Fluid Management Strategies in Heart Failure Cover Article

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
the stimulus for acute decompensated 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. Critical care, intermediate care, and telemetry nurses have roles in both
assessment and management of patients hospitalized with acute decompensated
heart failure and fluid retention. Nurse administrators and managers have heightened their attention to fluid retention because the Medicare performance measure
known as the risk-standardized 30-day all-cause readmission rate after heart failure
hospitalization can be attenuated by fluid management strategies initiated by
nurses during a patient’s hospitalization. (Critical Care Nurse. 2012;32[2]:20-32,34)
CEContinuing Education
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. 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
20 CriticalCareNurse Vol 32, No. 2, APRIL 2012
T
he term heart failure is
defined as a clinical syndrome of decreased exercise tolerance and fluid
retention due to structural
heart disease (eg, cardiomyopathy or
valvular disorders). Acute decompensated heart failure denotes development 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
may not have classic signs and symptoms of clinical congestion, such as
respiratory distress, crackles, interstitial/alveolar edema, elevated jugular venous pressure or jugular venous
distension, findings on chest radiographs, and an S3 heart sound.
Patients may have hemodynamic
congestion, defined as an increase in
left ventricular filling and/or intravascular pressures.3 Hemodynamic congestion is a form of fluid retention
that occurs earlier than does clinical
congestion and indicates that the
clinical manifestations of fluid retention may be imminent.3 Even when
signs and symptoms of clinical congestion are relieved, patients may
still have hemodynamic congestion
that could lead to progression of
heart failure and worsening prognosis.3 Thus, optimal assessment of
fluid status and management of both
hemodynamic and clinical congestion are integral components of
nursing care.
Congestion in any form is a hallmark of acute decompensated heart
failure that stems from a cyclical
detrimental process involving low
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cardiac output, arterial underfilling,
activation of neurohormonal systems, and dysregulation between
the heart and kidneys.4 Two large
US heart failure registries, Acute
Decompensated Heart Failure Registry (ADHERE)5 and Organized
Program to Initiate Lifesaving Treatment in Hospitalized Patients with
Heart Failure (OPTIMIZE-HF)6 collected data on the clinical features
of patients hospitalized for acute
decompensated heart failure. According to both registries, cardiogenic
shock was uncommon, accounting
for 2% or less of all cases. However,
hypervolemic states were prevalent
and often included dyspnea (89%
and 90%, respectively), crackles
(67% and 65%, respectively), and
peripheral edema (66% and 65%,
respectively) regardless of whether
or not the ejection fraction was less
than 40% (indicating systolic left
ventricular dysfunction) or normal
(indicating heart failure with preserved ejection fraction, or diastolic
dysfunction).
In this review, I briefly describe
the complex pathophysiological
processes of hypervolemia in hospitalized patients with decompensated
heart failure and discuss fluid management strategies, many of which
can be nurse-led or nurse-facilitated.
Critical care, intermediate care, telemetry, and general care nurses have
many opportunities to assess patients’
fluid status, correct hypervolemia,
and ensure that fluid management
strategies are in place before a
patient is discharged. Patients must
also understand their roles in
assessing, monitoring, and treating
hypervolemia at home to optimize
health-related clinical outcomes.
Pathophysiology of
Hypervolemia
In patients with normal hemodynamic, neurohormonal, cardiac,
and renal processes, an increase in
total blood volume is associated
with an increase in renal levels of
sodium and water excretion4,7 (Figure 1). Renal excretion of sodium
and water is due to a series of reflexes
that maintain normal total body
volume when atrial pressure increases.
Thus, any increase in atrial pressure
leads to a diminished release of arginine vasopressin (antidiuretic hormone), increased release of atrial
natriuretic peptide, and decreased
renal sympathetic tone.8
However, in patients with acute
decompensated heart failure, total
blood volume is not the determinant
of renal excretion of sodium and
water; the integrity of arterial circulation is a key factor in euvolemia.4
Patients with heart failure have
either decreased cardiac output that
causes underfilling of the arterial
circulation or high cardiac output
that prompts systemic arterial
vasodilatation and underfilling of
the arterial circulation.4 In order to
Author
Nancy M. Albert is the senior director, Nursing Research and Innovation, Nursing Institute,
and a clinical nurse specialist in the George M. and Linda H. Kaufman Center for Heart
Failure at the Cleveland Clinic Foundation, Cleveland, Ohio.
Corresponding author: Nancy M. Albert, PhD, CCNS, CHFN, CCRN, NE-BC, FAHA, FCCM, 9500 Euclid Ave, Mail code J3-4,
Cleveland, OH 44195 (e-mail: [email protected]).
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, [email protected].
www.ccnonline.org
compensate, total blood volume is
increased by expansion of blood
volume in the venous circulation and
systemic vascular resistance (afterload) increases.9 Increased afterload
combined with impaired systolic
performance also leads to an acute
increase in left ventricular enddiastolic pressure. An acute increase
in left ventricular end-diastolic and
pulmonary venous pressures causes
an increase of pressure in the alveoli.
When the absorptive capabilities of
the alveoli cells are overwhelmed,
pulmonary congestion occurs.9
Further, in acute decompensated
heart failure, normal reflexes stimulated by increased atrial pressure
are blunted by reflexes initiated in
the high-pressure arterial circulation.
For example, an increase in total
blood volume associated with
decompensated heart failure
prompts activation of the reninangiotensin-aldosterone system,
leading to production of angiotensin
II.3 Angiotensin II has many physiological effects, including peripheral
and renal vasoconstriction (to restore
arterial pressure and improve cardiac output), increased thirst, and
stimulation of the sympathetic nervous system. Angiotensin II increases
synthesis of aldosterone, leading to
renal reabsorption of sodium and
sodium retention.8,10 Activation of the
sympathetic nervous system leads
to elevated plasma levels of norepinephrine that stimulate α-receptors
in the nephron, enhancing reabsorption of sodium in the proximal
tubules.8,10 In addition, β-receptors
in the juxtaglomerular apparatus
stimulate the renin-angiotensinaldosterone system, further
enhancing proximal tubular reabsorption of sodium.8 Normally,
CriticalCareNurse Vol 32, No. 2, APRIL 2012 21
Normal cardiac output and
effective arterial blood
volume + fluid overload
↑ Distal tubule sodium reabsorption
↑ Atrial natriuretic peptide
↓ Plasma renin,
aldosterone,
norepinephrine, and
arginine vasopressin
↑ 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 excretion of water and sodium; however,
in advanced heart failure, these effects
are attenuated by renal vasoconstriction and a reduction in sodium
delivery to the distal nephron. Arginine vasopressin is released as a
result of arterial underfilling. Arginine vasopressin increases plasma
and urine osmolalities and leads to
22 CriticalCareNurse Vol 32, No. 2, APRIL 2012
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 neurohormonal systems leads to worsening
retention of sodium and water that
contributes to pulmonary congestion, hyponatremia, and edema.
Ultimately, a vicious cycle occurs,
with activation of neurohormonal
systems leading to worsening cardiac function and further stimulation of neurohormonal systems.4 In
addition to the pathophysiological
processes of acute decompensated
heart failure set in motion when
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Left ven
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Heart failure with
e a al r
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e
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Fluid overload
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Activation of the arterial baroreceptors
Nonosmotic
vasopressor stimulation
Renal water
retention
Stimulation of sympathetic
nervous system
↑ Peripheral arterial
resistance
↑ Renal vascular
resistance
Activation of the
renin-angiotensionaldosterone system
Renal sodium
retention
↓ Renal sodium and water excretion
* Hemodynamic congestion.
Edema and other signs and
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 ventricular dilatation) are also powerful mechanisms of neurohormonal activation
and hypervolemia that can further
impair cardiac function.2
Assessment of
Hypervolemia
Accurate assessment of hypervolemia is important, because freedom from hypervolemia after
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hospitalization has been associated
with improvement in long-term clinical outcomes. Lucas et al11 assessed
patients 4 to 6 weeks after hospital
discharge for 5 signs of hypervolemia: 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, worsened dyspnea, worsened orthopnea,
worsened paroxysmal nocturnal dyspnea, and increased jugular venous
distension, all of which are indications of hypervolemia. In 189 outpatients 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
CriticalCareNurse Vol 32, No. 2, APRIL 2012 23
mortality over a 2-year period, and
a greater likelihood of lower quality 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’ characteristics. Moreover, hemodynamic
congestion is not benign. In one
study,15 increased blood volume
was associated with increased pulmonary artery wedge pressure and
increased risk for death or urgent
heart transplantation at 1 year.
Although assessment of hypervolemia 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 symptoms assessed were present in
patients who actually had worsening 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 problem. Invasive hemodynamic monitoring may be needed to assess
intracardiac pressures.1
Second, Mueller et al16 characterized 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 symptoms differed between ambulatory
and hospitalized patients. Although
dyspnea was positively and significantly 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 failure16,17,19 and repeat hospitalization
for worsening heart failure,20 weight
gain may not occur in patients with
acute decompensated heart failure.21,22 Lack of association of body
weight with dyspnea or edema
could have many causes, including
failure to monitor a patient’s weight,
offset of weight gain from fluid by
weight loss from cachexia, and minimal weight gain because of diminished appetite due to ascites.17
Finally, hemodynamic congestion may not be associated with
physical findings of hypervolemia.
In a study15 of ambulatory nonedematous 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 pressures 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 correlated with New York Heart Association 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 longterm rather than instantaneous volume status.
Likewise, O’Neill 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 recommendations should be followed to ensure
optimal management with evidencebased therapies. 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 hemodynamic status without further
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damage of cardiac myocytes, and
minimization of preventable recurrences 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, elevation in left ventricular diastolic
pressures, and neuroendocrine
activation. Thus, managing hemodynamic 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 resynchronization therapies are first-line
strategies for managing hypervolemia because the interventions
attenuate neurohormonal activation and prevent progression, or
promote reversal, of left ventricular
remodeling that can worsen congestion.1,28 Unless contraindicated, all
patients should take an angiotensinconverting enzyme inhibitor (eg,
lisinopril, enalapril, or captopril)
or angiotensin II receptor blocker
(eg, valsartan or candesartan) and a
β-blocker (eg, carvedilol, metoprolol 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 combination therapy and cardiac resynchronization therapy.1,28 Finally, when
patients have hypoperfusion and
diuretic-resistant elevations in cardiac filling pressures, intravenous
inotropic or vasopressor therapies
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are indicated to maintain systemic
perfusion and preserve or improve
end-organ performance.1
Loop diuretics are the hallmark
pharmacological treatment for
hypervolemia.5 Because oral agents,
especially furosemide, have irregular intestinal absorption and can
have altered pharmacokinetics and
pharmacodynamics, intravenous
administration is preferred during
the early part of hospital therapy.8
When administered intravenously,
loop diuretics rapidly relieve signs
and symptoms of pulmonary congestion by lowering left ventricular
filling pressures.1 Initially, loop
diuretics should be administered at
a dose that is higher than the total
daily outpatient dosage. Urine output and signs and symptoms of
hypervolemia must be serially
assessed so that the dosage of a
diuretic can be titrated to a patient’s
needs.1 Adverse events associated
with use of diuretics include electrolyte imbalances (hypokalemia
and hypomagnesemia) leading to
serious dysrhythmias, hypotension
(especially when vasodilator therapy
is used concomitantly), and worsening renal function.8 Electrolyte levels, hemodynamic parameters, and
Table 1
overall fluid volume status must be
carefully monitored and managed.
Diuretic resistance is common in
patients with advanced heart failure
because of hypertrophy of distal
tubule epithelial cells,29 increased
activation of the renin-angiotensinaldosterone system,30 and decreased
glomerular filtration rate.7 Strategies to overcome diuretic resistance
are provided in Table 1.
Some therapies developed to
directly or indirectly relieve hypervolemia were promising in early
research but did not improve shortand long-term quality of life, morbidity, and mortality in large-scale
randomized controlled trials. A1
adenosine receptor antagonists,31
vasopressin receptor antagonists,32
and levosimenden33 resulted in
removal of excess fluid or improved
cardiac output in heart failure in
clinical trials but were not approved
by the Food and Drug Administration because the medications did
not decrease the number of hospitalizations for heart failure or mortality rates. Likewise, early clinical
outcomes did not differ between
treatment groups in acutely decompensated, hospitalized patients with
heart failure and stable hemodynamic
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 continuous intravenous infusion of milrinone 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 vasculature. Whole blood passes across a
the amount of sodium in the water
component of plasma.36 In addition,
diuretic therapy can cause hypovolemia, which enhances renal secretion of renin and activation of
neurohormones. In ultrafiltration,
fluid is removed from the blood at
the same rate at which fluid is reabsorbed from the edematous interstitium; 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
Other disadvantages of ultrafiltration therapy are patients’ costs,
need for training nurses in the procedure, nurse staffing, excessive volume removal (resulting in
hypotension and worsening prerenal 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 ultrafiltration has not been better than
aggressive intravenous diuretic therapy in improving signs and symptoms, causing weight loss, or
preventing complications.
Nurses must understand medically appropriate care
recommendations and advocate for patients during daily
rounds with physicians and pharmacy care providers.
hemofilter (a semipermeable membrane) to yield plasma water in
response to a pressure gradient created by the filtrate compartments
and hydrostatic pressures in blood
and also by oncotic pressure produced 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 primarily hypotonic, the sodium content in the ultrafiltrate is equal to
26 CriticalCareNurse Vol 32, No. 2, APRIL 2012
results of a multicenter, randomized,
controlled research trial38 corroborated 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
Interdisciplinary nurse-physician
or nurse-led programs, initiated and
maintained in a variety of environments of care, did not prevent worsening hypervolemia associated with
rehospitalization. Education before
hospital discharge41-43; counseling43-46;
and follow-up programs after discharge,47,48 including transition-tohome,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 mortality 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,
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Table 2
New York Heart Association functional classificationa and examples
Functional status
Definition
Example A: Stair climbing
Example B: Personal grooming
I, Asymptomatic
Ordinary physical activity does not cause
symptoms
A: Patient can climb 2 full flights (basement to second floor) with
out symptoms developing
B: Patient is not limited
II, Mild
Ordinary physical activity may be slightly
limited by symptoms but no symptoms
at rest
A: Symptoms occur after climbing 1 full flight (12 regular steps) or
8 steps while carrying 10.8 kg (24 lb)
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
of symptoms
A: Patient cannot climb 1 full flight without stopping
B: Symptoms occur during washing, dressing, or preparing meals;
patient needs to take a break
IV, Severe
Physical activity cannot be carried out
without symptoms; symptoms occur at rest
A: Patient cannot climb more than 1 or a few steps without taking
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 determine and enhance patients’ understanding. Additionally, not all
programs were effective in preventing hospitalizations, even if patients
had improvement in knowledge or
self-care.48-51
Nursing Implications
Assessment
Because of the nuances of hypervolemia assessment in heart failure,
nurses must not base decisions on
volume 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 (Table 2). 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
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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 technology. Portable, handheld, pocketsized ultrasound machines can be
used to determine left ventricular
function, detect pericardial effusions, predict intravenous fluid
responsiveness, and identify important valvular defects.64,65 For patients
with implantable cardioverter defibrillators that also measure intrathoracic impedance, impedance data
(on intrathoracic fluid) can be downloaded by using a wand system
similar to that used to download
pacemaker data. The impedance
report provides data about the presence of thoracic congestion. In a
study66 of 23 patients, impedance
values measured by using an
implantable cardioverter defibrillator were compared with pulmonary
artery wedge pressures measured
noninvasively by using echocardiography. 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 recommendations and actual practice. Disparities 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 pharmacy care providers. Nurses should
participate in quality improvement
programs that focus on monitoring
the adherence of health care
providers’ use of heart failure medications chosen on the basis of
research evidence and recommendations for use of cardiac devices. Nurses
should also participate in quality
improvement programs that focus
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 patient’s 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 patient’s 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 patient’s 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 hypervolemia.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 µg/L
or troponin T >0.1 µg/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
28 CriticalCareNurse Vol 32, No. 2, APRIL 2012
improve quality of care and conformity with recommended guidelines for management of heart
failure. The need is great for nurses
to develop and participate in programs that ease the transition of
patients and informal caregivers
from hospital to home and focus on
disease management. Nurse-led initiatives can facilitate safe and effective care before patients are
discharged, increase awareness of
patients’ and informal caregivers’
barriers to optimal self-care, and
prepare patients and informal caregivers to adhere to the plan of care.
www.ccnonline.org
Patients’ nonadherence to methods for managing heart failure has
been associated with acute decompensated heart failure leading to
hospitalization.71-73 Nonadherence to
diet, medication, or fluid restriction
was cited as a reason for readmission by 25% of patients and 26% of
informal caregivers.72 However, only
14% of cardiologists and 13% of
heart failure nurses thought nonadherence 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 primary intervention to prevent readmissions. Adequate professional
help was identified by 35% of family
caregivers as the most important
intervention. Cardiologists identified 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 failure 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 education 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 effectiveness of the interventions by studying clinical outcomes and cost of
care so that deficiencies can be corrected. Attention to emerging knowledge and evidence-based practices is
paramount to a successful program
focused on patients, patients’ families and patients’ informal caregivers.
Revised national guideline recommendations and new research that
provides important and generalizable
findings should be the basis for
standards of clinical care.
Summary
Hypervolemia (both hemodynamic and clinical congestion) is an
import predictor of worsening heart
failure, morbidity leading to hospitalization for heart failure, and mortality. Hypervolemia can be difficult
to recognize when common signs
and symptoms of clinical congestion are not manifested during an
acute congestive exacerbation.
Clinical congestion often occurs
later than elevated left ventricular
filling pressure (hemodynamic congestion) 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 education, counseling, and follow-up
programs after discharge from the
hospital promote patients’ and caregivers’ knowledge and expectations
for adherence to heart failure selfcare. During acute decompensated
heart failure, nursing care that conforms to the recommendations of
evidence-based guidelines to reconcile and prevent hypervolemia may
promote improved outcomes. CCN
Now that you’ve read the article, create or contribute
to an online discussion about this topic using eLetters.
Just visit www.ccnonline.org and click “Submit a
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article.
Financial Disclosures
None reported.
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CriticalCareNurse Vol 32, No. 2, APRIL 2012 31
CCN Fast Facts
CriticalCareNurse
The journal for high acuity, progressive, and critical care
Fluid Management Strategies in Heart Failure
Facts
In patients with chronic heart failure, fluid retention
(or hypervolemia) is often the stimulus for acute decompensated 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. Adherence to heart failure medications improves cardiac function, 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 hemodynamic status without further damage of cardiac myocytes,
and minimization of preventable recurrences of hypervolemia that require hospitalization for heart failure
decompensation.1,2 Strategies to overcome diuretic
resistance are provided in the Table.
Table
Because of the nuances of hypervolemia assessment
in heart failure, nurses must not base decisions on volume 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 Management 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 failure in adults: a report of the American College of Cardiology Foundation/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.
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
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
7. After initial treatment (first 24 hours) of hypervolemia in patients
with acute decompensated heart failure, what laboratory value is
not an accurate predictor of heart failure status?
a. Potassium
c. B-type natriuretic peptide
b. Sodium
d. Glomerular filtration rate
1. Which statement best defines features of heart failure due to
structural heart disease?
a. Orthopnea and sleep disordered breathing
b. Decreased exercise tolerance and fluid retention
c. Cough and orthopnea
d. Hypovolemia and decreased exercise tolerance
2. What is the key factor to ensure euvolemia in heart failure patients?
a. The integrity of the arterial circulation
b. Normal kidney function
c. Decreased levels of B-type natriuretic peptide
d. Increased level of renin
3. Which of the following are physiological effects of angiotensin II?
a. Activates peripheral vasoconstriction and sodium excretion
b. Activates renal vasodilatation and sodium retention
c. Inhibits the release of antidiuretic hormone and B-type natriuretic peptide
d. Activates renal vasoconstriction and stimulates the sympathetic nervous
system
4. What is the mechanism for the stimulation of the renin-angiotensinaldosterone system?
a. Decrease in arterial volume
b. Hyponatremia and antidiuretic hormone
c. Production of cortisol by the adrenal gland
d. β-Receptors in juxtaglomerular apparatus of the kidney
5. Which factor has been associated with long-term improvement in
heart failure patients?
a. Drinking fluids to prevent thirst
b. Freedom from hypervolemia after hospitalization
c. Weight loss when overweight, obese, or extremely obese
d. Keeping serum sodium levels between 130-135 mmol/L
6. What did multiple researchers find to be true regarding weight gain
in acute decompensated heart failure?
a. Weight gain was commonly reported when even mild dyspnea was present.
b. Weight gain was associated with systolic dysfunction (ejection fraction
of <40%).
c. Weight gain may not occur in patients, even if dyspnea or edema are present.
d. Weight gain was commonly observed in patients with edema.
8. What medications should all patients with heart failure take,
unless otherwise contraindicated?
a. Digoxin, β-blocker, and angiotensin-converting enzyme inhibitor
b. Angiotensin-converting enzyme inhibitor or angiotensin II receptor
blocker and β-blocker
c. Aldosterone inhibitor, loop diuretic, and angiotensin-converting
enzyme inhibitor
d. β-Blocker, thiazide diuretic, and hydralazine/nitrate combination
9. What class of medication is considered the hallmark pharmacological treatment for hypervolemia in heart failure?
a. Angiotensin-converting enzyme inhibitor
b. β-Blocker
c. Loop diuretic
d. Aldosterone inhibitor
10. What adverse events are associated with the use of loop diuretics?
a. Hypokalemia and hypomagnesemia
b. Hypocalcemia and hyperkalemia
c. Hyperphosphotemia and hyponatremia
d. Hypermagnesemia and hypercalcemia
11. Which strategies were most effective for promoting adherence to
prescribed therapies and preventing rehospitalization?
a. Sending patients home with written self-care materials
b. Ensuring patients know how to record daily weight and report changes
c. Education before discharge and remote monitoring
d. Diet class provided to family members after discharge
12. What percentage of patients and informal caregivers cited nonadherence to diet, medications, or fluid restriction as the reason for
readmission?
a. 46% and 38%, respectively
c. 12% and 15%, respectively
b. 14% and 46%, respectively
d. 25% and 26%, respectively
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
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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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