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Crit Care Nurs Q

Vol. 30, No. 2, pp. 94–103
Copyright  c 2007 Wolters Kluwer Health | Lippincott Williams & Wilkins

Management of Acute
Decompensated Heart Failure
Sheeba Varughese, MSN, RN, CNS, CCRN, APRN,BC

Heart failure, a debilitating complex clinical syndrome, affects nearly 5 million people in the United
States and presents a heavy socioeconomic burden. Neurohormonal abnormalities contribute to
the pathophysiology of heart failure. Acute decompensated heart failure (ADHF) has emerged as
a major health problem associated with poor prognosis, increased costs related to care, reduced
quality of life, and frequent readmissions. Symptoms of ADHF are primarily related to congestion
and/or low perfusion states. The use of biomakers such as B-natriuretic peptides is useful in distin-
guishing between cardiac and noncardiac causes of symptoms. Treatment for ADHF begins with
identification and treatment of precipitating factors for acute decompensation. Initial goal of ther-
apy is focused on symptom management followed by interventions that delay disease progression,
reduce readmission, and prolong survival. Key words: biomarkers, B-natriuretic peptides, de-
compensated, heart failure, nursing management

H EART FAILURE (HF) is a progressive,

complex clinical syndrome resulting
from structural and/or functional cardiac dis-
orders that impair systolic and/or diastolic
function. A series of neurohormonal mecha-
nisms are integrated into this syndrome and
impacts the overall outcomes associated with
the disease.1–3 Acute decompensated heart
failure (ADHF) has emerged as a major health
problem associated with poor prognosis, in-
creased costs related to care, and frequent
readmissions.1,4,5
Heart failure is a growing health problem
and affects nearly 5 million people in the
United States.4 Nearly 550,000 new patients
are diagnosed each year.4 The incidence of HF
is highest among those who are aged 65 years
or older.4 Despite modern therapies, the ex-
pected 5-year mortality is approximately 50%6
and the incidence of sudden cardiac death is 6
to 9 times the rate of the general population.4
More Medicare dollars are spent for the
diagnosis and management of HF than for
From the St Luke’s Episcopal Hospital, Houston, Tex.
Corresponding author: Sheeba Varughese, MSN, RN,
CNS, CCRN, APRN,BC, Cardiovascular and Transplant
Nursing, St Luke’s Episcopal Hospital, 6720 Bertner Ave,
Houston, TX 77030 (e-mail: svarughese1@ sleh.com).
any other disease. In 2006, it was estimated
that expenses related to HF would reach
$29.6 billion.4 The majority of these expenses
($15.4 billion) are directly related to hospi-
talized care.4 Each year, HF is a contributor
of approximately 1 million hospitalizations.6
From 1979 to 2003, the number of hospi-
tal discharges related to HF increased by
174%.4
The rise in HF has been attributed to sev-
eral factors, including the increasing propor-
tion of elderly individuals in the population,
improved short-term survival of patients with
myocardial infarction, and heightened aware-
ness of HF resulting in increased diagnosis and
reporting.7 Approximately 80% of patients
hospitalized with HF are older than 65 years.4
The incidence of HF is rising in both men and
women.4
The hospitalized HF population consists
of a mixed group of patients with low and
preserved left ventricular ejection fraction
(LVEF). Recent data from the Acute De-
compensated Heart Failure National Registry
(ADHERE) suggest that 40% of patients hos-
pitalized for ADHF have normal systolic
function,8 72% have history of hypertension,
and 29% have chronic renal insufficiency.5
However, congestion is the dominant feature
in all ADHF hospitalizations.5

94
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Management of Acute Decompensated Heart Failure
Table 1. Exacerbating factors that may lead
to decompensation1,9,10
Uncontrolled hypertension
Renal insufficiency
Atrial arrhythmias with rapid ventricular
response
Ventricular arrhythmias
Acute myocardial ischemia or infarction
Medication triggers (eg, thiazolidinediones,
nonsteroidal anti-inflammatory agents,
calcium channel blockers,
antiarrhythmics)
Infections
Obesity
Hyperthyroidism
Untreated anemia
Alcohol
Noncompliance (medications, diet)
Several factors that may predispose a pa-
tient to experience ADHF with or without
worsening of underlying cardiac structure or
function have been identified.1 Exacerbation
of comorbid factors such as a worsening of
renal function, persistent neurohormonal ac-
tivation, and progressive deterioration in my-
ocardial function all plays a role in ADHF.1
In addition, failure to adhere to prescribed
medication and treatment plan or an inade-
quate medical regimen may also contribute to
decompensation.1 Table 1 outlines some po-
tential exacerbating factors that may lead to
ADHF.
PATHOPHYSIOLOGY
Heart failure is a complex syndrome in
which myocardial injury results in a fall in
left ventricular (LV) performance.11 This can
be due to a systolic or diastolic dysfunc-
tion resulting in a drop in perfusion. The
body recognizes this and attempts to compen-
sate through neurohormonal activation. The
neurohormonal activation involves the renin-
angiotensin-aldosterone system, sympathetic
nervous system, endothelin, vasopressin, cy-
tokines, and natriuretic peptides (Table 2).11
When the compensatory mechanisms are un-
95
able to positively impact perfusion, symptoms
prevail. Over time, these compensatory mech-
anisms lead to remodeling and progressive
worsening of myocardial function and apop-
tosis (programmed cell death).11 The result is
the increased morbidity and mortality that is
associated with HF.
Heart failure can be due to systolic or di-
astolic dysfunction. Systolic dysfunction re-
sults from impaired ventricular contractility,
resulting in reduced ventricular emptying, el-
evated diastolic filling pressures, ventricular
dilatation, and reduction in stroke volume
and cardiac output.3,11 The most common
cause of systolic dysfunction is myocardial
ischemia/infarction, coronary artery disease,
and hypertensive heart disease. Less common
causes include valvular heart disease and di-
lated cardiomyopathy. Systolic dysfunction is
associated with an LVEF of less than 45%.13
Diastolic dysfunction causes impairment in
ventricular relaxation, which results in resis-
tance to filling of the ventricle.15 This impair-
ment can result in elevated diastolic filling
pressures. The contractility of the my-
ocardium may be normal, resulting in a
near-normal LVEF.15 However, the stiffened
left ventricle impedes normal ventricular
filling, which can result in a reduction of
cardiac output.15 The most common causes
of diastolic dysfunction include ventricular
hypertrophy due to chronic hypertension,
myocardial ischemia or infarction, coronary
artery disease, diabetes, and aging.15
CLASSIFICATION OF HF
Functional status is an important assess-
ment that is made for HF patients. The New
York Heart Association (NYHA) functional
classification system is utilized to make this
assessment. It assists in classifying HF patients
into 1 of 4 classes that are related to the degree
of functional limitations imposed by HF symp-
toms (Table 3).1 The most severe NYHA func-
tional class is class IV, where a patient expe-
riences symptoms of HF that limit functional
status even at rest.1 The other classification
system is the American College of Cardiology/
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96 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2007

Table 2. Neurohormonal response12–14,∗

SNS RAAS Natriuretic peptides

↑ HR Vasoconstriction Arterial and venous

↑ Contractility ↑ Vasopressin vasodilation
Vasoconstriction ↑ Aldosterone ↑ Sodium and water excretion
↑ RAAS ↑ SNS activity Myocardial relaxation
↑ Vasopressin Sodium & water retention ↓ Myocardial fibrosis
Direct cardiotoxicity ↑ Wall stress ↓ SNS activity
↑ Myocardial oxygen demand Direct cardiotoxicity ↓ RAAS activity
Myocardial hypertrophy Myocardial hypertrophy ↓ Endothelin
Endothelin-1 Cytokines Vasopressin
Vasoconstriction Vasoconstriction Vasoconstriction
Ventricular hypertrophy ↓ Contractility Free water reabsorption
Ventricular remodeling Ventricular hypertrophy Dilutional hyponatremia
Ventricular remodeling ↓ Contractility
Contribute to cardiac Ventricular hypertrophy
cachexia

*SNS indicates sympathetic nervous system; RAAS, renin-angiotensin-aldosterone system; HR, heart rate.

American Heart Association (ACC/AHA) stag-
ing system for HF.1,2 It encompasses 4 stages
of heart failure (Table 4).2 Stages A and B are
asymptomatic stages. Patients who are at risk
for developing HF are in these 2 stages. Stage
C is symptomatic HF, which is responsive to
treatment. Stage D is end-stage refractory HF.
In 2005, The ACC/AHA Guideline Update for
the Diagnosis and Management of Chronic
Heart Failure in the Adult was published.2
These guidelines provide recommendations
for nonacute care and include both rationale
and level of evidence for the support of each
management strategy identified for each stage
of HF. Recommended therapies focus on mod-
ifying or suppressing the neurohormonal pro-
cesses and preventing or delaying the disease
progression.2

Table 4. ACC/AHA stages of heart failure1 :

The development of heart failure
Table 3. The New York Heart Association
classification of heart failure1 : Degree of func-
tional limitation imposed by heart failure Stages Criteria

A At risk for heart failure but

Class Criteria without structural heart disease
or symptoms of heart failure
I Symptoms elicited only at levels of B Structural heart disease but
exertion that would limit normal without signs or symptoms of
individuals heart failure
II Symptoms elicited on ordinary C Structural heart disease with prior
exertion or current symptoms of heart
III Symptoms elicited on less than failure
ordinary exertion D Refractory heart failure requiring
IV Symptoms elicited at rest specialized interventions
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Management of Acute Decompensated Heart Failure
Figure 1. Two-minute assessment of hemodynamic profile. Hemodynamic profiles for patients with heart
failure. Most patients can be classified in a rapid bedside assessment according to the signs and symp-
toms shown. This classification helps guide the use of initial therapy. Reprinted with permission from
Dr Stevenson.
TREATMENT
Although in HF management the priority
of treatment is related to delaying disease
progression and prolonging survival,2 dur-
ing ADHF hospitalizations, the initial prior-
ities of treatment are related to symptom
management.1,9 This initial treatment strategy
for ADHF involves a 3-step process. The first
step is a search for potential reversible factors
that may be the cause of the exacerbation
(Table 1).9 Second, an evaluation of symp-
toms related to congestion and/or low per-
fusion is completed.9 The symptoms that are
being evaluated are related to functional sta-
tus. The use of the hemodynamic profile
(Fig 1) may be helpful in accomplishing this
step. The last step is the determination of ap-
propriate treatment strategies based on the as-
sessment findings.9
Several triggers or exacerbating factors that
predispose a patient with HF to experience
worsened symptoms and the development of
ADHF have been identified (Table 1).9,10 It is
important to evaluate the ADHF patient for
the presence of any of these reversible fac-
tors and attempt to address them as quickly
as possible.9,10 A common factor is atrial
arrhythmias where the rapid ventricular re-
sponse may contribute to exacerbation. Sys-
temic hypertension is another exacerbating
factor seen with ADHF admissions.1,5 Other
factors include implications from comorbidi-
ties, new ischemic event, heavy alcohol con-
97
sumption, infection, medication interactions,
and lack of compliance with the prescribed
treatment plan.9,10
Evaluation of symptoms is the next step in
the treatment plan. The major symptoms of
ADHF include shortness of breath, conges-
tion, and fatigue.1 Unfortunately, these symp-
toms are not specific to only ADHF. They
can be seen with other conditions such as
chronic pulmonary disorders, or infections.
Therefore, differential diagnosis becomes
essential.
Most patients will display evidence of vol-
ume overload as manifested by signs and
symptoms of congestion or elevated filling
pressures.4,8 These signs and symptoms may
include weight gain, dyspnea, orthopnea,
paroxysmal nocturnal dyspnea, rales, pleural
effusion, pulmonary edema, hypoxemia, third
heart sound, worsening regurgitation of mi-
tral valve, generalized edema, elevated jugular
venous pressure (JVP), hepatic enlargement,
ascites, and hepatojugular reflux.1,5,9
In chronic HF, orthopnea and elevated JVP
are the 2 primary symptoms or findings of ele-
vated filling pressure.16 Rales are absent in the
majority of patients with chronically elevated
filling pressures because the chronic move-
ment of fluid into the pulmonary interstitium
is associated with increased pulmonary lym-
phatic drainage.9
The other signs and symptoms of ADHF are
related to inadequate perfusion. Symptoms
of low perfusion are nonspecific and may
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98 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2007
include complaints of lack of energy and fa-
tigue, mental status changes, or weakness.9
The complaints of daytime sleepiness or dif-
ficulty concentrating may be reflective of dis-
turbed sleep patterns, severely reduced per-
fusion to the brain, or depression.9 The signs
of hypoperfusion may include narrow pulse
pressure, pulsus alternans, cool extremities,
hypotension, or renal dysfunction.9 A quick
estimate of cardiac index is the proportional
pulse pressure. If this value is less than 25%,
the estimated cardiac index is below 2.2
L/min.16 The formula to determine propor-
tional pulse pressure is given below.15
Systolic BP − diastolic BP Proportional pulse
=
Systolic BP pressure
As was previously mentioned, signs and
symptoms associated with ADHF are not spe-
cific to only cardiac disorders, and so making
a differential diagnosis is important. The clin-
ical diagnosis of HF is based on history, physi-
cal examination, and diagnostic testing. Tests
done at the time of admission may include
chest radiograph, arterial blood gas, liver func-
tion tests, hematologic series, electrocardio-
gram, echocardiogram, basic metabolic pro-
file, and a B-natriuretic peptide (BNP) assay.2
The BNP assay can be utilized as an aid to es-
tablish the diagnosis, estimate prognosis, and
monitor the response to therapy of patients
with ADHF.17,18 The BNP is a cardiac hormone
secreted by the ventricular myocytes in re-
sponse to wall stretch. The results of this as-
say may be especially useful when the diag-
nosis of HF is uncertain because of other co-
morbid factors.1 The Breathing Not Properly
Study provided important evidence support-
ing the clinical use of BNP in the assessment of
patients presenting with possible HF.19,20 The
results of this study indicate that the diagnos-
tic accuracy of BNP, using a cutoff value of 100
pg/mL, was 83% when compared to the as-
sessment made by independent cardiologists,
whereas the negative predictive value of BNP
for HF, when levels were less than 50 pg/mL,
was 96%.19,20 Therefore, assessment of BNP
assay may serve as a useful tool in the diagno-
sis of a patient presenting with HF symptoms.
To continue further symptom evaluation,
the hemodynamic profile (Fig 1) may be
utilized.9 The hemodynamic profile has 4 sub-
sets relating to the presence or absence of 2
fundamental abnormalities in HF: congestion
and hypoperfusion.9 A patient who has con-
gestion is profiled as being “wet,” whereas
a patient without congestion is profiled as
being “dry.” Inadequate perfusion leads to
the patient being profiled as being “cold,”
whereas a patient with adequate perfusion
is profiled as being “warm.”9 A patient can
be rapidly assessed according to these crite-
ria and classified into 1 of 4 subsets (warm
and dry, warm and wet, cold and wet, and
cold and dry).9 Most patients presenting with
ADHF experience congestion without low
perfusion (warm and wet). Severely decom-
pensated patients may present with both con-
gestion and low perfusion (cold and wet).9
For those patients in whom the initial hemo-
dynamic profile is unclear or early responses
to treatment are not as anticipated, inva-
sive hemodynamic monitoring may be a use-
ful tool. Invasive hemodynamic measurement
in the form of a pulmonary artery catheter
may be utilized in tailoring therapy for the
ADHF patient21 but the use of these catheters
is associated with several risks for the pa-
tient, including infection, bleeding, and vessel
damage.22,23
Bioimpedance cardiography is a noninva-
sive alternative to hemodynamic monitoring
that is now available and being evaluated. This
technology enables the calculation of hemo-
dynamic values (eg, stroke volume, cardiac
output, cardiac index, and systemic vascular
resistance) based on the impedance of flow
of electricity through the chest wall.23 Re-
sults from the study conducted by Albert et
al indicate that impedance cardiography pro-
vides accurate measurements of cardiac out-
put and cardiac index when compared with
the invasive bolus thermodilution method.23
This noninvasive method may lead to timely
interventions, resulting in clinical improve-
ment and a shorter stay in the intensive care
unit.23
Once adequate information is obtained
regarding the patient, it is time to employ a
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Management of Acute Decompensated Heart Failure
treatment strategy. Although improving the
signs and symptoms (related to congestion
and hypoperfusion) is the principal immedi-
ate goal, treatments should be applied in a
way that limits adverse effects of treatment
and reduces the risk of morbidity.1,9 The
Heart Failure Society of America (HFSA)
has developed some comprehensive prac-
tice guidelines for the management of
patients with ADHF. The treatment goals
identified by the HFSA practice guide-
lines include optimizing volume status,
identifying etiology, identifying precipitating
factors, optimizing chronic oral therapy,
minimizing side effects, identifying patients
who may benefit from revascularization,
educating patients concerning medications
and self-assessment of HF, and considering
initiating a disease management program.1
Adequate perfusion, no evidence
of congestion
A patient who is warm and dry according
to the hemodynamic profile9 is one who does
not reflect evidence of elevated filling pres-
sures or hypoperfusion. The goal of therapy
for the patient is focused on disease manage-
ment and prevention of disease progression.9
This patient generally does not fit the crite-
ria for ADHF. Treatment strategies for this sub-
group of patients are directed by the 2005
AHA/ACC guidelines.2
Evidence of congestion, adequate
perfusion
A patient who presents as wet and warm
has signs and symptoms of congestion but
perfusion appears to be adequate.9 Therapy
needs to be directed at dealing with con-
gestion. If they are already on angiotensin-
converting enzyme (ACE) inhibitors, their
diuretic regimen needs to be enhanced.2,9
By the time these patients present in the
acute care setting, some may have already
been treated on an outpatient basis to man-
age their congestion.9 Hospitalization occurs
when there is inadequate relief of symptoms.
In this context, the addition of intravenous
loop diuretics or supplementation with other
99
diuretics can be utilized to achieve symptom
relief.1 Initial improvement in symptoms can
also be accelerated by intravenous vasodila-
tors such as nitroglycerin (Nitrospan and Ni-
trostat) or natrecor (Nesiritide).25 Intravenous
inotropes are generally not utilized unless ev-
idence of fluid overload persists because of
poor response to intravenous diuretics or di-
minished renal function.1,9,26
Diuretics have been the standard of therapy
for the management of the congested ADHF
patients because of their ability to rapidly de-
crease volume overload and congestion.1,27
Complications associated with diuretic use
have also been reported. These compli-
cations include reduced glomerular filtra-
tion rate, neurohormonal activation, and di-
uretic resistance.1,27–33 The neurohormonal
activation results in further vasoconstric-
tion. Other concerns are related to the
fact that diuretics create electrolyte imbal-
ances (eg, hypokalemia), which may con-
tribute to the development of potentially fa-
tal arrhythmias.28–33 These adverse effects are
thought to increase mortality within the HF
patient population.27 The HFSA recommenda-
tions are that diuretics should be administered
at a dose that produces sufficient diuresis to
relieve congestion and to achieve optimal vol-
ume status. This treatment strategy should be
done without inducing an excessively rapid
reduction in volume, whereby symptomatic
hypotension and/or worsening renal function
is created.1 Patients should be closely mon-
itored for adverse effects, electrolyte imbal-
ances, intake and output, and weight status.1
In addition, sodium and fluid restriction may
also need to be instituted.
Mechanical methods of fluid removal are
also being actively investigated as a potential
alternative to pharmacologic diuresis.34,35 In
a study conducted by Costanzo et al, early
ultrafiltration in patients admitted with fluid
overload and diuretic resistance resulted in
reduced length of stay (compared to the
length of stay indicated for ADHF patients
in ADHERE database), aggressive fluid with-
drawal (approximately 8500 mL), sustained
drop in plasma BNP, and reduced hospi-
talizations within 30 days.35 Ultrafiltration
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100 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2007
was not associated with worsening renal
failure, electrolyte abnormalities, or symp-
tomatic hypotension.35 Clinical benefits per-
sisted at 3 months after the treatment.35
Natrecor (exogenous BNP) is one of the
agents that may be used in a patient who
exhibits congestion but adequate perfusion
(warm and wet). It has a combined action of
vasodilation, diuresis, and natriuresis.36 These
effects lead to a reduction in preload, after-
load, and congestion.36 Natrecor has no in-
otropic effects and thus does not increase
myocardial oxygen demand. It is contraindi-
cated in patients with symptomatic hypoten-
sion and cardiogenic shock.37 In ADHF, the
counterregulatory effects of endogenous BNP
(BNP produced by myocytes) are not suf-
ficient; therefore, natrecor may be adminis-
tered to achieve the desired physiologic ef-
fect. The most common side effect of natrecor
therapy is dose-related hypotension.36,37 If
this occurs, the natrecor dose should be
reduced or discontinued and measures to
support blood pressure (eg, intravenous flu-
ids, changes in body position) should be
instituted.37 Recent findings relating natrecor
to increased incidence of renal dysfunction
and mortality may impact the use of natrecor
in the ADHF patient population.38,39
Evidence of congestion and
low perfusion
Patients who present with congestion
and low perfusion (wet and cold) require
interventions to improve perfusion and
reduce congestion.9 For these patients, it
is usually necessary to impact perfusion
issues first and then the congestion issues.9
β-Blockers and ACE inhibitors may need to
be withdrawn until stabilization is achieved,
especially if the patient is experiencing symp-
tomatic hypotension.9 For many patients,
low cardiac output is associated with high
systemic vascular resistance and predictable
improvement may be experienced with
vasodilator therapy alone.9 There is consid-
erable controversy about the relative role
of vasodilators and inotropic-vasodilator
agents such as dobutamine (dobutrex),
low-dose dopamine (Intropin), and milri-
none (Primacor).12,40 The investigators from
Vasodilation in the Management of Acute
CHF (VMAC) study concluded that natrecor
may be the drug of choice in these patients
because it is less potent and less toxic than
intravenous nitroprusside (Nipride) and
more easily administered than intravenous
nitroglycerin.36
It is well understood that contractility is a
determinant of cardiac output and when car-
diac output is low, clinicians often consider
utilizing an inotrope first. It is important to
also remember that increased afterload im-
pacts cardiac output. Since vasodilators are
very effective in reducing afterload, it is a
group of drugs that may be considered within
this group of patients.1,9
Medications such as nitroprusside, nitro-
glycerin, and natrecor can be used to reduce
afterload and thereby improve cardiac output,
organ perfusion, and diuresis. It is definitely a
challenge to use these agents in patients who
start out hypotensive, even if asymptomatic.9
The routine use of intravenous inotropes
(eg, dobutamine or milrinone) in HF may
be detrimental.2,26 However, in select ADHF
patients, inotropes may be administered to
relieve symptoms and improve end-organ
function.1,26 These patients are character-
ized by LV dilation, reduced LVEF, dimin-
ished systemic perfusion, and symptomatic
hypotension.1 Inotropes are also utilized
when initial hemodynamic status is unclear
and temporary stability is needed until a more
definitive profile can be determined.9,26 Con-
comitant use of β-blockers and inotropes that
are beta agonists (eg, dobutamine) are also
controversial since both groups of drugs com-
pete for the same beta receptor. The response
to dobutamine is inhibited in patients receiv-
ing high doses of β-blockers.41
Low perfusion and no evidence
of congestion
Patients who present with low perfusion
and no clinical evidence of congestion (cold
and dry) reflect a very small subgroup of the
ADHF patients.9 These patients may be stable
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Management of Acute Decompensated Heart Failure
clinically and often do not present with ur-
gent symptoms.9 Unappreciated congestion
may exist and requires further evaluation to
determine.9 Treatment strategies for this sub-
group will focus on improving the low perfu-
sion state.1,9
CARDIORENAL SYNDROME
Cardiorenal syndrome is a condition seen in
HF where renal and cardiac dysfunction coex-
ists. As the disease of HF advances, a decline
in the renal function is evident. Diuretics and
other treatment modalities become less effec-
tive. Worsening cardiac function contributes
to a further decline in renal function.31,42 The
cardiorenal syndrome is one of the major fac-
tors leading to frequent inotropic infusions for
diuretic resistant congestion. Upon initiation
of inotropic infusion, symptoms of congestion
are temporarily relieved. Once inotropic ther-
apy is discontinued, the symptoms reappear.9
Multiple factors are involved in the devel-
opment of renal failure in these patients. Re-
nal failure may occur because of reduced re-
nal perfusion, neurohormonal mediated vaso-
constriction, medication side effects (eg, non-
steroidal anti-inflammatory agents), and/or
comorbidities (eg, hypertension, diabetes).42
Renal insufficiency is a significant component
of the morbidity and mortality associated with
HF. The presence of cardiorenal syndrome sig-
nals a marked worsening of prognosis for the
HF patient.42 This is one of the most common
reasons why patients during late stages of HF
have unrelieved symptoms, despite aggressive
management.9,31,42
CASE STUDY
A 70-year-old man was admitted with symp-
toms of increasing dyspnea and fatigue. He
stated that his activity level declined substantially
over the past few weeks. This was his second
admission in the past 3 months with a similar
presentation. His history is significant for non-
insulin-dependent diabetes, coronary artery dis-
ease, and chronic bronchitis. His ejection fraction
during his last hospitalization was noted as be-
101
ing 20%. He was determined to be a New York
Heart Association class IV. Upon physical exam-
ination, 2+ edema to the mid-calf region, jugular
venous distention, weight gain of 10 lb since his
last follow-up visit 2 weeks ago, and cold upper
and lower extremities bilaterally were evident. His
BNP assay was 1000 pg/mL. His current medica-
tions were ACE inhibitor, loop diuretic, β-blocker,
antiarrhythmic, and bronchodilators.
This patient was presenting with signs and
symptoms of ADHF. According to the hemody-
namic profile, this patient was cold and wet.
Evaluation for exacerbating factors revealed that
he had a respiratory tract infection. He was
started on antibiotics and breathing treatments.
His symptoms of congestion and low perfusion
were addressed on the basis of the cold and wet
profile discussed earlier. Patient education was
begun in the intensive care unit and continued
throughout his hospitalization.
NURSING IMPLICATIONS
Nurses are challenged to have a thorough
knowledge base related to the disease state
of HF and the eliciting factors that impact
readmissions for ADHF. For patients admitted
to the intensive care unit, appropriate assess-
ment of signs and symptoms of congestion
and hypoperfusion is essential. It is important
to utilize diagnostic tools such as the BNP
assay to decipher the presented symptoms
as it relates to HF versus other comorbid
factors. The use of the hemodynamic profile
is helpful in developing treatment strategies.
To evaluate the effectiveness of the treatment
plan, an understanding of what the antici-
pated outcomes should be is necessary. Since
readmissions are frequent within this patient
population, prevention strategies should be
evaluated and employed. Effective treatment
plans are dependent on ongoing communica-
tion and collaboration by all members of the
healthcare team.12
In 2002, the Joint Commission on Accredi-
tation of Healthcare Organizations developed
the HF core measure set.43 The 4 standardized
core measures set for hospitalized HF patients
are documentation of discharge instruction in
6 areas (medication management, low-sodium
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102 CRITICAL CARE NURSING QUARTERLY/APRIL–JUNE 2007
diet, activity and exercise, signs and symp-
toms of worsening condition, weight mon-
itoring, and when to contact a healthcare
provider), assessment of LV function, use
of an ACE inhibitor or angiotensin receptor
blocker in patients with LV dysfunction, and
smoking cessation counseling.43 The health-
care team needs to be aware of these core
measures and address each element through-
out the hospitalization for all HF patients.
CONCLUSION
Patients hospitalized with ADHF are com-
plex and clinically challenging. Hospitaliza-
REFERENCES
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