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doi: 10.4037/ccn20128772012;32:20-32Crit Care NurseNancy M. AlbertFluid Management Strategies in Heart Failure

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may not have classic signs and symp-

toms of clinical congestion, such as

respiratory distress, crackles, inter-

stitial/alveolar edema, elevated jugu-

lar venous pressure or jugular venous

distension, findings on chest radi-

ographs, and an S3 heart sound.

Patients may have hemodynamic

congestion, defined as an increase in

left ventricular filling and/or intravas-cular pressures.3 Hemodynamic con-

gestion is a form of fluid retention

that occurs earlier than does clinical

congestion and indicates that the

clinical manifestations of fluid reten-

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 ofheart 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

Fluid Management

Strategies inHeart Failure

Cover Article

This article has been designated for CE credit.A closed-book, multiple-choice examination fol-lows this article, which tests your knowledge ofthe following objectives:

1. Describe the pathophysiological processesrelated to fluid overload (hypervolemia) inheart failure

2. Recognize the signs, symptoms anddiagnostic information needed to determinehypervolemia in heart failure

3. Identify strategies to manage hypervolemiaassociated with decompensated heart failureduring hospitalization and after discharge

Nancy M. Albert, PhD, CCNS, CHFN, CCRN, NE-BC

CEContinuing Education

The term heart failure is

defined as a clinical syn-

drome of decreased exer-

cise tolerance and fluid

retention due to structuralheart 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

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 height-

ened 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 patients hospitalization. (Critical Care Nurse. 2012;32[2]:20-32,34)

2012 American Association of Critical-Care Nurses

doi: http://dx.doi.org/10.4037/ccn2012877

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

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3/15

cardiac output, arterial underfilling,

activation of neurohormonal sys-

tems, and dysregulation between

the heart and kidneys.4 Two large

US heart failure registries, Acute

Decompensated Heart Failure Reg-

istry (ADHERE)5

and OrganizedProgram to Initiate Lifesaving Treat-

ment in Hospitalized Patients with

Heart Failure (OPTIMIZE-HF)6 col-

lected data on the clinical features

of patients hospitalized for acute

decompensated heart failure. Accord-

ing 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 pre-

served ejection fraction, or diastolic

dysfunction).In this review, I briefly describe

the complex pathophysiological

processes of hypervolemia in hospi-

talized patients with decompensated

heart failure and discuss fluid man-

agement strategies, many of which

can be nurse-led or nurse-facilitated.

Critical care, intermediate care, tele-

metry, 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 ofHypervolemia

In patients with normal hemo-

dynamic, 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 (Fig-

ure 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 argi-

nine vasopressin (antidiuretic hor-

mone), increased release of atrial

natriuretic peptide, and decreased

renal sympathetic tone.8

However, in patients with acute

decompensated heart failure, totalblood volume is not the determinant

of renal excretion of sodium and

water; the integrity of arterial circu-

lation 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

compensate, total blood volume is

increased by expansion of blood

volume in the venous circulation and

systemic vascular resistance (after-

load) increases.9 Increased afterload

combined with impaired systolic

performance also leads to an acuteincrease in left ventricular end-

diastolic 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 stimu-

lated 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 renin-

angiotensin-aldosterone system,

leading to production of angiotensin

II.3 Angiotensin II has many physio-

logical effects, including peripheraland renal vasoconstriction (to restore

arterial pressure and improve car-

diac output), increased thirst, and

stimulation of the sympathetic nerv-

ous 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 norepi-

nephrine that stimulate-receptors

in the nephron, enhancing reab-

sorption of sodium in the proximal

tubules.8,10 In addition, -receptors

in the juxtaglomerular apparatus

stimulate the renin-angiotensin-

aldosterone system, further

enhancing proximal tubular reab-

sorption of sodium.8Normally,

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 HeartFailure at the Cleveland Clinic Foundation, Cleveland, Ohio.

Author

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]).

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4/15

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

Figure 1 Events in adults with normal cardiac output and effective blood volume when fluid overload occurs.

Adapted from Schrier,7 with permission.

No edema formation and other signsand symptoms of fluid overload

Renal sodium and water excretion

Glomerular filtration rate

Atrial natriuretic peptide

Distal tubule sodium reabsorption

Extracellular fluid volume

Proximal tubule sodium reabsorption

Plasma renin,aldosterone,

norepinephrine, andarginine vasopressin

Enhanced sodium and water deliveryto the distal tubule

Normal cardiac output andeffective arterial blood

volume + fluid overload




5/15

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 ofHypervolemia

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

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.

Edema and other signs and

symptoms of fluid overload

Renal waterretention

Renal sodiumretention

Peripheral arterialresistance

Renal vascularresistance

Renal sodium and water excretion

Activation of the arterial baroreceptors

Heart failure withlow cardiac output

and arterial

underfilling+

Fluid overload(high preload)*

Left

vent

ricula

r myoc

ardial re

modeling Leftventricularmyocardialrem

odeling

Incr

ease

afterlo

ad Increaseafterload

Stimulation of sympatheticnervous system

Nonosmoticvasopressor stimulation

Activation of therenin-angiotension-aldosterone system

* Hemodynamic congestion.




6/15

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 associatedwith 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 emergencydepartment, 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 andsymptoms 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

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

StrategiesThe 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

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




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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 ofthe 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

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 irregu-lar 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 con-

gestion 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 out-

put and signs and symptoms of

hypervolemia must be serially

assessed so that the dosage of a

diuretic can be titrated to a patients

needs.1 Adverse events associated

with use of diuretics include elec-

trolyte imbalances (hypokalemia

and hypomagnesemia) leading toserious dysrhythmias, hypotension

(especially when vasodilator therapy

is used concomitantly), and worsen-

ing renal function.8 Electrolyte lev-

els, hemodynamic parameters, and

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-angiotensin-aldosterone system,30 and decreased

glomerular filtration rate.7 Strate-

gies to overcome diuretic resistance

are provided in Table 1.

Some therapies developed to

directly or indirectly relieve hyper-

volemia were promising in early

research but did not improve short-

and long-term quality of life, mor-

bidity, 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 Administra-

tion because the medications did

not decrease the number of hospi-

talizations for heart failure or mor-tality rates. Likewise, early clinical

outcomes did not differ between

treatment groups in acutely decom-

pensated, hospitalized patients with

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/h2. 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 oralfurosemide 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




8/15

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 patientswho 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

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. Vascularcatheters 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

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-relatedor 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 fewerrehospitalizations 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,

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 atthe 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 anddiuretic 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

Nurses must understand medically appropriate carerecommendations and advocate for patients during dailyrounds with physicians and pharmacy care providers.




9/15

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 ImplicationsAssessment

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 systemsimilar 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 ofevidence-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 improvementprograms 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

Table 2 New York Heart Association functional classificationa and examples

Functional status

I, Asymptomatic

II, Mild

III, Moderate

IV, Severe

Definition

Ordinary physical activity does not causesymptoms

Ordinary physical activity may be slightlylimited by symptoms but no symptomsat rest

Physical activity is markedly limited becauseof symptoms

Physical activity cannot be carried outwithout symptoms; symptoms occur at rest

Example A: Stair climbingExample B: Personal grooming

A: Patient can climb 2 full flights (basement to second floor) without symptoms developing

B: Patient is not limited

A: Symptoms occur after climbing 1 full flight (12 regular steps) or8 steps while carrying 10.8 kg (24 lb)

B: Symptoms occur during or after washing, dressing, preparingmeals, but patient does not need to stop

A: Patient cannot climb 1 full flight without stoppingB: Symptoms occur during washing, dressing, or preparing meals;

patient needs to take a break

A: Patient cannot climb more than 1 or a few steps without takinga break because of symptoms

B: Symptoms occur when patient initiates personal groomingbehaviors

a Signs and symptoms: dyspnea, fatigue, chest pain, palpitations.




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http://ccn.aacnjournals.org/


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Patients nonadherence to meth-

ods for managing heart failure has

been associated with acute decom-

pensated heart failure leading to

hospitalization.71-73Nonadherence 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 asequally 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 theheart failure plan of care so that an

individualized approach can be

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 decompensatedheart failure, nursing care that con-

forms to the recommendations of

evidence-based guidelines to recon-

cile and prevent hypervolemia may

promote improved outcomes. CCN

Financial DisclosuresNone reported.

References1. Jessup M, Abraham WT, Casey DE, et al;

2009 Writing Group to Review New Evi-dence and Update the 2005 Guideline forthe Management of Patients with ChronicHeart Failure Writing on Behalf of the 2005Heart Failure Writing Committee. 2009Focused update: ACCF/AHA guidelines forthe diagnosis and management of heartfailure in adults: a report of the AmericanCollege of Cardiology Foundation/Ameri-can Heart Association Task Force on Prac-tice Guidelines: Developed in CollaborationWith the International Society for Heartand Lung Transplantation. Circulation. 2009;119(14):1977-2016.

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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 deliveryof 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.

SummaryHypervolemia (both hemody-

namic and clinical congestion) is animport 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 ventricularfilling 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.

Now that youve read the article, create or contributeto an online discussion about this topic using eLetters.

Just visit www.ccnonline.org and click Submit aresponse in either the full-text or PDF view of thearticle.

To learn more about caring for heart fail-ure patients, read Caregiving for PatientsWith Heart Failure: Impact on PatientsFamilies by Hwang et al in theAmericanJournal of Critical Care, 2011;20: 431-442.Available at www.ajcconline.org.




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congestive heart failure.J Am Coll Cardiol.2001;38:963-968.

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ultrafiltration device as a treatment strategyfor diuretic resistant, refractory heart fail-ure: initial clinical experience in a singlecenter.J Card Fail. 2006;12(9):707-714.

40. Shin JT, Dec GW. Ultrafiltration should notreplace diuretics for the initial treatment ofacute decompensated heart failure. CircHeart Fail. 2009;2:505-511.

41. Koelling TM, Johnson ML, Cody RJ, Aaron-son KD. Discharge education improves clin-ical outcomes in patients with chronic heartfailure. Circulation. 2005;111(5):179-185.

42. Caldwell MA, Peters KJ, Dracup KA. A sim-plified education program improves knowl-edge, self-care behavior, and disease severityin heart failure patients in rural settings.Am Heart J. 2005;150:983e7-983e12.

43. Anderson C, Deepak BV, Amoateng-AdjepongY, Zarich S. Benefits of comprehensiveinpatient education and discharge planningcombined with outpatient support in eld-erly patients with congestive heart failure.Congest Heart Fail. 2005;11(6):315-321.

44. Blue L, Lang E, McMurray JJ, et al. Random-ised controlled trial of specialist nurse inter-vention in heart failure.BMJ. 2001;225:715-718.

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CCN Fast Facts CriticalCareNurseThe journal for high acuity, progressive, and critical care

Fluid Management Strategies in Heart Failure

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 hospitalizationfor 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

References1. 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 the2005 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 Heartand Lung Transplantation.

Circulation.2009;119(14):1977-2016.

2. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA2010 Comprehensive Heart Failure Practice Guideline.J Card Fail.2010;16(6):e1-e194.

FactsIn 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.

Albert NM. Fluid management strategies in heart failure. Crit Care Nurse. 2012;32(2):20-32,34.

Table Strategies to overcome diuretic resistancea

1. Infuse the agent as a continuous intravenous infusion: for example, furosemide at5-40 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 anagent 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 oralfurosemide 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 al 1 and the Heart Failure Society of America.2




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CE Test Test ID C122: Fluid Management Strategies in Heart FailureLearning objectives: 1. Describe the pathophysiological processes related to fluid overload (hypervolemia) in heart failure 2. Recognize the signs, symptomsand diagnostic information needed to determine hypervolemia in heart failure 3. Identify strategies to manage hypervolemia associated with decompensatedheart failure during hospitalization and after discharge

Program evaluationYes No

Objective 1 was met q qObjective 2 was met q qObjective 3 was met q qContent was relevant to my

nursing practice q qMy expectations were met q qThis method of CE is effective

for this content q qThe level of difficulty of this test was:

q easy q medium q difficultTo complete this program,

it took me hours/minutes.

1. Which statement best defines features of heart failure due tostructural heart disease?a. Orthopnea and sleep disordered breathingb. Decreased exercise tolerance and fluid retentionc. 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 circulationb. Normal kidney functionc. Decreased levels of B-type natriuretic peptided. Increased level of renin

3. Which of the following are physiological effects of angiotensin II?a. Activates peripheral vasoconstriction and sodium excretionb. Activates renal vasodilatation and sodium retentionc. Inhibits the release of antidiuretic hormone and B-type natriuretic peptided. Activates renal vasoconstriction and stimulates the sympathetic nervous

system

4. What is the mechanism for the stimulation of the renin-angiotensin-aldosterone system?a. Decrease in arterial volumeb. Hyponatremia and antidiuretic hormonec. Production of cortisol by the adrenal glandd. -Receptors in juxtaglomerular apparatus of the kidney

5. Which factor has been associated with long-term improvement inheart failure patients?a. Drinking fluids to prevent thirstb. Freedom from hypervolemia after hospitalizationc. Weight loss when overweight, obese, or extremely obesed. Keeping serum sodium levels between 130-135 mmol/L

6. What did multiple researchers find to be true regarding weight gainin 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

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