Cover Article

Fluid Management
Strategies in
Heart Failure
Nancy M. Albert, PhD, CCNS, CHFN, CCRN, NE-BC

In patients with chronic heart failure, fluid retention (or hypervolemia) is often may not have classic signs and symp-
the stimulus for acute decompensated heart failure that requires hospitalization. toms of clinical congestion, such as
The pathophysiology of fluid retention is complex and involves both hemodynamic respiratory distress, crackles, inter-
and clinical congestion. Signs and symptoms of both hemodynamic and clinical stitial/alveolar edema, elevated jugu-
congestion should be assessed serially during hospitalization. Core heart failure lar venous pressure or jugular venous
drug and cardiac device therapies should be provided, and ultrafiltration may be
distension, findings on chest radi-
warranted. Critical care, intermediate care, and telemetry nurses have roles in both
ographs, and an S3 heart sound.
assessment and management of patients hospitalized with acute decompensated
Patients may have hemodynamic
heart failure and fluid retention. Nurse administrators and managers have height-
ened their attention to fluid retention because the Medicare performance measure congestion, defined as an increase in
known as the risk-standardized 30-day all-cause readmission rate after heart failure left ventricular filling and/or intravas-
hospitalization can be attenuated by fluid management strategies initiated by cular pressures.3 Hemodynamic con-
nurses during a patients hospitalization. (Critical Care Nurse. 2012;32[2]:20-32,34) gestion is a form of fluid retention
that occurs earlier than does clinical
congestion and indicates that the
clinical manifestations of fluid reten-

CEContinuing Education
This article has been designated for CE credit.
A closed-book, multiple-choice examination fol-
lows this article, which tests your knowledge of
the following objectives:
1. Describe the pathophysiological processes
related to fluid overload (hypervolemia) in
heart failure
2. Recognize the signs, symptoms and
diagnostic information needed to determine
hypervolemia in heart failure
3. Identify strategies to manage hypervolemia
associated with decompensated heart failure
during hospitalization and after discharge
2012 American Association of Critical-Care Nurses
doi: http://dx.doi.org/10.4037/ccn2012877
T
he term heart failure is
defined as a clinical syn-
drome of decreased exer-
cise tolerance and fluid
retention due to structural
heart disease (eg, cardiomyopathy or
valvular disorders). Acute decom-
pensated heart failure denotes devel-
opment of progressive signs and
symptoms of distress that require
hospitalization in patients with a
previous diagnosis of heart failure.1
Although many markers of acute
decompensated heart failure are
related to fluid retention,2 patients
tion may be imminent.3 Even when
signs and symptoms of clinical con-
gestion are relieved, patients may
still have hemodynamic congestion
that could lead to progression of
heart failure and worsening progno-
sis.3 Thus, optimal assessment of
fluid status and management of both
hemodynamic and clinical conges-
tion are integral components of
nursing care.
Congestion in any form is a hall-
mark of acute decompensated heart
failure that stems from a cyclical
detrimental process involving low

20 CriticalCareNurse Vol 32, No. 2, APRIL 2012 www.ccnonline.org

cardiac output, arterial underfilling, and ensure that fluid management compensate, total blood volume is
activation of neurohormonal sys- strategies are in place before a increased by expansion of blood
tems, and dysregulation between patient is discharged. Patients must volume in the venous circulation and
the heart and kidneys.4 Two large also understand their roles in systemic vascular resistance (after-
US heart failure registries, Acute assessing, monitoring, and treating load) increases.9 Increased afterload
Decompensated Heart Failure Reg- hypervolemia at home to optimize combined with impaired systolic
istry (ADHERE)5 and Organized health-related clinical outcomes. performance also leads to an acute
Program to Initiate Lifesaving Treat- increase in left ventricular end-
ment in Hospitalized Patients with Pathophysiology of diastolic pressure. An acute increase
Heart Failure (OPTIMIZE-HF)6 col- Hypervolemia in left ventricular end-diastolic and
lected data on the clinical features In patients with normal hemo- pulmonary venous pressures causes
of patients hospitalized for acute dynamic, neurohormonal, cardiac, an increase of pressure in the alveoli.
decompensated heart failure. Accord- and renal processes, an increase in When the absorptive capabilities of
ing to both registries, cardiogenic total blood volume is associated the alveoli cells are overwhelmed,
shock was uncommon, accounting with an increase in renal levels of pulmonary congestion occurs.9
for 2% or less of all cases. However, sodium and water excretion4,7 (Fig- Further, in acute decompensated
hypervolemic states were prevalent ure 1). Renal excretion of sodium heart failure, normal reflexes stimu-
and often included dyspnea (89% and water is due to a series of reflexes lated by increased atrial pressure
and 90%, respectively), crackles that maintain normal total body are blunted by reflexes initiated in
(67% and 65%, respectively), and volume when atrial pressure increases. the high-pressure arterial circulation.
peripheral edema (66% and 65%, Thus, any increase in atrial pressure For example, an increase in total
respectively) regardless of whether leads to a diminished release of argi- blood volume associated with
or not the ejection fraction was less nine vasopressin (antidiuretic hor- decompensated heart failure
than 40% (indicating systolic left mone), increased release of atrial prompts activation of the renin-
ventricular dysfunction) or normal natriuretic peptide, and decreased angiotensin-aldosterone system,
(indicating heart failure with pre- renal sympathetic tone.8 leading to production of angiotensin
served ejection fraction, or diastolic However, in patients with acute II.3 Angiotensin II has many physio-
dysfunction). decompensated heart failure, total logical effects, including peripheral
In this review, I briefly describe blood volume is not the determinant and renal vasoconstriction (to restore
the complex pathophysiological of renal excretion of sodium and arterial pressure and improve car-
processes of hypervolemia in hospi- water; the integrity of arterial circu- diac output), increased thirst, and
talized patients with decompensated lation is a key factor in euvolemia.4 stimulation of the sympathetic nerv-
heart failure and discuss fluid man- Patients with heart failure have ous system. Angiotensin II increases
agement strategies, many of which either decreased cardiac output that synthesis of aldosterone, leading to
can be nurse-led or nurse-facilitated. causes underfilling of the arterial renal reabsorption of sodium and
Critical care, intermediate care, tele- circulation or high cardiac output sodium retention.8,10 Activation of the
metry, and general care nurses have that prompts systemic arterial sympathetic nervous system leads
many opportunities to assess patients vasodilatation and underfilling of to elevated plasma levels of norepi-
fluid status, correct hypervolemia, the arterial circulation.4 In order to nephrine that stimulate -receptors
in the nephron, enhancing reab-
sorption of sodium in the proximal
Author
Nancy M. Albert is the senior director, Nursing Research and Innovation, Nursing Institute, tubules.8,10 In addition, -receptors
and a clinical nurse specialist in the George M. and Linda H. Kaufman Center for Heart in the juxtaglomerular apparatus
Failure at the Cleveland Clinic Foundation, Cleveland, Ohio. stimulate the renin-angiotensin-
Corresponding author: Nancy M. Albert, PhD, CCNS, CHFN, CCRN, NE-BC, FAHA, FCCM, 9500 Euclid Ave, Mail code J3-4, aldosterone system, further
Cleveland, OH 44195 (e-mail: albertn@ccf.org).
enhancing proximal tubular reab-
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org. sorption of sodium.8 Normally,

www.ccnonline.org CriticalCareNurse Vol 32, No. 2, APRIL 2012 21

 Normal cardiac output and
effective arterial blood
volume + fluid overload

Plasma renin,
Distal tubule sodium reabsorption aldosterone,
norepinephrine, and
arginine vasopressin
Atrial natriuretic peptide Extracellular fluid volume

Glomerular filtration rate Proximal tubule sodium reabsorption

Enhanced sodium and water delivery

to the distal tubule

Renal sodium and water excretion

No edema formation and other signs

and symptoms of fluid overload

Figure 1 Events in adults with normal cardiac output and effective blood volume when fluid overload occurs.
Adapted from Schrier,7 with permission.

atrial natriuretic peptide increases
glomerular filtration rate and excre-
tion of water and sodium; however,
in advanced heart failure, these effects
are attenuated by renal vasocon-
striction and a reduction in sodium
delivery to the distal nephron. Argi-
nine vasopressin is released as a
result of arterial underfilling. Argi-
nine vasopressin increases plasma
and urine osmolalities and leads to
peripheral arterial vasoconstriction
and water reabsorption in the cells
of the distal tubule and collecting
duct in the kidney, promoting
hyponatremia.8 Figure 2 provides a
global depiction of interacting events
and responses that occur in patients
with reduced cardiac output and
fluid overload.7,10
Thus, activation of neurohor-
monal systems leads to worsening
retention of sodium and water that
contributes to pulmonary conges-
tion, hyponatremia, and edema.
Ultimately, a vicious cycle occurs,
with activation of neurohormonal
systems leading to worsening car-
diac function and further stimula-
tion of neurohormonal systems.4 In
addition to the pathophysiological
processes of acute decompensated
heart failure set in motion when

22 CriticalCareNurse Vol 32, No. 2, APRIL 2012 www.ccnonline.org

 ling
mode Left ven
ial re tricu
yo card lar m
m yo
lar In reas cardi
icu rload Heart failure with c
en t r
e afte low cardiac output
e a al r
fte e
tv ea
s rlo mod
cr and arterial
f

e
Le

In

ad
underfilling

lin
g
+
Fluid overload
(high preload)*

Activation of the arterial baroreceptors

Stimulation of sympathetic
nervous system Activation of the
Nonosmotic renin-angiotension-
vasopressor stimulation aldosterone system

Renal water Peripheral arterial Renal vascular Renal sodium

retention resistance resistance retention

Renal sodium and water excretion

Edema and other signs and

* Hemodynamic congestion. symptoms of fluid overload

Figure 2 Events in adults with low cardiac output and ineffective blood volume (arterial underfilling) when fluid overload occurs
(high preload).
Adapted from Schrier,7 with permission.

total blood volume increases because
of arterial underfilling, increased left
ventricular filling (diastolic) pressure
and myocardial stretch (left ventricu-
lar dilatation) are also powerful mech-
anisms of neurohormonal activation
and hypervolemia that can further
impair cardiac function.2
Assessment of
Hypervolemia
Accurate assessment of hyper-
volemia is important, because free-
dom from hypervolemia after
hospitalization has been associated
with improvement in long-term clini-
cal outcomes. Lucas et al11 assessed
patients 4 to 6 weeks after hospital
discharge for 5 signs of hyperv-
olemia: orthopnea, peripheral
edema, weight gain, need to increase
baseline diuretic dose, and jugular
venous distension. Patients with any 3
of the 5 signs 6 weeks after discharge
had a 3-fold increase in mortality at 2
years after the index hospitalization.
In another study,12 investigators
defined clinical exacerbation of heart
failure as the occurrence of at least 2
of the following: new or worsening
edema, increased body weight, wors-
ened dyspnea, worsened orthopnea,
worsened paroxysmal nocturnal dys-
pnea, and increased jugular venous
distension, all of which are indica-
tions of hypervolemia. In 189 outpa-
tients with heart failure, episodes of
clinical exacerbation were assessed
over time. More episodes of clinical
exacerbation were associated with an
increased rate of hospitalization for
heart failure, an increased risk of

www.ccnonline.org CriticalCareNurse Vol 32, No. 2, APRIL 2012 23

mortality over a 2-year period, and
a greater likelihood of lower qual-
ity of life, lower functional status,
and poorer exercise tolerance.
In other studies,13,14 repeated
hospitalizations for heart failure
decompensation were associated
with all-cause mortality, even after
adjustments for patients charac-
teristics. Moreover, hemodynamic
congestion is not benign. In one
study,15 increased blood volume
was associated with increased pul-
monary artery wedge pressure and
increased risk for death or urgent
heart transplantation at 1 year.
Although assessment of hyper-
volemia is important, some
nuances are worth mentioning.
First, although some signs and
symptoms (weight gain, nocturia,
elevated jugular venous pressure,
lower extremity edema, positive
hepatojugular reflux, paroxysmal
nocturnal dyspnea, and crackles)
were significant predictors of
decompensated heart failure in
patients treated in an emergency
department, the overall sensitivity
(the probability that signs or symp-
toms assessed were present in
patients who actually had worsen-
ing heart failure) of each sign or
symptom was low, even though
specificity (the probability that
signs or symptoms were absent in
patients without worsening heart
failure) was high.16 Thus, signs and
symptoms commonly associated
with decompensated heart failure
were not helpful in diagnosing
heart failure as the current prob-
lem. Invasive hemodynamic moni-
toring may be needed to assess
intracardiac pressures.1
Second, Mueller et al16 charac-
terized daily dyspnea, edema, and
24 CriticalCareNurse Vol 32, No. 2, APRIL 2012
body weight in patients with heart
failure for 1 month, and Albert et
al17 determined if signs and symp-
toms differed between ambulatory
and hospitalized patients. Although
dyspnea was positively and signifi-
cantly associated with edema,
changes in body weight were not
routinely associated with dyspnea
or edema.18 Hence, although changes
in body weight might be associated
with hospitalization for heart fail-
ure16,17,19 and repeat hospitalization
for worsening heart failure,20 weight
gain may not occur in patients with
acute decompensated heart fail-
ure.21,22 Lack of association of body
weight with dyspnea or edema
could have many causes, including
failure to monitor a patients weight,
offset of weight gain from fluid by
weight loss from cachexia, and min-
imal weight gain because of dimin-
ished appetite due to ascites.17
Finally, hemodynamic conges-
tion may not be associated with
physical findings of hypervolemia.
In a study15 of ambulatory nonede-
matous patients, physical findings
of hypervolemia were infrequent
and were not associated with
increased blood volume. In patients
with acutely decompensated heart
failure, pulmonary artery wedge
pressures can be elevated even though
crackles and edema are absent or
infrequent, and jugular venous pres-
sures may not be elevated.23,24
The biomarker B-type natriuretic
peptide (BNP) may not be an ideal
marker of volume status. In one
study,25 levels of BNP increased with
worsening heart failure and corre-
lated with New York Heart Associa-
tion functional class. However, in
another study,26 after treatment,
patients hemodynamic parameters
correlated better with changes in
blood volume than with changes in
BNP values. Although the sample
size was small, the researchers26
thought that BNP values changed
more slowly than did blood volume
and were better for showing long-
term rather than instantaneous vol-
ume status.
Likewise, ONeill et al27 found
that BNP levels were not accurate
predictors of serial hemodynamic
changes in hospitalized patients
with advanced heart failure. Even
though an initial decrease in BNP
levels was associated with early
improvement in hemodynamic
parameters, a change in BNP level
was not associated with a change in
pulmonary artery wedge pressure.
Research results1,8 reinforce the need
to use more than 1 method to assess
initial volume status, to determine
the effectiveness of therapies, and to
inform clinical decisions.
Fluid Management
Strategies
The guidelines of the American
College of Cardiology and American
Heart Association1 and the Heart
Failure Society of America28 include
recommendations for management
of patients with chronic heart failure
during acute episodes that require
hospitalization. The recommenda-
tions should be followed to ensure
optimal management with evidence-
based therapies. During both hospi-
talization and outpatient care, the
aims of fluid management strategies
for left ventricular systolic dysfunc-
tion and left ventricular dysfunction
with preserved ejection fraction are
relief of signs and symptoms of
hypervolemia, stabilization of hemo-
dynamic status without further
www.ccnonline.org
damage of cardiac myocytes, and
minimization of preventable recur-
rences of hypervolemia that require
hospitalization for heart failure
decompensation.1,28
In patients with hypervolemia,
signs and symptoms are the tip of
the iceberg in regard to congestion.
Pathophysiological changes in
hypervolemia include low cardiac
output, arterial underfilling, eleva-
tion in left ventricular diastolic
pressures, and neuroendocrine
activation. Thus, managing hemo-
dynamic congestion manifested by
increased left ventricular filling
pressure but no constellation of
signs and symptoms is just as
important as managing clinical
congestion. Core medications for
heart failure and cardiac resynchro-
nization therapies are first-line
strategies for managing hyper-
volemia because the interventions
attenuate neurohormonal activa-
tion and prevent progression, or
promote reversal, of left ventricular
remodeling that can worsen conges-
tion.1,28 Unless contraindicated, all
patients should take an angiotensin-
converting enzyme inhibitor (eg,
lisinopril, enalapril, or captopril)
or angiotensin II receptor blocker
(eg, valsartan or candesartan) and a
-blocker (eg, carvedilol, metopro-
lol succinate, or bisoprolol). Patients
hospitalized with advanced systolic
heart failure often meet indications
for an aldosterone antagonist (eg,
spironolactone or eplerenone) or
hydralazine-and-nitrate combina-
tion therapy and cardiac resynchro-
nization therapy.1,28 Finally, when
patients have hypoperfusion and
diuretic-resistant elevations in car-
diac filling pressures, intravenous
inotropic or vasopressor therapies
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are indicated to maintain systemic overall fluid volume status must be
perfusion and preserve or improve carefully monitored and managed.
end-organ performance.1 Diuretic resistance is common in
Loop diuretics are the hallmark patients with advanced heart failure
pharmacological treatment for because of hypertrophy of distal
hypervolemia.5 Because oral agents, tubule epithelial cells,29 increased
especially furosemide, have irregu- activation of the renin-angiotensin-
lar intestinal absorption and can aldosterone system,30 and decreased
have altered pharmacokinetics and glomerular filtration rate.7 Strate-
pharmacodynamics, intravenous gies to overcome diuretic resistance
administration is preferred during are provided in Table 1.
the early part of hospital therapy.8 Some therapies developed to
When administered intravenously, directly or indirectly relieve hyper-
loop diuretics rapidly relieve signs volemia were promising in early
and symptoms of pulmonary con- research but did not improve short-
gestion by lowering left ventricular and long-term quality of life, mor-
filling pressures.1 Initially, loop bidity, and mortality in large-scale
diuretics should be administered at randomized controlled trials. A1
a dose that is higher than the total adenosine receptor antagonists,31
daily outpatient dosage. Urine out- vasopressin receptor antagonists,32
put and signs and symptoms of and levosimenden33 resulted in
hypervolemia must be serially removal of excess fluid or improved
assessed so that the dosage of a cardiac output in heart failure in
diuretic can be titrated to a patients clinical trials but were not approved
needs.1 Adverse events associated by the Food and Drug Administra-
with use of diuretics include elec- tion because the medications did
trolyte imbalances (hypokalemia not decrease the number of hospi-
and hypomagnesemia) leading to talizations for heart failure or mor-
serious dysrhythmias, hypotension tality rates. Likewise, early clinical
(especially when vasodilator therapy outcomes did not differ between
is used concomitantly), and worsen- treatment groups in acutely decom-
ing renal function.8 Electrolyte lev- pensated, hospitalized patients with
els, hemodynamic parameters, and heart failure and stable hemodynamic
Table 1 Strategies to overcome diuretic resistancea
1. Infuse the agent as a continuous intravenous infusion: for example, furosemide at
5-40 mg/h or bumetanide at 0.1-0.5 mg/h
2. Administer 2 diuretic agents at the same time: for example, a loop diuretic and an
agent that blocks the distal tubule
Intravenous chlorothiazide (500-1000 mg), given 30 minutes before administration
of an intravenous loop diuretic
Oral metolazone (2.5-10 mg) given with an oral loop agent
3. Rotating loop diuretic agents: for example, switching or alternating between oral
furosemide and torsemide
a No large, randomized trials that provide evidence of the effectiveness of these strategies have been done.
Based on data from Jessup et al1 and the Heart Failure Society of America.28
CriticalCareNurse Vol 32, No. 2, APRIL 2012 25
status who were randomized to con-
tinuous intravenous infusion of mil-
rinone or placebo.34 More patients
sustained hypotension requiring
intervention and had new atrial
arrhythmias in the milrinone group.
Further, use of milrinone in patients
who had worsening renal function
(increasing serum levels of urea
nitrogen) during hospitalization did
not have improved outcomes
despite minor improvements in
renal function.35
As a therapeutic procedure,
ultrafiltration is the mechanical
removal of fluid from the vascula-
ture. Whole blood passes across a
Nurses must understand medically appropriate care
recommendations and advocate for patients during daily
rounds with physicians and pharmacy care providers.
hemofilter (a semipermeable mem-
brane) to yield plasma water in
response to a pressure gradient cre-
ated by the filtrate compartments
and hydrostatic pressures in blood
and also by oncotic pressure pro-
duced by plasma proteins.36 The
ultrafiltration device extracts blood
from and then returns it to the venous
circulation via separate access points
with large venous catheters (known
as a venovenous technique) and an
extracorporeal blood pump. Vascular
catheters can be placed in the femoral,
internal jugular, or subclavian veins
and in large peripheral veins. The
procedure can be performed only
once, continuously or intermittently.
Unlike the situation in fluid
removal with diuretics, which is pri-
marily hypotonic, the sodium con-
tent in the ultrafiltrate is equal to
26 CriticalCareNurse Vol 32, No. 2, APRIL 2012
the amount of sodium in the water
component of plasma.36 In addition,
diuretic therapy can cause hypo-
volemia, which enhances renal secre-
tion of renin and activation of
neurohormones. In ultrafiltration,
fluid is removed from the blood at
the same rate at which fluid is reab-
sorbed from the edematous intersti-
tium; therefore, prolonged
intravascular hypovolemia does not
occur and neurohormonal activation
is not stimulated.37
Ultrafiltration became a more
clinically relevant option after a
portable, peripheral venovenous
system became available and the
results of a multicenter, randomized,
controlled research trial38 corrobo-
rated the usefulness of the treatment.
When peripheral ultrafiltration was
compared with diuretic therapy in
patients with acute decompensated
heart failure, patients treated with
ultrafiltration had greater weight
loss, decreased need for vasoactive
drugs, and reduced 90-day rate of
rehospitalization.38 However, in a
small single-center study39 in patients
with very advanced heart failure and
diuretic resistance, ultrafiltration
was associated with variable fluid
removal, and renal function worsened
in 45% of patients during therapy.
Overall, in 3 of 5 trials of peripheral
ultrafiltration with a portable system,
readmission was not improved in 3
studies, and signs and symptoms were
significantly reduced in only 1 study.40
Other disadvantages of ultrafil-
tration therapy are patients costs,
need for training nurses in the pro-
cedure, nurse staffing, excessive vol-
ume removal (resulting in
hypotension and worsening prere-
nal azotemia), and catheter-related
or system complications, such as
infection, thrombosis, air
embolism, or hemorrhage due to
disconnection of the venous return
catheter.40 To date, peripheral ultra-
filtration has not been better than
aggressive intravenous diuretic ther-
apy in improving signs and symp-
toms, causing weight loss, or
preventing complications.
Interdisciplinary nurse-physician
or nurse-led programs, initiated and
maintained in a variety of environ-
ments of care, did not prevent wors-
ening hypervolemia associated with
rehospitalization. Education before
hospital discharge41-43; counseling43-46;
and follow-up programs after dis-
charge,47,48 including transition-to-
home,43,46 telephone, and other forms
of remote monitoring48,49 programs,
were associated with adherence to
prescribed therapies and fewer
rehospitalizations after discharge.
However, most strategies used to
minimize preventable hypervolemia
and subsequent morbidity and mor-
tality were not well described and
therefore are hard to replicate.
Investigators provided a global
overview of programs but did not
provide details of key components,
www.ccnonline.org
 Table 2 New York Heart Association functional classificationa and examples
Example A: Stair climbing
Functional status Definition Example B: Personal grooming
I, Asymptomatic Ordinary physical activity does not cause A: Patient can climb 2 full flights (basement to second floor) with
symptoms out symptoms developing
B: Patient is not limited
II, Mild Ordinary physical activity may be slightly A: Symptoms occur after climbing 1 full flight (12 regular steps) or
limited by symptoms but no symptoms 8 steps while carrying 10.8 kg (24 lb)
at rest B: Symptoms occur during or after washing, dressing, preparing
meals, but patient does not need to stop
III, Moderate Physical activity is markedly limited because A: Patient cannot climb 1 full flight without stopping
of symptoms B: Symptoms occur during washing, dressing, or preparing meals;
patient needs to take a break
IV, Severe Physical activity cannot be carried out A: Patient cannot climb more than 1 or a few steps without taking
without symptoms; symptoms occur at rest a break because of symptoms
B: Symptoms occur when patient initiates personal grooming
behaviors
a Signs and symptoms: dyspnea, fatigue, chest pain, palpitations.

the depth or breadth of content
delivered (program intensity), or
assessment methods used to deter-
mine and enhance patients under-
standing. Additionally, not all
programs were effective in prevent-
ing hospitalizations, even if patients
had improvement in knowledge or
self-care.48-51
Nursing Implications
Assessment
Because of the nuances of hyper-
volemia assessment in heart failure,
nurses must not base decisions on
volume status on a single method
of assessment or on only a few vari-
ables. Physical signs and symptoms
must be assessed along with patients
subjective perceptions of clinical
changes in status, such as worsen-
ing exercise intolerance or changes
in New York Heart Association func-
tional class (Table 2). A valuable
assessment variable for hypervolemia
may be history of recent hospitaliza-
tion for heart failure. Nurses should
ask patients about recent hospital
events, especially if patients use more
than a single health care center to
meet health needs. Specific issues
and tips for assessing hypervolemia
are provided in Table 3.
In lieu of invasive hemodynamic
monitoring to measure intracardiac
pressures and definitively determine
hemodynamic congestion, clinicians
can be trained to use other technol-
ogy. Portable, handheld, pocket-
sized ultrasound machines can be
used to determine left ventricular
function, detect pericardial effu-
sions, predict intravenous fluid
responsiveness, and identify impor-
tant valvular defects.64,65 For patients
with implantable cardioverter defib-
rillators that also measure intratho-
racic impedance, impedance data
(on intrathoracic fluid) can be down-
loaded by using a wand system
similar to that used to download
pacemaker data. The impedance
report provides data about the pres-
ence of thoracic congestion. In a
study66 of 23 patients, impedance
values measured by using an
implantable cardioverter defibrilla-
tor were compared with pulmonary
artery wedge pressures measured
noninvasively by using echocardiog-
raphy. The results indicated a strong
correlation between high wedge
pressure and low intrathoracic
impedance.
Fluid Management
Currently, a gap exists between
clinical expectations for use of
evidence-based treatment recom-
mendations and actual practice. Dis-
parities are prevalent in the quality
of care in heart failure at both the
patient67-69 and hospital level.67,68,70
Nurses must understand medically
appropriate care recommendations
and advocate for patients during daily
rounds with physicians and phar-
macy care providers. Nurses should
participate in quality improvement
programs that focus on monitoring
the adherence of health care
providers use of heart failure med-
ications chosen on the basis of
research evidence and recommenda-
tions for use of cardiac devices. Nurses
should also participate in quality
improvement programs that focus

www.ccnonline.org CriticalCareNurse Vol 32, No. 2, APRIL 2012 27

 Table 3 Hypervolemia assessment issues and tips

Issue 1: Insensitivity of common signs and symptoms of heart failure15-17

Ask multiple questions, in a variety of ways, to obtain a well-rounded picture of the incidence and level (mild, moderate, or severe) of
signs and symptoms.
- For example, when assessing dyspnea, do not just ask if it had worsened before the patient came to the hospital or outpatient clinic.
Patients may decrease activity level to prevent worsening of dyspnea.
Ask what activities the patient has given up or is doing more slowly or less frequently because of dyspnea.
Ask if caregivers have changed behaviors to minimize patients dyspnea.
Obtain an individualized history of events that might be the reason for new or worsening signs and symptoms of hypervolemia.
- For example, if a patient complains of difficulty sleeping, you might learn that he or she has nocturia. Once the problem is identified,
ask the patient about
Change in dietary behaviors (eating away from home or a change in purchasing practices)
Change in food preparation (new meal planner or cook)
Recent nonadherence to medications for heart failure
New or worsening thirst leading to increased fluid intake
Use of ibuprofen or other over-the-counter drugs that cause sodium and water retention
Use noninvasive and internal monitoring features of cardiac devices to aid in assessment when elevations in pulmonary artery wedge
pressure cannot be directly assessed.52
- When measurement of thoracic impedance is available as a feature of an implantable cardioverter-defibrillator device, assess
thoracic impedance levels.53
- If respiratory distress or clinical evidence of impaired perfusion and intracardiac filling pressures cannot be assessed clinically,
use invasive hemodynamic monitoring.1
Issue 2: Neuroendocrine activation leading to hypervolemia could be due to nonoptimal medication regimen or medication nonadherence.1,28,54
Obtain medication reconciliation related to therapies used before hospitalization.
- Report findings and patients rationale for not taking medications as prescribed.
- Report core medications not prescribed for heart failure.
- Report identified contraindications to medications for heart failure.
- Report medications not for heart failure that could worsen heart failure.
Issue 3: Nonadherence to self-care program for heart failure may have multiple, patient-specific causes that may be related to or
beyond knowledge and skills deficits.26,55-58
Carefully assess patients rationale for nonadherence. Consider economic issues (transportation or costs of care), social issues
(caregiver support, loneliness),57 psychological issues (depression, anxiety),58 and cognition issues.59
Assess health literacy.60
Assess number of heart failure health care provider services as patients may be receiving mixed or confusing advice.61
Issue 4: Be aware of laboratory and clinical parameters that may be helpful in determining hypervolemia, renal dysfunction that aggravates
hypervolemia,8 or other medical conditions associated with decreased cardiac output and neuroendocrine activation leading to hyper-
volemia.1,28,62,63
Assess creatinine clearance (estimated glomerular filtration rate).
Assess increases ion serum levels of urea nitrogen and creatinine during hospitalization.
Assess hemoglobin level for presence of anemia that could be due to hemodilution.
Assess serum sodium level for hyponatremia, which is a marker of an increase in plasma levels of arginine vasopressin (and water
retention).
Assess for elevated blood pressure that may be associated with stimulation of the sympathetic nervous system.
Assess QRS duration 120 ms associated with cardiac dyssynchronization that can lead to mitral regurgitation and pulmonary
congestion as well as hypervolemia from neuroendocrine activation associated with poor cardiac performance.
Assess serum levels of troponins I and T, which are highly sensitive markers of myocardial injury. Elevated values (troponin I >1 g/L
or troponin T >0.1 g/L) could indicate cardiac myocyte damage as the precipitant of hypervolemia.
Assess worsening burden of comorbid conditions that could cause acute deterioration in renal function (eg, worsening diabetes or
hypertension).

on the understanding of patients
and patients families of education
received, adherence to early (7-day)
follow-up care, and adherence to the
nonpharmacological plan of care.
Nurses should participate on
interdisciplinary collaborative
teams to implement strategies to
improve quality of care and con-
formity with recommended guide-
lines for management of heart
failure. The need is great for nurses
to develop and participate in pro-
grams that ease the transition of
patients and informal caregivers
from hospital to home and focus on
disease management. Nurse-led ini-
tiatives can facilitate safe and effec-
tive care before patients are
discharged, increase awareness of
patients and informal caregivers
barriers to optimal self-care, and
prepare patients and informal care-
givers to adhere to the plan of care.

28 CriticalCareNurse Vol 32, No. 2, APRIL 2012 www.ccnonline.org

 Patients nonadherence to meth-
ods for managing heart failure has
been associated with acute decom-
pensated heart failure leading to
hospitalization.71-73 Nonadherence to
diet, medication, or fluid restriction
was cited as a reason for readmis-
sion by 25% of patients and 26% of
informal caregivers.72 However, only
14% of cardiologists and 13% of
heart failure nurses thought nonad-
herence was the primary reason for
hospitalization.72 Cardiologists and
heart failure nurses were more likely
to cite other diseases, nonoptimal
medical regimens, knowledge
deficits, and delay in seeking help as
reasons for hospitalization. Among
participants in the study,72 33% of
patients and 23% of heart failure
nurses cited improving adherence to
heart failure therapies as the pri-
mary intervention to prevent read-
missions. Adequate professional
help was identified by 35% of family
caregivers as the most important
intervention. Cardiologists identi-
fied 2 primary interventions as
equally important: improving
adherence and adequate professional
help. Nurses have an opportunity
and a responsibility to help patients
improve adherence to regimens for
managing heart failure.
Research results highlight the
need for greater vigilance in optimal
assessment of possible causes of
patients nonadherence with the
heart failure plan of care so that an
individualized approach can be
To learn more about caring for heart fail-
ure patients, read Caregiving for Patients
With Heart Failure: Impact on Patients
Families by Hwang et al in the American
Journal of Critical Care, 2011;20: 431-442.
Available at www.ajcconline.org.
www.ccnonline.org
developed. Nurses must ensure
consistency of hospital-based educa-
tion and counseling related to fluid
management (weight monitoring,
fluid restriction when ordered, and
low-sodium diet). Nurses must also
ensure consistency in the delivery
of interventions to manage heart
failure (including those targeting
clinicians and informal caregivers)
and in assessment of the effective-
ness of the interventions by study-
ing clinical outcomes and cost of
care so that deficiencies can be cor-
rected. Attention to emerging knowl-
edge and evidence-based practices is
paramount to a successful program
focused on patients, patients fami-
lies and patients informal caregivers.
Revised national guideline recom-
mendations and new research that
provides important and generalizable
findings should be the basis for
standards of clinical care.
Summary
Hypervolemia (both hemody-
namic and clinical congestion) is an
import predictor of worsening heart
failure, morbidity leading to hospi-
talization for heart failure, and mor-
tality. Hypervolemia can be difficult
to recognize when common signs
and symptoms of clinical conges-
tion are not manifested during an
acute congestive exacerbation.
Clinical congestion often occurs
later than elevated left ventricular
filling pressure (hemodynamic con-
gestion) does, necessitating use of
multiple measures and methods of
monitoring hypervolemia.
Nurse-led or nurse-facilitated
delivery of interventions to manage
heart failure may decrease practice
gaps associated with worsening
heart failure due to hypervolemia.
Nurse-led or nurse-facilitated educa-
tion, counseling, and follow-up
programs after discharge from the
hospital promote patients and care-
givers knowledge and expectations
for adherence to heart failure self-
care. During acute decompensated
heart failure, nursing care that con-
forms to the recommendations of
evidence-based guidelines to recon-
cile and prevent hypervolemia may
promote improved outcomes. CCN
Now that youve read the article, create or contribute
to an online discussion about this topic using eLetters.
Just visit www.ccnonline.org and click Submit a
response in either the full-text or PDF view of the
article.
Financial Disclosures
None reported.
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www.ccnonline.org CriticalCareNurse Vol 32, No. 2, APRIL 2012 31

CCN Fast Facts
Fluid Management Strategies in Heart Failure
Facts
In patients with chronic heart failure, fluid retention
(or hypervolemia) is often the stimulus for acute decom-
pensated heart failure that requires hospitalization. The
pathophysiology of fluid retention is complex and involves
both hemodynamic and clinical congestion. Signs and
symptoms of both hemodynamic and clinical congestion
should be assessed serially during hospitalization. Core
heart failure drug and cardiac device therapies should be
provided, and ultrafiltration may be warranted. Adher-
ence to heart failure medications improves cardiac func-
tion, leading to improvement in volume status.
During both hospitalization and outpatient care, the
aims of fluid management strategies for left ventricular
systolic dysfunction and left ventricular dysfunction
with preserved ejection fraction are relief of signs and
symptoms of hypervolemia, stabilization of hemody-
namic status without further damage of cardiac myocytes,
and minimization of preventable recurrences of hyper-
volemia that require hospitalization for heart failure
decompensation.1,2 Strategies to overcome diuretic
resistance are provided in the Table.
Table Strategies to overcome diuretic resistancea
1. Infuse the agent as a continuous intravenous infusion: for example, furosemide at
5-40 mg/h or bumetanide at 0.1-0.5 mg/h
2. Administer 2 diuretic agents at the same time: for example, a loop diuretic and an
agent that blocks the distal tubule
Intravenous chlorothiazide (500-1000 mg), given 30 minutes before administration
of an intravenous loop diuretic
Oral metolazone (2.5-10 mg) given with an oral loop agent
3. Rotating loop diuretic agents: for example, switching or alternating between oral
furosemide and torsemide
a No large, randomized trials that provide evidence of the effectiveness of these strategies have been done.
Based on data from Jessup et al1 and the Heart Failure Society of America.2
Albert NM. Fluid management strategies in heart failure. Crit Care Nurse. 2012;32(2):20-32,34.
32 CriticalCareNurse Vol 32, No. 2, APRIL 2012
CriticalCareNurse
The journal for high acuity, progressive, and critical care
Because of the nuances of hypervolemia assessment
in heart failure, nurses must not base decisions on vol-
ume status on a single method of assessment or on only
a few variables. Physical signs and symptoms must be
assessed along with patients subjective perceptions of
clinical changes in status, such as worsening exercise
intolerance or changes in New York Heart Association
functional class. A valuable assessment variable for
hypervolemia may be history of recent hospitalization
for heart failure. Nurses should ask patients about recent
hospital events, especially if patients use more than a
single health care center to meet health needs. CCN
References
1. Jessup M, Abraham WT, Casey DE, et al; 2009 Writing Group to
Review New Evidence and Update the 2005 Guideline for the Manage-
ment of Patients with Chronic Heart Failure Writing on Behalf of the
2005 Heart Failure Writing Committee. 2009 Focused update:
ACCF/AHA guidelines for the diagnosis and management of heart fail-
ure in adults: a report of the American College of Cardiology Founda-
tion/American Heart Association Task Force on Practice Guidelines:
Developed in Collaboration With the International Society for Heart
and Lung Transplantation. Circulation. 2009;119(14):1977-2016.
2. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA
2010 Comprehensive Heart Failure Practice Guideline. J Card Fail.
2010;16(6):e1-e194.
www.ccnonline.org
CE Test Test ID C122: Fluid Management Strategies in Heart Failure
Learning objectives: 1. Describe the pathophysiological processes related to fluid overload (hypervolemia) in heart failure 2. Recognize the signs, symptoms
and diagnostic information needed to determine hypervolemia in heart failure 3. Identify strategies to manage hypervolemia associated with decompensated
heart failure during hospitalization and after discharge

1. Which statement best defines features of heart failure due to 7. After initial treatment (first 24 hours) of hypervolemia in patients
structural heart disease? with acute decompensated heart failure, what laboratory value is
a. Orthopnea and sleep disordered breathing not an accurate predictor of heart failure status?
b. Decreased exercise tolerance and fluid retention a. Potassium c. B-type natriuretic peptide
c. Cough and orthopnea b. Sodium d. Glomerular filtration rate
d. Hypovolemia and decreased exercise tolerance
8. What medications should all patients with heart failure take,
2. What is the key factor to ensure euvolemia in heart failure patients? unless otherwise contraindicated?
a. The integrity of the arterial circulation a. Digoxin, -blocker, and angiotensin-converting enzyme inhibitor
b. Normal kidney function b. Angiotensin-converting enzyme inhibitor or angiotensin II receptor
c. Decreased levels of B-type natriuretic peptide blocker and -blocker
d. Increased level of renin c. Aldosterone inhibitor, loop diuretic, and angiotensin-converting
enzyme inhibitor
3. Which of the following are physiological effects of angiotensin II? d. -Blocker, thiazide diuretic, and hydralazine/nitrate combination
a. Activates peripheral vasoconstriction and sodium excretion
b. Activates renal vasodilatation and sodium retention 9. What class of medication is considered the hallmark pharmaco-
c. Inhibits the release of antidiuretic hormone and B-type natriuretic peptide logical treatment for hypervolemia in heart failure?
d. Activates renal vasoconstriction and stimulates the sympathetic nervous a. Angiotensin-converting enzyme inhibitor
system b. -Blocker
c. Loop diuretic
4. What is the mechanism for the stimulation of the renin-angiotensin- d. Aldosterone inhibitor
aldosterone system?
a. Decrease in arterial volume 10. What adverse events are associated with the use of loop diuretics?
b. Hyponatremia and antidiuretic hormone a. Hypokalemia and hypomagnesemia
c. Production of cortisol by the adrenal gland b. Hypocalcemia and hyperkalemia
d. -Receptors in juxtaglomerular apparatus of the kidney c. Hyperphosphotemia and hyponatremia
d. Hypermagnesemia and hypercalcemia
5. Which factor has been associated with long-term improvement in
heart failure patients? 11. Which strategies were most effective for promoting adherence to
a. Drinking fluids to prevent thirst prescribed therapies and preventing rehospitalization?
b. Freedom from hypervolemia after hospitalization a. Sending patients home with written self-care materials
c. Weight loss when overweight, obese, or extremely obese b. Ensuring patients know how to record daily weight and report changes
d. Keeping serum sodium levels between 130-135 mmol/L c. Education before discharge and remote monitoring
d. Diet class provided to family members after discharge
6. What did multiple researchers find to be true regarding weight gain
in acute decompensated heart failure? 12. What percentage of patients and informal caregivers cited non-
a. Weight gain was commonly reported when even mild dyspnea was present. adherence to diet, medications, or fluid restriction as the reason for
b. Weight gain was associated with systolic dysfunction (ejection fraction readmission?
of <40%). a. 46% and 38%, respectively c. 12% and 15%, respectively
c. Weight gain may not occur in patients, even if dyspnea or edema are present. b. 14% and 46%, respectively d. 25% and 26%, respectively
d. Weight gain was commonly observed in patients with edema.
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
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qc qc qc qc qc qc qc qc qc qc qc qc
qd qd qd qd qd qd qd qd qd qd qd qd
Test ID: C122 Form expires: April 1, 2014 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP: Category A
Test writer: Diane Byrum, RN, MSN, CCRN, CCNS, FCCM

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