Nancy M. Albert, Cathy A. Eastwood and Michelle L.

Edwards
Evidence-Based Practice for Acute Decompensated Heart Failure
Published online http://www.cconline.org
2004 American Association of Critical-Care Nurses
2004, 24:14-29. Crit Care Nurse

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14 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Nancy M. Albert is certified as a clinical nurse specialist and has a dual role of director of nursing research in the division of nursing
and clinical nurse specialist at the George M. and Linda H. Kaufman Center for Heart Failure of the Cleveland Clinic Foundation,
Cleveland, Ohio. She codeveloped heart failure programs along the continuum of care, including emergency care, critical care, and acute
care, at the Cleveland Clinic Foundation.
Cathy A. Eastwood graduated with a master of nursing degree from the University of Calgary, Canada, after specializing in the care of
patients with heart failure. She developed and managed the outpatient heart failure center and oversaw the flow of inpatients with heart
failure at St. Lukes Episcopal Hospital, Houston, Tex. Currently, she is a lecturer at Memorial University of Newfoundland, School of
Nursing, in St. Johns, Newfoundland, Canada.
Michelle L. Edwards earned a master of science degree in nursing from the University of Alabama at Birmingham and is a board-
certified family and acute care nurse practitioner. She practiced several years in critical care, specializing in the care of cardiovascular
patients. She currently is a cardiology nurse practitioner/outcomes manager at St. Lukes Episcopal Hospital.
Each year, chronic left ventric-
ular systolic and diastolic dysfunc-
tion, or heart failure, causes 1
million hospitalizations in the
United States.
1
Heart failure is the
most common Medicare diagnosis
related group at discharge
1,2
and is
associated with poor survival and
quality of life. In addition, cost of
care is high; in 1998, Medicare paid
out $3.6 billion for care related to
heart failure.
1
The Acute Decompensated Heart
Failure National Registry (ADHERE)
3
recently reported data on 14716
patients hospitalized for heart failure
in the United States (Tables 1 and 2).
Generally, patients admitted to the
hospital for heart failure were elderly,
were female, had a history of heart
CoverArticle
Authors
CE This article has been designated for
CE credit. A closed-book, multiple- choice
examination follows this article, which tests
your knowledge of the following objectives:
1. Identify the core drug therapies for
decompensated heart failure
2. Describe the role of B-type natriuretic
peptide in decompensated heart failure
3. Explain the pharmacological management
of decompensated heart failure
Nancy M. Albert, RN, MSN, CCNS, CCRN, CNA
Cathy A. Eastwood, RN, MN
Michelle L. Edwards, RN, MSN, FNP, ACNP
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail,
reprints@aacn.org.
CE
Continuing Education
Evidence-Based
Practice for
Acute Decompensated
Heart Failure
by guest on September 28, 2014 http://ccn.aacnjournals.org/ Downloaded from
failure, and were unable to carry out
activities of daily living without exer-
cise intolerance. The most common
symptom was dyspnea, which was
most often associated with other signs
and symptoms of fluid retention.
Comorbid conditions were common,
and patients were equally likely to
be admitted with systolic dysfunction
(reduced ventricular contractility;
ejection fraction 0.40) or diastolic
dysfunction (impaired ventricular
relaxation or ventricular stiffness
tion that led to signs and symptoms
was impaired ventricular relaxation,
which was associated with increased
age, obesity, hypertension, and car-
diovascular disease.
4
In addition,
ADHERE data were comparable to
data from other reports
6-8
in that
retention of fluid and sodium, as
evidenced by admitting signs and
symptoms, was a primary factor in
hospitalization. This knowledge pro-
vides an opportunity for care improve-
ment that can be championed by
nurses, because hospitalization for
fluid and sodium retention in patients
with systolic or diastolic dysfunction
may be avoidable, especially when
such retention is due to patients fail-
ure to adhere to medication regimens
or self-care instructions.
In this article, we discuss evidence-
based practices for managing patients
with acutely decompensated heart
failure because in-hospital actions
may facilitate an improved experience
for patients after hospitalization.
The intent is to provide management
that decreases the
ventricles ability
to fill). One quar-
ter of patients were
rehospitalized
within 6 months
of a previous hos-
pitalization, and
Medicare was the
primary hospital
payor. Most
patients spent
time in the emer-
gency department
before admission as an inpatient, and
the most common level of initial care
was telemetry. Median length of stay
was 4.4 days.
3
The ADHERE data are similar to
data from other studies
4,5
in which
investigators found an equal split of
patients with impaired and preserved
left ventricular systolic function, sig-
nifying hospitalization of patients
with systolic dysfunction and patients
with diastolic dysfunction. The pri-
mary mechanism of diastolic dysfunc-
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 15
Table 2 Outpatient medications before hospitalization and
medications at discharge: data from the Acute Decompensated
Heart Failure National Registry
3
Medication class
% of patients
87
58
13
4
5
33
72
54
22
37
27
48
34
3
72
42
11
3
4
28
54
44
23
30
23
38
30
7
Diuretic
Angiotensin-converting
enzyme inhibitor
Angiotensin II receptor blocker
Hydralazine plus nitrate
Hydralazine
Nitrate
Angiotensin-converting enzyme
inhibitor, hydralazine, plus
nitrate or angiotensin II
receptor blocker
-Blocker
Calcium channel blocker
Digoxin
Warfarin
Aspirin
Lipid-lowering agent
Nonsteroidal anti-inflammatory
drugs
Before hospitalization
(n=14716)
At discharge
(n = 11 187)
Table 1 Characteristics of patients, clinical signs and
symptoms, and hospital placement: data from the Acute
Decompensated Heart Failure National Registry
3
Characteristics at hospital admission % of patients
52
68
50
77
25
43
32
71
31
58
30
44
28
16
8
92
34
72
69
35
38
49
20
77
22
65
13
8
Female
Medicare, primary payer
Ejection fraction <0.40
History of heart failure
Hospitalized for heart failure within past 6 months
Baseline New York Heart Association functional class
III*
IV

History of hypertension
History of myocardial infarction
History of coronary artery disease
Atrial fibrillation, asthma, or chronic obstructive
pulmonary disease

Diabetes
Chronic renal insufficiency
Stroke or transient ischemic attack
Ventricular tachycardia
Clinical signs and symptoms

Any dyspnea
Dyspnea at rest
Crackles
Peripheral edema
Fatigue
New York Heart Association functional class
III
IV
Creatinine >177 mol/L (2.0 mg/dL)
Point of entry to the hospital
Emergency department
Direct admission
First inpatient unit
Telemetry
Ward or intensive or coronary care
Stepdown
*Dyspnea, fatigue, palpitations, or chest pain with minimal activity.

Dyspnea, fatigue, palpitations, or chest pain at rest.

Percentage of each.

Mean serum level of sodium was 138 mmol/L, and median level of B-type
natriuretic peptide was 784 pg/mL.
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goals and actions associated with the
most common clinical manifestation,
fluid retention, and not to focus on
management of cardiogenic shock,
profound hypoperfusion, or complex
decompensation (severe hyper-
volemia, hypoperfusion, and acidosis
or other conditions such as pneumo-
nia). Assessment of patients, man-
agement strategies, and education of
patients are highlighted. Myths
associated with acute care manage-
ment are discussed so that nurses
will be more aware of appropriate
interventions that are safe and effec-
tive. Heart failure management has
progressed rapidly in recent years.
Ultimately, nurses must be proactive
in ensuring that their behaviors are
based on current evidence.
Heightened Expectations
for Evidence-Based Care
Nurses are challenged to plan and
provide care that promotes the best
possible clinical and health-related
outcomes. The Joint Commission on
Accreditation of Healthcare Organi-
zations
9
recently established 4 core
measures in the acute management
of patients with heart failure to pro-
mote adherence to basic standards of
evidence-based care (Table 3). Because
of the large number of patients and
the high cost of care associated with
hospital readmissions, acute and
critical care nurses must develop
and implement strategies that are
associated with improved outcomes
for patients and hospitals. In addi-
tion, in 2001, the American College
of Cardiology (ACC) and the Ameri-
can Heart Association (AHA) pub-
lished practice guidelines
10
for adults
with chronic heart failure. These
guidelines provide caregivers with
recommendations for nonacute care
and include the rationale and level
of evidence for support of each man-
agement strategy. Table 4 provides
a list of management strategies,
including core drug therapies, that
should be a part of each patients
treatment plan at discharge after
an admission for decompensated
heart failure stemming from vol-
ume overload.
10,11
If the medica-
tion expectations
listed in Table 4
are compared with
the actual med-
ication therapies
before hospital-
ization and at dis-
charge indicated
in the ADHERE
data (Table 2), a
need for change is
evident. New
efforts must be
undertaken to
promote use of
consensus guidelines and therapies
to meet the overall goal of manag-
ing heart failure: promoting regres-
sion and preventing progression of
left ventricular enlargement (remod-
eling) to decrease disease progres-
sion and improve survival.
11-14
See
Figure 1 and Table 5 for definition
and description of consequences of
ventricular remodeling.
16 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Table 3 The 4 core measures of the Joint Commission on
Accreditation of Healthcare Organizations
Written discharge instructions or educational material must be
given to the patient or caregiver and include all of the follow-
ing: activity level, diet, discharge medications, follow-up
appointment, weight monitoring, and symptom management
Left ventricular function must be documented in the hospital
record to indicate that it was assessed before or during hos-
pitalization, or will be assessed after discharge
Patients with known systolic dysfunction of moderate to
severe impairment (ejection fraction <0.40) and without con-
traindication to angiotensin-converting enzyme inhibitor will
be prescribed an angiotensin-converting enzyme inhibitor at
hospital discharge
Patients who are current smokers or former smokers who quit
in the past 12 months will be given smoking cessation advice
or counseling during the hospital stay
Table 4 Practice guidelines that apply to stage C* patients
Nonpharmacological management
Core pharmacological management
Encourage exercise
Promote smoking cessation
Discourage alcohol consumption and illicit drug use
Restrict dietary sodium (2000-mg sodium diet)
Assess cause of heart failure to determine if surgical options are appropriate
Revascularization for chronic coronary artery disease without angina but with viable
myocardial tissue or if symptomatic angina
Repair of mitral valve or replacement of aortic valve for valve disease
Assess for cardiac dyssynchronization, wide QRS (>130 ms), and other inclusion
criteria to determine if cardiac resynchronization devices are appropriate
Angiotensin-converting enzyme inhibitors
-Blockers
Digitalis
Diuretics
Spironolactone (if condition is unstable with preceding drugs and patient is in New
York Heart Association functional class IV)
*Stage C is referenced in American College of Cardiology/American Heart Association practice guidelines
10
and is part of a 4-stage classification of heart failure by evolution and progression of the disease. In stage
C, patients have structural heart disease of the myocardium, pericardium, or cardiac valves with prior or
current symptoms (shortness of breath, fatigue, exercise intolerance) of heart failure.
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No standardized evidence-based
guidelines are available to direct acute
care; however, randomized, placebo-
controlled research studies provide
strong support for actions that are
effective and safe. In addition, many
actions promoted in the current
guidelines for long-term outpatient
management of heart failure can be
translated to the acute setting and
are not in cardiogenic shock or do
not have profound hypoperfusion or
complex decompensation. Imple-
mentation of the following strategies
might require a change in the philos-
ophy of care, further education, and
continuous quality monitoring to
ensure that evidence-based strategies
are used regardless of the type of
physician, a patients placement
(telemetry or nonmonitored bed), a
nurses background (cardiac, heart
failure, or generalist), or a hospitals
resources.
Assessment of Patients
Before planning interventions for
a patient hospitalized with heart fail-
ure, the healthcare team must conduct
a systematic assessment that includes
identification of the cause of the heart
failure, aggravating factors, potential
risk factors that may influence survival
and quality of life, and current clinical
status. Patients comorbid conditions,
especially active chronic conditions,
may act as exacerbating factors
(Table 6), affecting the planning of
patients care and influencing the
timing and intensity of therapies. The
treatment plan must include modifi-
cation of correctable causes of
decompensation. Examples include
education for sodium indiscretion,
alcohol abstinence programs for over-
consumption of alcohol, or revascu-
larization strategies for hibernating
myocardium (ie, viable but under-
perfused myocardial tissue with
decreased contractility). In addition,
risks related to heart failure must be
considered, such as the need for
anticoagulation to prevent embolic
events or the need for an implantable
cardioverter-defibrillator to prevent
sudden cardiac death, so that appro-
priate consultations and therapies are
provide a uniform plan of care based
on large, multicenter, randomized
research studies that focus on the pri-
mary management goal of prevent-
ing progression of heart failure.
10
Nurses can facilitate some practi-
cal assessment and management
strategies that apply to patients
admitted to the hospital with a pri-
mary diagnosis of heart failure who
18 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Table 5 Ventricular remodeling: definition and consequences
Definition
Consequences
A cascade of changes in genome expression, cells, molecules, and interstitium that
alters the size, shape, and function of the left ventricle after injury.
Alterations in heart size and shape (volume) that are not associated with preload-
mediated increase in myocyte length.
Hallmarks leading to change in shape of left ventricle from a V to a U. Combination of
Dilatation (myocyte lengthening and cell slippage)
Cell loss/death (apoptosis)
Interstitial fibrosis
Heart failure after myocardial infarction: formation of a discrete collagen scar
Nonischemic heart failure: isolated fibrosis
Hypertrophy (see Figure 1b and c)
Initially concentric (thickening of myocytes)
Then becomes eccentric (thinning of the left ventricular walls)
High pressure (wall stress) in the ventricle during systole and diastole heightens
myocardial oxygen consumption, a situation that promotes further hypertrophy and
activates neurohormonal systems
Reduction in ejection fraction
Reduced ventricular performance
Morbidity and mortality
Figure 1 Ventricular remodeling. Cross-sectional view of left and right ventricles:
a, normal; b, concentric hypertrophy; and c, eccentric hypertrophy.
Abbreviations: LV, left ventricle; RV, right ventricle.
Produced and printed with permission from The Cleveland Clinic Foundation; Cleveland, Ohio.
a
RV RV
RV
LV
LV LV
b c
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discussed and initiated before patients
are discharged from the hospital.
Hemodynamic Status:
Volume and Perfusion
Volume and perfusion status
provide useful clues to a patients
cardiac performance and help shape
the treatment plan. Nurse caregivers
must frequently reassess the patients
hemodynamic status to determine
volume and perfusion status. Volume
status is determined by assessing if
the patient is wet, dry, or has a bal-
anced fluid level (ie, has hypervolemia,
hypovolemia, or euvolemia, respec-
tively), and perfusion is assessed by
determining if the patient is cold,
cool/lukewarm, or warm (ie, has
perfusion that is very low, slightly
low, or normal, respectively). Evi-
dence of congestion includes the
signs of neck vein distension, ele-
vated pressure in the right internal
jugular vein, positive abdominal-
jugular neck vein reflex, edema,
ascites, and crackles (rarely) and the
symptoms of dyspnea, orthopnea,
and paroxysmal nocturnal dyspnea.
15
Nurses must be careful not to count
on the presence of crackles as an indi-
cator of congestion because chronic
movement of fluid into the intersti-
tium (common in patients with a
history of chronic heart failure) is
associated with increased lymphatic
drainage so that crackles are absent
and the alveoli remain relatively dry.
16
Evidence of very low perfusion
includes symptomatic hypotension,
especially in patients receiving
angiotensin-converting enzyme (ACE)
inhibitors, cool extremities (arms and
legs, not just hands and feet), mental
obtundation or constant sleepiness,
worsening renal function (elevation
in serum levels of creatinine and
urea nitrogen), hyponatremia, nar-
row pulse pressure, and, most impor-
tant, a proportional pulse pressure of
25% or less.
15,16
Acute care nurses
should be educated in calculating pro-
portional pulse pressure. The calcula-
tion is simple to do and can provide
valuable information about cardiac
contractility and perfusion, especially
when trends over time are assessed.
The formula to determine pro-
portional pulse pressure is (systolic
blood pressure - diastolic blood
pressure)/systolic blood pressure,
resulting in a proportion or percent-
age.
16
An example of a calculation of
proportional pulse pressure is (108 -
66)/108 = 42/108 = 0.389 or 39%.
In a hemodynamic study
16
of 50
patients with a history of heart fail-
ure, 91% of patients with a propor-
tional pulse pressure of 25% or lower
had a cardiac index (calculated as
cardiac output in liters per minute
divided by body surface area in
square meters) of less than 2.2; how-
ever, systolic and mean arterial blood
pressure were poorly correlated with
cardiac index or stroke volume index.
In a study
17
of hemodynamic profiles
(wet, dry, cold, and warm) and clini-
cal characteristics of advanced heart
failure, a low proportional pulse pres-
sure was the only predictor of wet
patients, and among wet patients,
proportional pulse pressure was the
only predictor of patients in the cold
category. A patients hemodynamic
profile should influence initiation of
pharmacological and other treat-
ment strategies and also guide the
adjustment of therapies during the
hospitalization.
Of note, patients who are admit-
ted in a congestive or wet state with
a high preload (passive stretch of
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 19
Table 6 Exacerbating factors in chronic heart failure that lead to decompensation
Uncontrolled hypertension
Atrial fibrillation or flutter with fast ventricular response
Frequent premature ventricular contractions or ventricular tachycardia
Acute myocardial ischemia
Worsening bundle branch block or intraventricular conduction delay due to desynchro-
nized ventricular electrical cell conduction and myocyte contraction
Treatment of diabetes with thiazolidinediones (Actos or Avandia)
Treatment of arthritis, muscular, or pain conditions with routinely administered
nonsteroidal anti-inflammatory drugs or high doses of aspirin
Concurrent infections (pneumonia, viral illnesses)
Obesity
Hyperthyroidism or hypothyroidism
Untreated anemia (hemoglobin <110 g/L; hematocrit <0.35)
Electrolyte imbalances (hypomagnesemia, hypokalemia) from heart failure drug
therapies that promote new arrhythmias
Salt/fluid indiscretion; nonadherence to medication regimen
Calculating proportional pulse pressure
is simple to do and can provide valuable
information about cardiac contractility
and perfusion.
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20 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Figure 2 Acute decompensated systolic heart failure (SHF) or diastolic heart failure (DHF) in patients with chronic heart failure: initial treatment of
Abbreviations: BNP, B-type natriuretic peptide; EKG, electrocardiographic; INR, international normalized ratio; IV, intravenous; PT, prothrombin time.
*Treatment decisions based on serum BNP results in acute decompensated heart failure DO NOT apply to patients with chronic, stable heart failure who are not acutely dyspneic.

Profiles: patient is wet, dry, or has a balanced fluid level (ie, has hypervolemia, hypovolemia, or euvolemia, respectively), and is cold, cool/ lukewarm, or warm (ie, has perfusion that is
very low, slightly low, or normal, respectively).
Dyspnea and chest pain: if cardiac markers
are positive and/or EKG findings are abnormal:
Follow Acute Coronary Syndrome protocol.
Admit to hospital or
23-hour observation/short-
stay unit on the basis of results
of workup and signs and
symptoms
Admit
to hospital for IV
and oral pharmacological
and nondrug therapies and
monitoring; consider cardiac
resynchronization, implantable
defibrillator, and/or surgical
therapies; treat comorbid
factors that affect
heart failure
BNP >600 pg/mL*
Meets Wet and Cold

profile
and systolic blood pressure
is <90 mm Hg plus other
signs of profound hypoper-
fusion:
Consider this a complex
decompensation
Assess and monitor vital signs, initial signs and symptoms,
urine output, and response to vasodilator therapies:
Monitor perfusion status and diuresis; assess for
signs or symptoms of worsening low perfusion
Assess volume status to ensure signs and symp-
toms of congestion/dyspnea are not developing
or worsening
Assess and monitor vital signs, initial signs
and symptoms, urine output, and
response to diuretic therapy in 2 hours
Is systolic blood
pressure 90 mm
Hg? Are signs and
symptoms of
hypoperfusion
resolving?
Is blood pres-
sure stable?
Weaned off IV
vasodilators?
No
No
Yes
Yes
Is diuresis
adequate (as
defined above)
and dyspnea
resolving?
Continue IV vasodilator therapy
Consider treatment in a 23-hour observation or
short-stay unit
Continue core nonvasodilator heart failure therapies
(aldosterone agonist, -blocker, and digitalis)
Reintroduce core oral vasodilator therapy
(angiotensin-converting enzyme inhibitor,
angiotensin-receptor blocker, or
hydralazine/nitrates) to wean off IV vasodilators
Give second dose of IV loop diuretic at 2
times the first dose (up to a maximum
of the equivalent of 360 mg
furosemide)
Consider treatment in a 23-hour
observation or short-stay unit
Continue core heart failure therapies
(angiotensin-converting enzyme
inhibitor, angiotensin-receptor blocker,
or hydralazine/nitrates; -blocker,
digitalis, and aldosterone agonist)
Meets Dry and Cool to Cold

profile
but does NOT have signs of profound
hypoperfusion; systolic blood
pressure is 90 mm Hg:
IV vasodilators and oxygen
Nesiritide, nitroglycerin, or nitroprusside
(drug choice based on other initial
signs and symptoms)
IV fluids if hypovolemic
Meets Wet and Cool to Cold

profile and systolic blood

pressure is 90 mm Hg:
IV loop diuretic plus vasodilator
and oxygen
First dose of IV loop diuretic should
equal total oral daily dose (up to
a maximum of the equivalent of
180 mg furosemide)
IV vasodilators: nesiritide,
nitroglycerin, or nitroprusside
(drug choice based on initial
signs and symptoms)
Meets Wet and Warm

profile: IV loop
diuretic and oxygen
First dose of IV loop
diuretic should equal
total oral daily dose
(up to a maximum of
the equivalent of 180 mg
furosemide)
BNP >100 pg/mL but 600 pg/mL*
Dyspnea
Workup: history/physical examination; oxygen
saturation; laboratory tests: BNP, PT/INR, liver
function, basic metabolic profile, hematology, arterial blood
gases, troponin or other markers of cardiac injury; electrocardio-
gram, chest radiograph, and other tests on basis of history
Admit to coronary or intensive
care unit
Consider invasive or noninvasive
hemodynamically guided care
IV inotropic therapy may be
warranted
No
Consider
discharge home with
instructions to follow
up with primary
healthcare provider
in 1-3 days
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myocardial fibers; reflects left ven-
tricular end-diastolic pressure and
volume) often have a high afterload
(pressure the heart must pump
against; reflects systemic vascular
resistance, systolic stress, and systolic
impedance) that impairs stroke vol-
ume and is reflected as a cool or
lukewarmperfusion state. When
hemodynamic measurements were
recorded in 750 patients with heart
failure before tailored therapy at a
large university teaching hospital,
the mean pulmonary artery occlusive
pressure was 26 mm Hg (normal is
4-12 mm Hg; in heart failure treat-
ment, the goal is 8-15 mm Hg) and
the mean systemic vascular resistance
was 1640 dynes sec cm
-5
(normal
is 800-1200 dynes sec cm
-5
),
15
reflecting a vasoconstricted state and
the need for vasodilator therapy in
addition to diuresis and natriuresis
(sodium excretion).
Diagnostic Tests
In addition to results of tests done
at the time of admission (chest radi-
ographs, arterial blood gas levels,
liver function tests, hematologic tests,
electrocardiograms, basic metabolic
profile) and findings on physical
examination, the results of point-of-
care assays of serum levels of natri-
uretic peptides can be used to guide
treatment in patients with acute
decompensated heart failure (Figure
2). B-type natriuretic peptide (BNP) is
secreted mainly from the ventricular
myocardium in response to elevations
in end-diastolic pressure and ventric-
ular volume expansion.
18
Not only
can rapid measurement of BNP aid
in diagnosis of heart failure,
19-23
but
BNP level can also be used to assess
clinical status and the effectiveness
of therapies during an admission for
acute decompensation.
24
Point-of-care BNP testing can be
a useful adjunct in determining
which patients are receiving effective
care, which patients are not progress-
ing on the current treatment plan,
and which patients might be candi-
dates for end-of-life care. Nurses
should consider all components of
assessment of patients (etiology,
aggravating factors, risks, and clini-
cal status) when communicating and
collaborating with members of the
healthcare team so that patients
have the best opportunity for care
strategies that optimize outcomes
and promote comfort.
Myths and Realities
of Management
An algorithm provides a system-
atic approach to decision making as
patients with chronic heart failure
are assessed and managed during an
acute exacerbation (Figure 2). The
myths associated with management
of acute heart failure are replaced with
evidence-based actions that con-
tribute to the best possible outcomes.
Myth 1: The Goals of Treatment
for Acute and Chronic Heart
Failure Are Different
One of the hurdles in management
of heart failure is to overcome the
myth that the goals of managing acute
decompensated and stable heart fail-
ure are different. Today, it is impor-
tant to gear therapies toward reversal
of ventricular remodeling. Reversing
ventricular remodeling is important
regardless of whether patients are in
stable condition or in a decompen-
sated state. Historically, the primary
goal of treatment of acute decom-
pensated heart failure was to quickly
reduce the circulating fluid volume
to relieve patients of the pulmonary
and peripheral edema. Diuretics
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 21
Consider
discharge home
with instructions to
follow up with primary
healthcare provider
in 1-3 days
Heart failure an unlikely
cause; consider other causes:
pulmonary embolism, pneumothorax,
pulmonary diseases, pneumonia,
arrhythmias, liver or kidney
diseases
BNP <100 pg/mL
Is diuresis adequate?
Urine output >500 mL (DHF)
or 1000 mL (SHF) with normal
renal function or >250 mL (DHF)
or 500 mL (SHF) with renal
insufficiency)?
Is dyspnea resolving?
No
Yes
Yes
Consider comorbid conditions
causing dyspnea
If meets Wet and Cold, Dry
and Cool to Cold, Wet and Cool
to Cold, or Wet and Warm

profile: treat as appropriate

dyspnea in the emergency department.
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have long been the standard type of
drug used for decreasing volume
and improving hemodynamic status
and signs and symptoms.
25
Through
research studies, however, it was
learned that acute intravenous
diuretic therapy was associated with
many hazards, including increased
mortality. Nonpotassium-sparing
diuretic therapy was associated with
an increased risk of arrhythmic
(sudden) death, increased cardiac
mortality, aggravated renal dysfunc-
tion, further activation of the renin-
angiotensin and sympathetic nervous
systems with a concomitant increase
in systemic vascular resistance that
was compounded by a decrease in
cardiac output from a reduction in
preload, and electrolyte imbalances
that caused muscle weakness,
depression, reduced contractility
(from reduced conductivity), and
peripheral vasoconstriction.
26-31
In
patients with acute decompensation,
preventing or limiting further activa-
tion of neuroendocrine systems by
using strategies that target excess
intravascular and extravascular vol-
ume and vascular resistance will
help meet the overall goals of pre-
venting progression of and promoting
reversal of ventricular remodeling.
Myth 2: Managing Fluid
Overload Equals Use of Diuretics
Administration of intravenous
and oral loop diuretic agents is an
important therapy aimed at decreas-
in patients with mild to severe heart
failure, as summarized in the consen-
sus guidelines.
10
Researchers reported
improvements in exercise tolerance,
ejection fraction, and survival along
with decreased rehospitalization
rates.
10
Therefore, diuretics are nec-
essary to relieve signs and symptoms
but should be used with ACE inhibitor
therapy for survival benefit and to
counterbalance the alterations in
renal and adrenal mechanisms
responsible for sodium and water
retention. Nurses must proactively
recommend increases in dosage of
ACE inhibitors based on the ACC/
AHA practice guidelines
10
during the
acute hospitalization period so that
patients dosing regimens are on tar-
get before the patients are discharged
from the hospital.
Diuretics and Intravenous Vasodilator
Therapy When patients are admit-
ted with a wet and lukewarm/cool
or cold profile without indications of
profound hypoperfusion, a combi-
nation of intravenous diuretics and
vasodilator therapy leads to improved
acute outcomes, without the need for
inotropic agents (Figure 2). Many
studies were conducted in the late
1970s and early 1980s in patients
with New York Heart Association
functional class IV decompensated
heart failure to study the effectiveness
of intravenous diuretic and vasodila-
tor (nitroprusside and nitroglycerin)
therapy in reducing filling pressures
(preload) and systemic vascular
resistance (afterload) and improving
cardiac output. The results indicated
that nitroprusside was a clinically
effective and powerful agent for
reducing afterload that also decreased
ventricular systolic and diastolic vol-
umes and improved ventricular dias-
ing preload (through initial venodi-
latation and then through diuresis
and natriuresis) and ultimately reliev-
ing signs and symptoms, but these
agents should not be used alone to
improve overall morbidity and sur-
vival in patients with heart failure. In
order to address increased afterload
associated with both exacerbation of
heart failure and intravenous loop
diuretic therapy, pharmacological
therapies must include agents that
reduce neuroendocrine activation
and vasoconstriction because these
mechanisms can worsen the heart
failure syndrome by worsening ven-
tricular remodeling.
Diuretics and ACE Inhibitor Therapy
Although only limited data are avail-
able, when an ACE inhibitor was
combined with loop diuretics, the
combination therapy reduced the
pressor (vasoconstriction) response
of diuretics.
32
ACE inhibitors reduced
the increase in plasma angiotensin II,
thus decreasing the sympathetic acti-
vation (and associated deterioration
in left ventricular pump function)
that preceded the diuretic action of
diuretics.
32
ACE inhibitors ultimately
decreased reabsorption of sodium
in the distal tubule and decreased
aldosterone stimulation in the adre-
nal glands.
33,34
Many randomized,
controlled research studies were
conducted from the early 1980s
through the mid-1990s that added
an ACE inhibitor to diuretic therapy
22 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
One of the hurdles in management of heart
failure is to overcome the myth that the
goals of managing acute decompensated
and stable heart failure are different.
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tolic properties. It provided rapid
symptomatic relief for patients and
improved, stabilized, and optimized
hemodynamic parameters.
35-39
Intravenous nitroglycerin is
known predominantly as an agent for
reducing preload. However, at high
doses, intravenous nitroglycerin
reduces systemic and pulmonary
vascular resistance. In patients with
decompensated chronic heart failure,
nitroglycerin was less powerful than
nitroprusside in reducing afterload
but was effective in reducing preload,
increasing cardiac output, and con-
trolling signs and symptoms and
hemodynamic derangements.
40-42
Table 7 is a summary of the dose
ranges, actions, and indications of
vasoactive medications used in the
management of patients with acute
decompensated heart failure.
43
As the overall goal of managing
patients with heart failure has
shifted from improving hemody-
namic status to improving neuroen-
docrine abnormalities in the hope
that ventricular remodeling will be
favorably affected, researchers have
studied the effectiveness of intra-
venous vasodilator therapy in modu-
lating the neuroendocrine axis. In a
recent study
44
of 34 patients with
decompensated heart failure who
received intravenous diuretics and
vasodilator therapies (nitroprusside
and ACE inhibitors) to reduce pre-
load and afterload, neurohormonal
activation (endothelin, norepine
phrine, and BNP levels) decreased
rapidly and was associated with
improved hemodynamic status.
Similar to results of studies con-
ducted in previous decades, in this
study,
44
the mean cardiac index
increased from 1.70 before treat-
ment to 2.58 after treatment. Pul-
monary artery occlusive pressure
decreased from a mean of 31 to 18
mm Hg, and systemic vascular
resistance decreased from a mean of
1780 to 1109 dynes sec cm
-5
from
before to after treatment. This
research provided further evidence
that hemodynamic parameters in
patients at rest were significantly
modulated by improving preload
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 23
Table 7 Intravenous vasoactive medications indicated in acute decompensated heart failure
43
Characteristic
Typical dose range
Action
Venodilator
Arterial vasodilator
Diuretic
Inotropic
Indication
Primary effect
Preload
Afterload
Diuresis
Natriuresis
Cardiac output
Stroke volume
Comments
Nitroglycerin
10-200
g/min
X
X (coronary)
Myocardial
ischemia,
elevated
PAOP,
hypertension

mild
Rapid onset
Nitroprusside
0.1-5 g/kg per
minute
X
X
Hypertensive crisis,
elevated PAOP,
acute aortic or
mitral
regurgitation

, indirectly
Risk coronary steal
from hypotension,
assess for
thiocyanate
poisoning
Nesiritide
Bolus 2 g/kg then
0.01 g/kg per
minute
X
X
X
Congestion and
vasoconstriction
from acute
decompensated
heart failure

, indirectly
More rapid onset
than nitroglycerin,
minimal dosage
adjustment, no
tachycardia
Milrinone
Bolus 50 g/kg* then
0.375-0.75 g/kg per
minute
X
X
Very low cardiac output,
high PAOP, pulmonary
hypertension

Long half-life, risk

hypotension,
proarrhythmia
Dobutamine
2.5-15 g/kg per minute
X
Very low cardiac output
with or without
congestion or
hypotension

Assess for tachyphylaxis,

tachycardia, ischemia,
proarrhythmia
Abbreviations and symbols: PAOP, pulmonary artery occlusive pressure; X denotes that the drug has the specified action; denotes decrease; denotes increase. No
entry indicates action or effect does not occur.
*Consider eliminating the bolus dose when systolic blood pressure is 100 mm Hg or less; just begin infusion and wait 2 hours to assess patient for desired effects (delay
to peak effect if bolus omitted).
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and afterload, rather than by using
agents that increased contractility
and cardiac workload. In addition,
decreased activation of neuroen-
docrine hormones might improve
short- and long-term outcomes.
A newer vasodilator, nesiritide, is
indicated for reducing dyspnea and
improving hemodynamic status in
patients with acute decompensated
heart failure. Nesiritide, a recombi-
nant form of human BNP, has
actions identical to those of the
endogenous BNP molecule.
45
Nesiri-
tide produced balanced arterial and
venous vasodilatation that resulted
in rapid reduction in ventricular fill-
ing pressures. This reduction was
manifested clinically as a dose-
dependent decrease in pulmonary
artery occlusive pressure, pul-
monary artery pressures, and sys-
temic blood pressure.
46
Nesiritide
caused diuresis and natriuresis by
suppressing the renin-angiotensin-
aldosterone system.
47
When intravenous nesiritide
was compared with intravenous
nitroglycerin during the first 72 hours
of signs and symptoms in patients
hospitalized with acute heart failure,
47
the results favored nesiritide. Nesiri-
tide produced a significantly quicker
and greater reduction in pulmonary
artery occlusive pressure than did
nitroglycerin. Patients reported and
caregivers measured a greater reduc-
tion in dyspnea when the patients
received nesiritide rather than nitro-
glycerin. The combined actions of
vasodilatation, diuresis, and natri-
uresis led to preload and afterload
reduction to achieve the goal of
enhanced cardiac output and reduced
pulmonary and systemic congestion.
The investigators
47
concluded that
nesiritide should be the drug of choice
guidelines)
10
may actually improve
signs and symptoms and quality of
life by antagonizing mechanisms
that cause excessive sodium and
water retention.
Myth 3: Low Systolic Blood
Pressure Requires Treatment
With Intravenous Inotropic Agents
Some myths are associated with
interventions when patients with
heart failure have low systolic blood
pressure. One belief is that a systolic
blood pressure of less than 90 mm
Hg requires intravenous infusion of
inotropic agents. Unless the hypoten-
sion is severe (systolic blood pressure
<80 mm Hg), it is important to
assess for indications of hypoperfu-
sion and not to rely just on systolic
blood pressure readings when deter-
mining whether intravenous
inotropic agents are needed. Is the
patient mentally obtunded or olig-
uric? Does the patient have cold arms
or legs or long-lasting orthostasis (ie,
dizziness and lightheadedness that
lasts longer than 15 minutes after a
change in body position from lying to
sitting or standing)? Is the propor-
tional pulse pressure less than 25%?
In combination, these signs are more
reflective of profound hypoperfusion
and low cardiac output than is sys-
tolic blood pressure.
16
Patients who
do not have these signs generally tol-
erate ACE inhibitor, -blocker, and
diuretic therapies, especially when the
dosing scheme is staggered so that
therapies do not reach peak effective-
ness at the same time.
It is important to consider that a
lower systolic blood pressure reflects
lower myocardial wall tension (stress)
and afterload. Afterload reduction
decreases activation of the neuroen-
docrine axis to promote regression
in patients admitted with a wet and
cool to cold hemodynamic profile
because it was less potent and less
toxic than intravenous nitroprusside
and more easily administered than
intravenous nitroglycerin. During
the first 24 hours of infusion, neither
symptomatic nor asymptomatic
hypotension differed significantly
between patients receiving intra-
venous nitroglycerin, patients
receiving nesiritide, and control
subjects.
47
During the research trial,
hypotension, which was dose-
dependent, was easily assessed with
regular monitoring of blood pres-
sure (ie, noninvasively every 15 min-
utes for an hour, then every 4
hours). Thus, infusion of nesiritide
does not require placement of an
arterial catheter for blood pressure
monitoring and admission to a criti-
cal care unit (as nitroprusside infu-
sion does) or telemetry monitoring.
Diuretics and -Blocker Therapy
-Blocker therapy also affects mech-
anisms in the kidneys and the renin-
angiotensin system. -Blockers are
the only oral medications in the core
pharmacological therapy for heart
failure that decrease renin release,
thereby indirectly decreasing proximal
reabsorption of sodium (by decreas-
ing angiotensin II levels).
34
When a
nonselective -blocker/-blocker
such as carvedilol is used, renal blood
flow may improve from a reduction
in renal vascular resistance.
34
Nurses
should not assume that an acute
exacerbation of heart failure requires
termination of treatment with or
decrease in dosage of -blockers. In
actuality, maintenance of -blockers
(and eventual increase to target
dosage once hypervolemia is con-
trolled, based on AHA/ACC practice
24 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
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of cardiac remodeling and improve
clinical outcomes. Nurses must edu-
cate patients about the benefits of
maintaining a low systolic blood
pressure and adhering to core phar-
macological therapies that decrease
neuroendocrine activation and
decrease blood pressure.
Additionally, use of intravenous
inotropic agents is not supported in
patients in an acute setting except
as temporary treatment of diuretic-
refractory complex decompensation.
48
Intravenous inotropic therapies
(continuous or intermittent infusion
of milrinone or dobutamine) have
been associated with increased mor-
tality when used in patients requiring
inotropic support, even though these
agents improve hemodynamic sta-
tus
10
(Table 7). In an effort to learn if
a short-term infusion (48 hours)
might lead to short- or intermediate-
term improvements in patients hos-
pitalized for exacerbation of heart
failure who had a wet and cool to
cold profile but in whom intravenous
inotropic support was not essential,
the study called Outcomes of a
Prospective Trial of Intravenous Mil-
rinone for Exacerbations of Chronic
Heart Failure (OPTIME-HF) was
conducted.
49
Investigators random-
ized patients to receive short-term
intravenous milrinone or placebo.
The 2 groups did not differ signifi-
cantly in hospital and 60-day posthos-
pitalization mortality or in the median
number of days patients were hospi-
talized for cardiovascular causes in
the first 60 days after discharge. In
addition, sustained hypotension or
new atrial arrhythmias were signifi-
cantly more likely to develop in the
patients receiving milrinone than in
the patients receiving placebo. The
results of this research, that receiving
an inotropic agent without clear evi-
dence of significant hemodynamic
compromise does not enhance clini-
cal or economic outcomes, led to a
tempering of the use of intravenous
inotropic agents unless absolutely
warranted.
Further, concomitant use of -
blocker (-antagonist) and intra-
venous dobutamine (-agonist)
therapies is controversial. The phar-
macological response of dobutamine
is inhibited in patients receiving high
doses of -blockers because both
drugs compete for the same -adren-
ergic receptors.
48
This conflict is
especially apparent with carvedilol
because it blocks both
1
and
2
receptors.
48,50
Myth 4: ACE Inhibitors and
-Blocker Therapies Should Be
Temporarily Decreased or Dis-
continued During Decompensation
Another belief is that ACE inhibit-
ors and -blocker therapies must be
decreased or discontinued or should
not be initiated when the patients
blood pressure is low. These agents
help suppress maladaptive neu-
roendocrine responses that lead to
increased wall stress, ventricular
hypertrophy, and worsening cardiac
remodeling and cardiac output.
51
Unless symptomatic low blood pres-
sure occurs or intravenous vasodila-
tor agents are used, core oral
therapies used to manage patients
with chronic heart failure should be
maintained whenever possible.
Blood pressure may not decrease or
the reduction may be self-limiting
when vasodilator (ACE inhibitor or
angiotensin-receptor blocker) and
-blocker therapies are initiated and
maintained in patients with a low
baseline blood pressure (85-90 mm
Hg). If blood pressure decreases but
indications of hypoperfusion are
absent, nurses should assess patients
for hypovolemia (from overdiuresis).
In addition, nurses must communi-
cate expected effects of core agents
for treating heart failure to patients
so that patients are prepared for
potential dizziness or other symp-
toms associated with drug actions
and interactions and understand the
self-limiting nature of these changes.
52
Myth 5: Once Core Therapies
Are Unsuccessful, They Should
Not Be Tried Again
Some may believe that once ACE
inhibitor or -blocker therapy is
unsuccessful in a patient because of
low blood pressure, these therapies
should not be tried again. Assessment
and correction of mechanisms that
cause low blood pressure (such as
initiating ACE inhibition when the
serum level of sodium is less than
130 mmol/L) may make the preceding
statement a false claim. Core pharma-
cological therapies known to improve
health-related outcomes can be suc-
cessfully implemented without
episodes of low blood pressure in most
patients, as evidenced by low dropout
rates in randomized controlled stud-
ies. The acute care episode is a perfect
setting for trying ACE inhibitors or
-blockers again, when appropriate,
because patients can be carefully
monitored and resources are readily
available. Low-dose, shorter-acting
agents in each drug class (such as
captopril and carvedilol) are the drugs
of choice in patients with a history of
low blood pressure.
Nursing Considerations
In addition to assessment of
patients, nursing actions that are cen-
26 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
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tral to patients outcomes are admin-
istration of medications, evaluation
of treatment effectiveness, and edu-
cation and ongoing communication
with patients, patients families, and
the healthcare team. If a patients
dyspnea improves but weight loss,
urination, intake and output, or
proportional pulse pressure do not
improve, nurses must be assertive in
providing timely communication of
these findings to peers and the physi-
cian team because delays can diminish
high-quality care, hinder achievement
of clinical goals, and harm the hospi-
tal financially. Table 8 outlines nurs-
ing actions and goals that reflect
critical thinking and foster commu-
nication when managing patients
with heart failure.
Nurses often take an active role
in prompting initiation and adjust-
ment of medication therapies. Nurses
must know the actions, dosing, and
effects of heart failure medications
and must promote decisions that will
affect the overall goal of management
of heart failure (reversal of cardiac
remodeling). This goal can be
achieved during the acute hospital-
ization by adding, maintaining, and
increasing dosages of vasodilators
(ACE inhibitors) and maintaining
-blocker therapy per consensus
recommendations. Nurses must not
focus on pharmacological therapies
that simply improve symptoms (eg,
diuretics), because these therapies
also increase cardiac workload, acti-
vate adverse neuroendocrine systems,
and increase mortality. When in
doubt about therapeutic priorities,
it is always helpful to reassess the
patients clinical status. When patients
have congestion and inadequate organ
or peripheral perfusion (cool/luke-
warm to touch), intravenous diuretic
blood pressure unless the patient has
orthostatic hypotension or other
signs and symptoms reflecting
hypoperfusion or hypovolemia.
Nurses must use multiple clinical
parameters, not just blood pressure
values, to determine that withhold-
ing drugs will benefit a patients clin-
ical status.
Critical evaluation of each
patients progress involves ongoing
assessment of electrolyte and fluid
and vasodilator therapy (along with
maintenance of prehospital -blocker
therapy) may decrease afterload and
preload to improve perfusion and
cardiac index. When profound
hypoperfusion compromises organ
function, an intravenous inotropic
agent may be the preferred agent of
choice (Figure 2). It is especially
important for nurses not to withhold
doses of vasodilators, -blockers, or
diuretics because of a patients low
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 27
Table 8 Nursing considerations: critical thinking and communication
Nursing role
Critically evaluate
effectiveness of
interventions
Communicate to
patient, patients
family and team
members
Actions/goals
Monitor vital signs; maintain systolic blood pressure >80 mm Hg
and <110 mm Hg unless having signs of orthostatic hypoten-
sion at higher pressures
Resting heart rate <80/min
Respirations <16/min
Maintain hemodynamic values in normal ranges:
Right atrial pressure 3-8 mm Hg
Pulmonary artery occlusive pressure <16 mm Hg
(if moderate or severe pulmonary hypertension, 16-19 mm Hg)
Systemic vascular resistance 800-1200 dynes sec cm
-5
Cardiac output >4.0 L/min
Cardiac index* >2.2
Monitor urine output: After initial diuresis from intravenous
diuretics, maintain equivalent of 0.5 mL/kg per hour if normal
renal function; decrease by 50% in renal dysfunction
Maintain serum electrolytes in normal ranges:
Potassium 4.0-5.0 mmol/L
Magnesium >0.74 mmol/L (>1.8 mg/dL)
Sodium >138 and <145 mmol/L
B-type natriuretic peptide <600 pg/mL
Assess for dyspnea and fatigue at rest and with exertion/activity;
notify healthcare team if lack of continual improvement
Assess for subclinical and clinical congestion
Assess for signs or symptoms of hypoperfusion
Assist patient with progressive ambulation
Encourage progression in self-care activities of daily living
Use daily weight values and intake and output changes to facilitate
discussion of principles of fluid management
Use daily menu to facilitate discussion of low-sodium diet choices
Provide information to enhance perceived control of changes in
clinical status
Medication rationale, actions, expected and adverse effects, and
when to notify the healthcare provider of issues
Listen to concerns, facilitate communication with team members,
and answer questions to maximize patients satisfaction
Identify psychosocial concerns that may affect patients status
after discharge: depression, social isolation, emotional distress
or anxiety, inability to care for self physically due to environmen-
tal, social, cultural, religious issues or heart failure or other ill-
ness; refer to social services as appropriate.
*Cardiac index is calculated as cardiac output in liters per minute divided by body surface area in square
meters.
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status. Such assessment is especially
important in managing patients
with heart failure because activation
of neuroendocrine systems, renal
dysfunction, and current drug thera-
pies may disrupt the fine balance of
electrolytes and cause shifts in
sodium, potassium, calcium, and
magnesium.
53
It is important for
nurses to develop and use advanced
measurement and cardiac ausculta-
tion skills to monitor fluid status
(eg, assessment of jugular venous
pressure and the presence or wors-
ening of systolic murmurs and S
3
or
S
4
heart sounds) because patients
may still have intravascular volume
overload after obvious interstitial
fluid retention (crackles, edema) dissi-
pates. Freedom from congestion in
the early weeks after hospital dis-
charge was an independent predictor
of survival in patients hospitalized
with New York Heart Association
functional class IV symptoms.
54
In
order to prevent readmission and
maintain clinical stability, patients
who have evidence of clinical and
subclinical congestion before dis-
charge should be considered for
aggressive follow-up (cardiologist
specializing in heart failure) and
interventions aimed at promoting
euvolemia (eg, increased restriction
in sodium diet or fluid intake, diuretic
self-management program, heart
failure nurse clinic).
Serum BNP values provide
another mechanism for monitoring
fluid status in the early hours after
hospitalization and for assessing
patients outcomes. In patients with
symptomatic, functional class III or
IV heart failure who were undergo-
ing tailored therapy for their con-
gested state, hourly changes in BNP
levels were significantly correlated
with hourly changes in pulmonary
artery occlusive pressure.
55
When
BNP levels at initial hospital assess-
ment and within 24 hours of discharge
or death were compared as an out-
come variable,
24
successfully treated
patients (as compared with patients
who died during the index hospital-
ization or were readmitted within 30
days of discharge) had a mean
decrease in BNP level of 216 pg/mL.
Patients who were readmitted or died
had levels that increased during the
course of hospitalization.
Last, communication between
healthcare providers and patients
and patients families about the
patients clinical status and manage-
ment plan is essential. Proactively
assessing the knowledge base of
patients and their families to promote
understanding of the current plan of
care and asking if there are questions
can aid communication and infor-
mation sharing. Information sharing
and ongoing communication with
patients and their families enhances
perceived control, potentially decreas-
ing stress.
56
This communication is
especially important because loss of
functional mobility and role changes
that occur with the progression of
heart failure lead to a perceived loss
of control
57
that can ultimately affect
coping, lifestyle modifications, and
behaviors. Examples of important
factors to address in patients educa-
tion are found in the first item in
Table 3 and in Table 4. It is well rec-
ognized that improving patients
knowledge of heart failure and pro-
viding support, encouragement, and
positive reinforcement of self-care
behaviors improves outcomes in
patients with heart failure.
58
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CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 29
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30 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
CE Test Form
Evidence-Based Practice for
Acute Decompensated Heart Failure
Objectives:
1. Identify the core drug therapies for decompensated heart failure
2. Describe the role of B-type natriuretic peptide in decompensated heart failure
3. Explain the pharmacological management of decompensated heart failure
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CE Test Instructions
1. a 2. a 3. a 4. a 5. a 6. a 7. a 8. a 9. a 10. a 11. a 12. a 13. a 14. a
b b b b b b b b b b b b b b
c c c c c c c c c c c c c c
d d d d d d d d d d d d d d
CE
Continuing Education
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CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 31
7. Which of the following is not a direct effect of
nesiritide?
a. Decreased preload
b. Decreased afterload
c. Increased diuresis
d. Increased contractility
8. What is the typical dosage range of nesiritide in the
treatment of acute decompensated HF?
a. 0.001 ug/kg/min
b. 0.01 ug/kg/min
c. 0.1 ug/kg/min
d. 1 ug/kg/min
9. Which of the following drugs inhibits renin release
and indirectly decreases proximal reabsorption of
sodium?
a. Diuretics
b. -Blockers
c. ACE inhibitors
d. Digitalis
10. Which one of the following medications has been
associated with increased mortality when used in
patients requiring inotropic support?
a. Dobutamine
b. Dopamine
c. Digoxin
d. Levophed
11. Which of the following goals indicates effective HF
management?
a. Resting heart rate <100/min
b. Cardiac index >4 L/min/m
2
c. Pulmonary artery occlusive pressure
<22 mm Hg
d. Systemic vascular resistance 800-1200
dynes/sec/cm
-5
12. In patients with symptomatic New York Heart
Association Class III or IV HF who underwent ther-
apy for their congested state, hourly changes in
BNP levels correlated with hourly changes in which
of the following?
a. Pulmonary artery occlusive pressure
b. Systemic vascular resistance
c. Mean arterial blood pressure
d. Cardiac output
1. The Acute Decompensated Heart Failure National
Registry reported which of the following as a pri-
mary factor in hospitalization?
a. Ejection fraction <0.40
b. Systolic blood pressure <90 mm Hg
c. Sodium and fluid retention
d. B-type natriuretic peptide (BNP) level
>100 pg/mL
2. Patients with moderate to severe systolic dysfunc-
tion and with an ejection fraction <0.40 should be
prescribed which of the following drugs after hos-
pital discharge?
a. Angiotensin-converting enzyme (ACE)
inhibitor
b. Angiotensin receptor blocker
c. Nitrate
d. Calcium channel blocker
3. Which of the following is not a core drug therapy
in the management of heart failure (HF)?
a. Diuretic
b. ACE inhibitor
c. -Blocker
d. Sodium channel blocker
4. What is the overall goal of HF management?
a. Sodium and fluid restriction
b. Reversal of ventricular remodeling
c. BNP level <100 pg/mL
d. Preload reduction
5. BNP, a neurohormone, is secreted from the ven-
tricular myocardium in response to which of the
following?
a. Increased systemic vascular resistance
b. Decreased cardiac output
c. Increased end-diastolic pressure and volume
d. Decreased contractility
6. To counterbalance the alterations in renal and
adrenal mechanisms responsible for sodium and
water retention, diuretics should be used with
which of the following medications?
a Dobutamine
b. -Blockers
c. ACE inhibitors
d. Digoxin
CE Test Questions
Evidence-Based Practice for Acute Decompensated Heart Failure
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