrenergic
receptor antagonists (beta-blockers). These medications
antagonize the effects of catecholamine inotropes, also
leading to higher dosages of the inotropes. Higher dos-
ages are associated with increased adverse effects.
18
Phosphodiesterase inhibitors (PDEIs) work by
increasing intracellular cyclic adenosine monophos-
phate levels, which produce a positive inotropic effect
on the heart, inducing peripheral vasodilatation and
reducing pulmonary vascular resistance. Overall, PDEIs
induce improvements in preload, afterload, and cardiac
output.
92
PDEIs have the advantage over catecholamine
inotropes of working independent of adrenoreceptor
activity, meaning they are unaffected by circulating cat-
echolamine levels or beta-blocker medications.
93
The
most well studied PDEI is milrinone, which has been
directly compared with dobutamine in patients with
severe acutely decompensated CHF and CPE, and mil-
rinone is consistently noted to produce equal or greater
improvements in stroke volume, cardiac output,
PCWP, and systemic vascular resistance. Milrinone is
well-tolerated, and is associated with fewer episodes
of tachycardia and sustained tachydysrhythmias than
dobutamine.
94–98
Despite apparent hemodynamic ben-
efi ts, however, it has not been demonstrated to improve
hospital length of stay or mortality.
96,98
Levosimendan, classifi ed as a “calcium sensitizer,” is
an inotrope suggested as an alternative to dobutamine
for patients presenting with acutely decompensated
ACUTE HEART FAILURE
179
ADHERE) of patients hospitalized with decom-
pensated heart failure identifi es: (1) high admission
blood urea nitrogen (43 mg/dL), followed by (2)
low admission systolic blood pressure (115 mmHg),
followed by (3) high levels of serum creatinine (2.75
mg/dL) as the best predictors for inhospital mortal-
ity.
109
Unfortunately, even a patient presenting with
AHF syndrome without any of the above criteria still
has a predicted 2.1% “low risk” of mortality.
Patients with any of these criteria, as well as
patients unable to complete close outpatient fol-
low-up (poor access or limited fi nancial capabilities),
should be admitted to ensure clinical resolution, and
to allow for arrangements for longer-term inpatient
or outpatient care. The goals of admission should
include improvement of a patient’s pulmonary edema
while simultaneously focusing on discovering and
treating the underlying cause.
18
In summary, until a
validated risk-stratifi cation tool based on ED data
from ED presentations of AHF syndrome is devel-
oped, admission to an inpatient or ED observation
unit is recommended.
The emergency department observation unit
Observation units allow for continued evaluation
and treatment for up to 24 hours, to either dis-
charge based on improved clinical status, or to have
an admission for further inpatient care. Preliminary
research suggests that an ED observation unit is a
safe and effi cient alternative for AHF patients with
mild symptoms.
111–114
With continued research, the
ED observation unit may become part of a viable dis-
position strategy of low risk patients presenting with
AHF syndrome.
18
Section IV: Decision making
Acute heart failure and cardiogenic pulmonary •
edema are at high risk for early morbidity or
mortality.
The diagnosis of AHF is based on history, physical •
examination, and chest radiography.
Laboratory testing adds little except in equivocal •
cases.
Early management should focus on aggressive •
preload and afterload reduction.
Diuresis plays a secondary role in the sickest of •
patients because of delayed effect and because most
cardiologist should be obtained if the cause of the
acute CHF exacerbation is AMI or acute valvular dys-
function, or if the patient requires inotropic support.
Consultation of a cardiac surgeon is also warranted if
severe valvular dysfunction is present.
Disposition for the non-critically ill patients Patients
who experience mild CHF decompensations that are
attributable to dietary indiscretions (excessive salt
intake) or medication noncompliance can receive
diuretics in the ED for symptomatic improvement,
and be discharged safely. This assumes a patient has
ready access to close outpatient follow-up, and the
ability to continue with medical interventions, either
begun or adjusted during the ED evaluation.
Patients who present with active signs of pulmo-
nary edema should be admitted to a cardiac-moni-
tored bed (inpatient or ED observation unit). Several
studies have evaluated ED-based risk models for
heart failure patients.
105
However, all models fail
to identify a truly low-risk patient, and many only
assess mortality but not morbidity from treatment
failures. Patients with presenting factors that have
been shown to be associated with in-hospital mor-
tality include advanced age, renal dysfunction,
hypotension, digoxin use, chest pain, and anemia
(Table 12-4).
106–110
Additional data from a large registry (Acute
Decompensated Heart Failure National Registry,
Table 12-4. Predictors of inhospital mortality in patients
who experience cardiogenic pulmonary edema.
• Need for mechanical ventilation
• Acute valvular dysfunction
• Need for inotropic support
• Elevated cardiac biomarkers
• EKG evidence of ischemia or dysrhythmias
• Advanced age
• Renal dysfunction (serum elevations of blood urea
nitrogen or creatinine)
• Hypotension
• Digoxin use
• Chest pain
• Anemia
Reprinted with permission from Elsevier from: Mattu
A, Martinez JP, Kelly BS. Modern management of
cardiogenic pulmonary edema. Emerg Med Clin N Am.
2005;23(4):1105–1125.
CHAPTER 12
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