-
Nancy M. Albert, Cathy A. Eastwood and Michelle L.
EdwardsEvidence-Based Practice for Acute Decompensated Heart
Failure
Published online http://www.cconline.org 2004 American
Association of Critical-Care Nurses
2004, 24:14-29. Crit Care Nurse
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14 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Nancy M. Albert is certified as a clinical nurse specialist and
has a dual role of director of nursing research in the division of
nursingand clinical nurse specialist at the George M. and Linda H.
Kaufman Center for Heart Failure of the Cleveland Clinic
Foundation,Cleveland, Ohio. She codeveloped heart failure programs
along the continuum of care, including emergency care, critical
care, and acutecare, at the Cleveland Clinic Foundation.
Cathy A. Eastwood graduated with a master of nursing degree from
the University of Calgary, Canada, after specializing in the care
ofpatients with heart failure. She developed and managed the
outpatient heart failure center and oversaw the flow of inpatients
with heartfailure at St. Lukes Episcopal Hospital, Houston, Tex.
Currently, she is a lecturer at Memorial University of
Newfoundland, School ofNursing, in St. Johns, Newfoundland,
Canada.
Michelle L. Edwards earned a master of science degree in nursing
from the University of Alabama at Birmingham and is a
board-certified family and acute care nurse practitioner. She
practiced several years in critical care, specializing in the care
of cardiovascularpatients. She currently is a cardiology nurse
practitioner/outcomes manager at St. Lukes Episcopal Hospital.
Each year, chronic left ventric-ular systolic and diastolic
dysfunc-tion, or heart failure, causes 1million hospitalizations in
theUnited States.1 Heart failure is themost common Medicare
diagnosisrelated group at discharge1,2 and isassociated with poor
survival andquality of life. In addition, cost ofcare is high; in
1998, Medicare paid
out $3.6 billion for care related toheart failure.1
The Acute Decompensated HeartFailure National Registry
(ADHERE)3
recently reported data on 14 716patients hospitalized for heart
failurein the United States (Tables 1 and 2).Generally, patients
admitted to thehospital for heart failure were elderly,were female,
had a history of heart
CoverArticle
Authors
CE This article has been designated forCE credit. A closed-book,
multiple-choiceexamination follows this article, which testsyour
knowledge of the following objectives:
1. Identify the core drug therapies for decompensated heart
failure
2. Describe the role of B-type natriuretic peptide in
decompensated heart failure
3. Explain the pharmacological managementof decompensated heart
failure
Nancy M. Albert, RN, MSN, CCNS, CCRN, CNACathy A. Eastwood, RN,
MNMichelle L. Edwards, RN, MSN, FNP, ACNP
To purchase reprints, contact The InnoVision Group, 101
Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949)
362-2050 (ext 532); fax, (949) 362-2049;
e-mail,[email protected].
CEContinuing EducationEvidence-Based Practice forAcute
DecompensatedHeart Failure
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failure, and were unable to carry outactivities of daily living
without exer-cise intolerance. The most commonsymptom was dyspnea,
which wasmost often associated with other signsand symptoms of
fluid retention.Comorbid conditions were common,and patients were
equally likely tobe admitted with systolic dysfunction(reduced
ventricular contractility;ejection fraction 0.40) or
diastolicdysfunction (impaired ventricularrelaxation or ventricular
stiffness
tion that led to signs and symptomswas impaired ventricular
relaxation,which was associated with increasedage, obesity,
hypertension, and car-diovascular disease.4 In addition,ADHERE data
were comparable todata from other reports6-8 in thatretention of
fluid and sodium, asevidenced by admitting signs andsymptoms, was a
primary factor inhospitalization. This knowledge pro-vides an
opportunity for care improve-ment that can be championed bynurses,
because hospitalization forfluid and sodium retention in
patientswith systolic or diastolic dysfunctionmay be avoidable,
especially whensuch retention is due to patients fail-ure to adhere
to medication regimensor self-care instructions.
In this article, we discuss evidence-based practices for
managing patientswith acutely decompensated heartfailure because
in-hospital actionsmay facilitate an improved experiencefor
patients after hospitalization.The intent is to provide
management
that decreases theventricles abilityto fill). One quar-ter of
patients wererehospitalizedwithin 6 monthsof a previous
hos-pitalization, andMedicare was theprimary hospitalpayor.
Mostpatients spenttime in the emer-gency department
before admission as an inpatient, andthe most common level of
initial carewas telemetry. Median length of staywas 4.4 days.3
The ADHERE data are similar todata from other studies4,5 in
whichinvestigators found an equal split ofpatients with impaired
and preservedleft ventricular systolic function, sig-nifying
hospitalization of patientswith systolic dysfunction and
patientswith diastolic dysfunction. The pri-mary mechanism of
diastolic dysfunc-
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 15
Table 2 Outpatient medications before hospitalization
andmedications at discharge: data from the Acute DecompensatedHeart
Failure National Registry3
Medication class
% of patients
8758
1345
3372
5422372748343
7242
1134
2854
4423302338307
DiureticAngiotensin-converting
enzyme inhibitorAngiotensin II receptor blockerHydralazine plus
nitrateHydralazineNitrateAngiotensin-converting enzyme
inhibitor, hydralazine, plusnitrate or angiotensin IIreceptor
blocker
-BlockerCalcium channel
blockerDigoxinWarfarinAspirinLipid-lowering agentNonsteroidal
anti-inflammatory
drugs
Before hospitalization(n = 14 716)
At discharge(n = 11 187)
Table 1 Characteristics of patients, clinical signs and
symptoms, and hospital placement: data from the AcuteDecompensated
Heart Failure National Registry3
Characteristics at hospital admission % of patients
5268507725
433271315830
442816
8
9234726935
384920
7722
6513
8
FemaleMedicare, primary payerEjection fraction 177 mol/L (2.0
mg/dL)Point of entry to the hospital
Emergency departmentDirect admission
First inpatient unitTelemetryWard or intensive or coronary
careStepdown
*Dyspnea, fatigue, palpitations, or chest pain with minimal
activity.Dyspnea, fatigue, palpitations, or chest pain at
rest.Percentage of each.Mean serum level of sodium was 138 mmol/L,
and median level of B-typenatriuretic peptide was 784 pg/mL.
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goals and actions associated with themost common clinical
manifestation,fluid retention, and not to focus onmanagement of
cardiogenic shock,profound hypoperfusion, or complexdecompensation
(severe hyper-volemia, hypoperfusion, and acidosisor other
conditions such as pneumo-nia). Assessment of patients, man-agement
strategies, and education ofpatients are highlighted.
Mythsassociated with acute care manage-ment are discussed so that
nurseswill be more aware of appropriateinterventions that are safe
and effec-tive. Heart failure management hasprogressed rapidly in
recent years.Ultimately, nurses must be proactivein ensuring that
their behaviors arebased on current evidence.
Heightened Expectations for Evidence-Based Care
Nurses are challenged to plan andprovide care that promotes the
bestpossible clinical and health-relatedoutcomes. The Joint
Commission onAccreditation of Healthcare Organi-zations9 recently
established 4 coremeasures in the acute managementof patients with
heart failure to pro-mote adherence to basic standards
ofevidence-based care (Table 3). Becauseof the large number of
patients andthe high cost of care associated withhospital
readmissions, acute andcritical care nurses must developand
implement strategies that areassociated with improved outcomesfor
patients and hospitals. In addi-tion, in 2001, the American
Collegeof Cardiology (ACC) and the Ameri-can Heart Association
(AHA) pub-lished practice guidelines10 for adultswith chronic heart
failure. Theseguidelines provide caregivers withrecommendations for
nonacute care
and include the rationale and levelof evidence for support of
each man-agement strategy. Table 4 providesa list of management
strategies,including core drug therapies, thatshould be a part of
each patientstreatment plan at discharge afteran admission for
decompensatedheart failure stemming from vol-ume overload.10,11
If the medica-tion expectationslisted in Table 4are compared
withthe actual med-ication therapiesbefore hospital-ization and at
dis-charge indicatedin the ADHEREdata (Table 2), aneed for change
isevident. Newefforts must beundertaken topromote use of
consensus guidelines and therapiesto meet the overall goal of
manag-ing heart failure: promoting regres-sion and preventing
progression ofleft ventricular enlargement (remod-eling) to
decrease disease progres-sion and improve survival.11-14 SeeFigure
1 and Table 5 for definitionand description of consequences
ofventricular remodeling.
16 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Table 3 The 4 core measures of the Joint Commission
onAccreditation of Healthcare Organizations
Written discharge instructions or educational material must
begiven to the patient or caregiver and include all of the
follow-ing: activity level, diet, discharge medications,
follow-upappointment, weight monitoring, and symptom management
Left ventricular function must be documented in the
hospitalrecord to indicate that it was assessed before or during
hos-pitalization, or will be assessed after discharge
Patients with known systolic dysfunction of moderate tosevere
impairment (ejection fraction 130 ms), and other inclusion
criteria to determine if cardiac resynchronization devices are
appropriate
Angiotensin-converting enzyme
inhibitors-BlockersDigitalisDiureticsSpironolactone (if condition
is unstable with preceding drugs and patient is in New
York Heart Association functional class IV)
*Stage C is referenced in American College of
Cardiology/American Heart Association practice guidelines10and is
part of a 4-stage classification of heart failure by evolution and
progression of the disease. In stageC, patients have structural
heart disease of the myocardium, pericardium, or cardiac valves
with prior orcurrent symptoms (shortness of breath, fatigue,
exercise intolerance) of heart failure.
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No standardized evidence-basedguidelines are available to direct
acutecare; however, randomized, placebo-controlled research studies
providestrong support for actions that areeffective and safe. In
addition, manyactions promoted in the currentguidelines for
long-term outpatientmanagement of heart failure can betranslated to
the acute setting and
are not in cardiogenic shock or donot have profound
hypoperfusion orcomplex decompensation. Imple-mentation of the
following strategiesmight require a change in the philos-ophy of
care, further education, andcontinuous quality monitoring toensure
that evidence-based strategiesare used regardless of the type
ofphysician, a patients placement(telemetry or nonmonitored bed),
anurses background (cardiac, heartfailure, or generalist), or a
hospitalsresources.
Assessment of PatientsBefore planning interventions for
a patient hospitalized with heart fail-ure, the healthcare team
must conducta systematic assessment that includesidentification of
the cause of the heartfailure, aggravating factors, potentialrisk
factors that may influence survivaland quality of life, and current
clinicalstatus. Patients comorbid conditions,especially active
chronic conditions,may act as exacerbating factors(Table 6),
affecting the planning ofpatients care and influencing thetiming
and intensity of therapies. Thetreatment plan must include
modifi-cation of correctable causes ofdecompensation. Examples
includeeducation for sodium indiscretion,alcohol abstinence
programs for over-consumption of alcohol, or revascu-larization
strategies for hibernatingmyocardium (ie, viable but under-perfused
myocardial tissue withdecreased contractility). In addition,risks
related to heart failure must beconsidered, such as the need
foranticoagulation to prevent embolicevents or the need for an
implantablecardioverter-defibrillator to preventsudden cardiac
death, so that appro-priate consultations and therapies are
provide a uniform plan of care basedon large, multicenter,
randomizedresearch studies that focus on the pri-mary management
goal of prevent-ing progression of heart failure.10
Nurses can facilitate some practi-cal assessment and
managementstrategies that apply to patientsadmitted to the hospital
with a pri-mary diagnosis of heart failure who
18 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Table 5 Ventricular remodeling: definition and consequences
Definition
Consequences
A cascade of changes in genome expression, cells, molecules, and
interstitium thatalters the size, shape, and function of the left
ventricle after injury.
Alterations in heart size and shape (volume) that are not
associated with preload-mediated increase in myocyte length.
Hallmarks leading to change in shape of left ventricle from a V
to a U. Combination ofDilatation (myocyte lengthening and cell
slippage)Cell loss/death (apoptosis)Interstitial fibrosisHeart
failure after myocardial infarction: formation of a discrete
collagen scarNonischemic heart failure: isolated fibrosis
Hypertrophy (see Figure 1b and c)Initially concentric
(thickening of myocytes) Then becomes eccentric (thinning of the
left ventricular walls)
High pressure (wall stress) in the ventricle during systole and
diastole heightensmyocardial oxygen consumption, a situation that
promotes further hypertrophy andactivates neurohormonal systems
Reduction in ejection fractionReduced ventricular
performanceMorbidity and mortality
Figure 1 Ventricular remodeling. Cross-sectional view of left
and right ventricles: a, normal; b, concentric hypertrophy; and c,
eccentric hypertrophy.
Abbreviations: LV, left ventricle; RV, right ventricle.Produced
and printed with permission from The Cleveland Clinic Foundation;
Cleveland, Ohio.
a
RV RV RVLV LV LV
b c
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discussed and initiated before patientsare discharged from the
hospital.
Hemodynamic Status: Volume and Perfusion
Volume and perfusion statusprovide useful clues to a
patientscardiac performance and help shapethe treatment plan. Nurse
caregiversmust frequently reassess the patientshemodynamic status
to determinevolume and perfusion status. Volumestatus is determined
by assessing ifthe patient is wet, dry, or has a bal-anced fluid
level (ie, has hypervolemia,hypovolemia, or euvolemia,
respec-tively), and perfusion is assessed bydetermining if the
patient is cold,cool/lukewarm, or warm (ie, hasperfusion that is
very low, slightlylow, or normal, respectively). Evi-dence of
congestion includes thesigns of neck vein distension, ele-vated
pressure in the right internaljugular vein, positive
abdominal-jugular neck vein reflex, edema,ascites, and crackles
(rarely) and thesymptoms of dyspnea, orthopnea,and paroxysmal
nocturnal dyspnea.15
Nurses must be careful not to counton the presence of crackles
as an indi-
cator of congestion because chronicmovement of fluid into the
intersti-tium (common in patients with ahistory of chronic heart
failure) isassociated with increased lymphaticdrainage so that
crackles are absentand the alveoli remain relatively dry.16
Evidence of very low perfusionincludes symptomatic
hypotension,especially in patients receivingangiotensin-converting
enzyme (ACE)inhibitors, cool extremities (arms andlegs, not just
hands and feet), mentalobtundation or constant sleepiness,worsening
renal function (elevationin serum levels of creatinine andurea
nitrogen), hyponatremia, nar-row pulse pressure, and, most
impor-tant, a proportional pulse pressure of25% or less.15,16 Acute
care nurses
should be educated in calculating pro-portional pulse pressure.
The calcula-tion is simple to do and can provide
valuable information about cardiaccontractility and perfusion,
especiallywhen trends over time are assessed.
The formula to determine pro-portional pulse pressure is
(systolicblood pressure - diastolic bloodpressure)/systolic blood
pressure,resulting in a proportion or percent-age.16 An example of
a calculation ofproportional pulse pressure is (108 -66)/108 =
42/108 = 0.389 or 39%.
In a hemodynamic study16 of 50patients with a history of heart
fail-ure, 91% of patients with a propor-tional pulse pressure of
25% or lowerhad a cardiac index (calculated ascardiac output in
liters per minutedivided by body surface area insquare meters) of
less than 2.2; how-ever, systolic and mean arterial bloodpressure
were poorly correlated withcardiac index or stroke volume index.In
a study17 of hemodynamic profiles(wet, dry, cold, and warm) and
clini-cal characteristics of advanced heartfailure, a low
proportional pulse pres-sure was the only predictor of wetpatients,
and among wet patients,proportional pulse pressure was theonly
predictor of patients in the coldcategory. A patients
hemodynamicprofile should influence initiation ofpharmacological
and other treat-ment strategies and also guide theadjustment of
therapies during thehospitalization.
Of note, patients who are admit-ted in a congestive or wet state
witha high preload (passive stretch of
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 19
Table 6 Exacerbating factors in chronic heart failure that lead
to decompensation
Uncontrolled hypertensionAtrial fibrillation or flutter with
fast ventricular responseFrequent premature ventricular
contractions or ventricular tachycardiaAcute myocardial
ischemiaWorsening bundle branch block or intraventricular
conduction delay due to desynchro-
nized ventricular electrical cell conduction and myocyte
contraction Treatment of diabetes with thiazolidinediones (Actos or
Avandia)Treatment of arthritis, muscular, or pain conditions with
routinely administered
nonsteroidal anti-inflammatory drugs or high doses of aspirin
Concurrent infections (pneumonia, viral
illnesses)ObesityHyperthyroidism or hypothyroidismUntreated anemia
(hemoglobin
-
20 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
Figure 2 Acute decompensated systolic heart failure (SHF) or
diastolic heart failure (DHF) in patients with chronic heart
failure: initial treatment of Abbreviations: BNP, B-type
natriuretic peptide; EKG, electrocardiographic; INR, international
normalized ratio; IV, intravenous; PT, prothrombin time.*Treatment
decisions based on serum BNP results in acute decompensated heart
failure DO NOT apply to patients with chronic, stable heart failure
who are not acutely dyspneic.Profiles: patient is wet, dry, or has
a balanced fluid level (ie, has hypervolemia, hypovolemia, or
euvolemia, respectively), and is cold, cool/ lukewarm, or warm (ie,
has perfusion that isvery low, slightly low, or normal,
respectively).
Dyspnea and chest pain: if cardiac markersare positive and/or
EKG findings are abnormal:Follow Acute Coronary Syndrome
protocol.
Admit to hospital or23-hour observation/short-
stay unit on the basis of resultsof workup and signs and
symptoms
Admitto hospital for IV
and oral pharmacologicaland nondrug therapies and
monitoring; consider cardiacresynchronization, implantable
defibrillator, and/or surgicaltherapies; treat comorbid
factors that affectheart failure
BNP >600 pg/mL*
Meets Wet and Cold profileand systolic blood pressureis 100
pg/mL but 600 pg/mL*
DyspneaWorkup: history/physical examination; oxygen saturation;
laboratory tests: BNP, PT/INR, liver
function, basic metabolic profile, hematology, arterial
bloodgases, troponin or other markers of cardiac injury;
electrocardio-
gram, chest radiograph, and other tests on basis of history
Admit to coronary or intensive care unit
Consider invasive or noninvasivehemodynamically guided care
IV inotropic therapy may be warranted
No
Consider discharge home withinstructions to follow
up with primaryhealthcare provider
in 1-3 days
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myocardial fibers; reflects left ven-tricular end-diastolic
pressure andvolume) often have a high afterload(pressure the heart
must pumpagainst; reflects systemic vascularresistance, systolic
stress, and systolicimpedance) that impairs stroke vol-ume and is
reflected as a cool orlukewarm perfusion state. Whenhemodynamic
measurements wererecorded in 750 patients with heartfailure before
tailored therapy at alarge university teaching hospital,the mean
pulmonary artery occlusivepressure was 26 mm Hg (normal is4-12 mm
Hg; in heart failure treat-ment, the goal is 8-15 mm Hg) andthe
mean systemic vascular resistancewas 1640 dynes sec cm-5 (normalis
800-1200 dynes sec cm-5),15
reflecting a vasoconstricted state andthe need for vasodilator
therapy inaddition to diuresis and natriuresis(sodium
excretion).
Diagnostic TestsIn addition to results of tests done
at the time of admission (chest radi-ographs, arterial blood gas
levels,liver function tests, hematologic tests,electrocardiograms,
basic metabolicprofile) and findings on physicalexamination, the
results of point-of-care assays of serum levels of natri-uretic
peptides can be used to guidetreatment in patients with
acutedecompensated heart failure (Figure2). B-type natriuretic
peptide (BNP) issecreted mainly from the ventricularmyocardium in
response to elevationsin end-diastolic pressure and ventric-ular
volume expansion.18 Not onlycan rapid measurement of BNP aidin
diagnosis of heart failure,19-23 butBNP level can also be used to
assessclinical status and the effectivenessof therapies during an
admission foracute decompensation.24
Point-of-care BNP testing can bea useful adjunct in
determiningwhich patients are receiving effectivecare, which
patients are not progress-ing on the current treatment plan,and
which patients might be candi-dates for end-of-life care.
Nursesshould consider all components ofassessment of patients
(etiology,aggravating factors, risks, and clini-cal status) when
communicating andcollaborating with members of thehealthcare team
so that patientshave the best opportunity for carestrategies that
optimize outcomesand promote comfort.
Myths and Realities of Management
An algorithm provides a system-atic approach to decision making
aspatients with chronic heart failureare assessed and managed
during anacute exacerbation (Figure 2). Themyths associated with
managementof acute heart failure are replaced withevidence-based
actions that con-tribute to the best possible outcomes.
Myth 1: The Goals of Treatmentfor Acute and Chronic HeartFailure
Are Different
One of the hurdles in managementof heart failure is to overcome
themyth that the goals of managing acutedecompensated and stable
heart fail-ure are different. Today, it is impor-tant to gear
therapies toward reversalof ventricular remodeling.
Reversingventricular remodeling is importantregardless of whether
patients are instable condition or in a decompen-sated state.
Historically, the primarygoal of treatment of acute decom-pensated
heart failure was to quicklyreduce the circulating fluid volumeto
relieve patients of the pulmonaryand peripheral edema.
Diuretics
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 21
Consider discharge home
with instructions tofollow up with primary
healthcare providerin 1-3 days
Heart failure an unlikelycause; consider other causes:
pulmonary embolism, pneumothorax,pulmonary diseases,
pneumonia,
arrhythmias, liver or kidneydiseases
BNP 500 mL (DHF)
or 1000 mL (SHF) with normalrenal function or >250 mL
(DHF)
or 500 mL (SHF) with renal insufficiency)?
Is dyspnea resolving?
No
Yes
Yes
Consider comorbid conditions causing dyspnea If meets Wet and
Cold, Dry
and Cool to Cold, Wet and Coolto Cold, or Wet and Warmprofile:
treat as appropriate
dyspnea in the emergency department.
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have long been the standard type ofdrug used for decreasing
volumeand improving hemodynamic statusand signs and symptoms.25
Throughresearch studies, however, it waslearned that acute
intravenousdiuretic therapy was associated withmany hazards,
including increasedmortality. Nonpotassium-sparingdiuretic therapy
was associated withan increased risk of arrhythmic(sudden) death,
increased cardiacmortality, aggravated renal dysfunc-tion, further
activation of the renin-angiotensin and sympathetic nervoussystems
with a concomitant increasein systemic vascular resistance that
was compounded by a decrease incardiac output from a reduction
inpreload, and electrolyte imbalancesthat caused muscle
weakness,depression, reduced contractility(from reduced
conductivity), andperipheral vasoconstriction.26-31 Inpatients with
acute decompensation,preventing or limiting further activa-tion of
neuroendocrine systems byusing strategies that target
excessintravascular and extravascular vol-ume and vascular
resistance willhelp meet the overall goals of pre-venting
progression of and promotingreversal of ventricular remodeling.
Myth 2: Managing Fluid Overload Equals Use of Diuretics
Administration of intravenousand oral loop diuretic agents is
animportant therapy aimed at decreas-
in patients with mild to severe heartfailure, as summarized in
the consen-sus guidelines.10 Researchers reportedimprovements in
exercise tolerance,ejection fraction, and survival alongwith
decreased rehospitalizationrates.10 Therefore, diuretics are
nec-essary to relieve signs and symptomsbut should be used with ACE
inhibitortherapy for survival benefit and tocounterbalance the
alterations inrenal and adrenal mechanismsresponsible for sodium
and waterretention. Nurses must proactivelyrecommend increases in
dosage ofACE inhibitors based on the ACC/AHA practice guidelines10
during theacute hospitalization period so thatpatients dosing
regimens are on tar-get before the patients are dischargedfrom the
hospital.
Diuretics and Intravenous VasodilatorTherapy When patients are
admit-ted with a wet and lukewarm/coolor cold profile without
indications ofprofound hypoperfusion, a combi-nation of intravenous
diuretics andvasodilator therapy leads to improvedacute outcomes,
without the need forinotropic agents (Figure 2). Manystudies were
conducted in the late1970s and early 1980s in patientswith New York
Heart Associationfunctional class IV decompensatedheart failure to
study the effectivenessof intravenous diuretic and vasodila-tor
(nitroprusside and nitroglycerin)therapy in reducing filling
pressures(preload) and systemic vascularresistance (afterload) and
improvingcardiac output. The results indicatedthat nitroprusside
was a clinicallyeffective and powerful agent forreducing afterload
that also decreasedventricular systolic and diastolic vol-umes and
improved ventricular dias-
ing preload (through initial venodi-latation and then through
diuresisand natriuresis) and ultimately reliev-ing signs and
symptoms, but theseagents should not be used alone toimprove
overall morbidity and sur-vival in patients with heart failure.
Inorder to address increased afterloadassociated with both
exacerbation ofheart failure and intravenous loopdiuretic therapy,
pharmacologicaltherapies must include agents thatreduce
neuroendocrine activationand vasoconstriction because
thesemechanisms can worsen the heartfailure syndrome by worsening
ven-tricular remodeling.
Diuretics and ACE Inhibitor TherapyAlthough only limited data
are avail-able, when an ACE inhibitor wascombined with loop
diuretics, thecombination therapy reduced thepressor
(vasoconstriction) responseof diuretics.32 ACE inhibitors
reducedthe increase in plasma angiotensin II,thus decreasing the
sympathetic acti-vation (and associated deteriorationin left
ventricular pump function)that preceded the diuretic action
ofdiuretics.32
ACE inhibitors ultimatelydecreased reabsorption of sodiumin the
distal tubule and decreasedaldosterone stimulation in the adre-nal
glands.33,34 Many randomized,controlled research studies
wereconducted from the early 1980sthrough the mid-1990s that
addedan ACE inhibitor to diuretic therapy
22 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
One of the hurdles in management of heartfailure is to overcome
the myth that thegoals of managing acute decompensatedand stable
heart failure are different.
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tolic properties. It provided rapidsymptomatic relief for
patients andimproved, stabilized, and optimizedhemodynamic
parameters.35-39
Intravenous nitroglycerin isknown predominantly as an agent
forreducing preload. However, at highdoses, intravenous
nitroglycerinreduces systemic and pulmonaryvascular resistance. In
patients withdecompensated chronic heart failure,nitroglycerin was
less powerful thannitroprusside in reducing afterloadbut was
effective in reducing preload,increasing cardiac output, and
con-trolling signs and symptoms andhemodynamic
derangements.40-42
Table 7 is a summary of the doseranges, actions, and indications
of
vasoactive medications used in themanagement of patients with
acutedecompensated heart failure.43
As the overall goal of managingpatients with heart failure
hasshifted from improving hemody-namic status to improving
neuroen-docrine abnormalities in the hopethat ventricular
remodeling will befavorably affected, researchers havestudied the
effectiveness of intra-venous vasodilator therapy in modu-lating
the neuroendocrine axis. In arecent study44 of 34 patients
withdecompensated heart failure whoreceived intravenous diuretics
andvasodilator therapies (nitroprussideand ACE inhibitors) to
reduce pre-load and afterload, neurohormonal
activation (endothelin, norepinephrine, and BNP levels)
decreasedrapidly and was associated withimproved hemodynamic
status.Similar to results of studies con-ducted in previous
decades, in thisstudy,44 the mean cardiac indexincreased from 1.70
before treat-ment to 2.58 after treatment. Pul-monary artery
occlusive pressuredecreased from a mean of 31 to 18mm Hg, and
systemic vascularresistance decreased from a mean of1780 to 1109
dynes sec cm-5 frombefore to after treatment. Thisresearch provided
further evidencethat hemodynamic parameters inpatients at rest were
significantlymodulated by improving preload
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 23
Table 7 Intravenous vasoactive medications indicated in acute
decompensated heart failure43
Characteristic
Typical dose range
ActionVenodilatorArterial vasodilatorDiureticInotropic
Indication
Primary effectPreloadAfterloadDiuresisNatriuresisCardiac
outputStroke volume
Comments
Nitroglycerin
10-200g/min
XX (coronary)
Myocardialischemia, elevatedPAOP,
hypertension
mild
Rapid onset
Nitroprusside
0.1-5 g/kg perminute
XX
Hypertensive crisis,elevated PAOP,acute aortic or
mitral regurgitation
, indirectly
Risk coronary stealfrom hypotension,
assess for thiocyanate poisoning
Nesiritide
Bolus 2 g/kg then0.01 g/kg per
minute
XXX
Congestion andvasoconstriction
from acute decompensated
heart failure
, indirectly
More rapid onsetthan nitroglycerin,minimal dosageadjustment,
no
tachycardia
Milrinone
Bolus 50 g/kg* then0.375-0.75 g/kg per
minute
X
X
Very low cardiac output,high PAOP, pulmonary
hypertension
Long half-life, riskhypotension,
proarrhythmia
Dobutamine
2.5-15 g/kg per minute
X
Very low cardiac outputwith or without congestion or
hypotension
Assess for tachyphylaxis,tachycardia, ischemia,
proarrhythmia
Abbreviations and symbols: PAOP, pulmonary artery occlusive
pressure; X denotes that the drug has the specified action; denotes
decrease; denotes increase. Noentry indicates action or effect does
not occur.*Consider eliminating the bolus dose when systolic blood
pressure is 100 mm Hg or less; just begin infusion and wait 2 hours
to assess patient for desired effects (delayto peak effect if bolus
omitted).
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and afterload, rather than by usingagents that increased
contractilityand cardiac workload. In addition,decreased activation
of neuroen-docrine hormones might improveshort- and long-term
outcomes.
A newer vasodilator, nesiritide, isindicated for reducing
dyspnea andimproving hemodynamic status inpatients with acute
decompensatedheart failure. Nesiritide, a recombi-nant form of
human BNP, hasactions identical to those of theendogenous BNP
molecule.45 Nesiri-tide produced balanced arterial andvenous
vasodilatation that resultedin rapid reduction in ventricular
fill-ing pressures. This reduction wasmanifested clinically as a
dose-dependent decrease in pulmonaryartery occlusive pressure,
pul-monary artery pressures, and sys-temic blood pressure.46
Nesiritidecaused diuresis and natriuresis bysuppressing the
renin-angiotensin-aldosterone system.47
When intravenous nesiritidewas compared with
intravenousnitroglycerin during the first 72 hoursof signs and
symptoms in patientshospitalized with acute heart failure,47
the results favored nesiritide. Nesiri-tide produced a
significantly quickerand greater reduction in pulmonaryartery
occlusive pressure than didnitroglycerin. Patients reported
andcaregivers measured a greater reduc-tion in dyspnea when the
patientsreceived nesiritide rather than nitro-glycerin. The
combined actions ofvasodilatation, diuresis, and natri-uresis led
to preload and afterloadreduction to achieve the goal ofenhanced
cardiac output and reducedpulmonary and systemic congestion.The
investigators47 concluded thatnesiritide should be the drug of
choice
guidelines)10 may actually improvesigns and symptoms and quality
oflife by antagonizing mechanismsthat cause excessive sodium
andwater retention.
Myth 3: Low Systolic BloodPressure Requires Treatment With
Intravenous Inotropic Agents
Some myths are associated withinterventions when patients
withheart failure have low systolic bloodpressure. One belief is
that a systolicblood pressure of less than 90 mmHg requires
intravenous infusion ofinotropic agents. Unless the hypoten-sion is
severe (systolic blood pressure
-
of cardiac remodeling and improveclinical outcomes. Nurses must
edu-cate patients about the benefits ofmaintaining a low systolic
bloodpressure and adhering to core phar-macological therapies that
decreaseneuroendocrine activation anddecrease blood pressure.
Additionally, use of intravenousinotropic agents is not
supported inpatients in an acute setting exceptas temporary
treatment of diuretic-refractory complex decompensation.48
Intravenous inotropic therapies(continuous or intermittent
infusionof milrinone or dobutamine) havebeen associated with
increased mor-tality when used in patients requiringinotropic
support, even though theseagents improve hemodynamic sta-tus10
(Table 7). In an effort to learn ifa short-term infusion (48
hours)might lead to short- or intermediate-term improvements in
patients hos-pitalized for exacerbation of heartfailure who had a
wet and cool tocold profile but in whom intravenousinotropic
support was not essential,the study called Outcomes of aProspective
Trial of Intravenous Mil-rinone for Exacerbations of ChronicHeart
Failure (OPTIME-HF) wasconducted.49 Investigators random-ized
patients to receive short-termintravenous milrinone or placebo.The
2 groups did not differ signifi-cantly in hospital and 60-day
posthos-pitalization mortality or in the mediannumber of days
patients were hospi-talized for cardiovascular causes inthe first
60 days after discharge. Inaddition, sustained hypotension ornew
atrial arrhythmias were signifi-cantly more likely to develop in
thepatients receiving milrinone than inthe patients receiving
placebo. Theresults of this research, that receiving
an inotropic agent without clear evi-dence of significant
hemodynamiccompromise does not enhance clini-cal or economic
outcomes, led to atempering of the use of intravenousinotropic
agents unless absolutelywarranted.
Further, concomitant use of -blocker (-antagonist) and
intra-venous dobutamine (-agonist)therapies is controversial. The
phar-macological response of dobutamineis inhibited in patients
receiving highdoses of -blockers because bothdrugs compete for the
same -adren-ergic receptors.48 This conflict isespecially apparent
with carvedilolbecause it blocks both 1 and 2receptors.48,50
Myth 4: ACE Inhibitors and -Blocker Therapies Should
BeTemporarily Decreased or Dis-continued During Decompensation
Another belief is that ACE inhibit-ors and -blocker therapies
must bedecreased or discontinued or shouldnot be initiated when the
patientsblood pressure is low. These agentshelp suppress
maladaptive neu-roendocrine responses that lead toincreased wall
stress, ventricularhypertrophy, and worsening cardiacremodeling and
cardiac output.51
Unless symptomatic low blood pres-sure occurs or intravenous
vasodila-tor agents are used, core oraltherapies used to manage
patientswith chronic heart failure should bemaintained whenever
possible.Blood pressure may not decrease orthe reduction may be
self-limitingwhen vasodilator (ACE inhibitor orangiotensin-receptor
blocker) and -blocker therapies are initiated andmaintained in
patients with a lowbaseline blood pressure (85-90 mm
Hg). If blood pressure decreases butindications of hypoperfusion
areabsent, nurses should assess patientsfor hypovolemia (from
overdiuresis).In addition, nurses must communi-cate expected
effects of core agentsfor treating heart failure to patientsso that
patients are prepared forpotential dizziness or other symp-toms
associated with drug actionsand interactions and understand
theself-limiting nature of these changes.52
Myth 5: Once Core Therapies Are Unsuccessful, They ShouldNot Be
Tried Again
Some may believe that once ACEinhibitor or -blocker therapy
isunsuccessful in a patient because oflow blood pressure, these
therapiesshould not be tried again. Assessmentand correction of
mechanisms thatcause low blood pressure (such asinitiating ACE
inhibition when theserum level of sodium is less than130 mmol/L)
may make the precedingstatement a false claim. Core
pharma-cological therapies known to improvehealth-related outcomes
can be suc-cessfully implemented withoutepisodes of low blood
pressure in mostpatients, as evidenced by low dropoutrates in
randomized controlled stud-ies. The acute care episode is a
perfectsetting for trying ACE inhibitors or-blockers again, when
appropriate,because patients can be carefullymonitored and
resources are readilyavailable. Low-dose, shorter-actingagents in
each drug class (such ascaptopril and carvedilol) are the drugsof
choice in patients with a history oflow blood pressure.
Nursing ConsiderationsIn addition to assessment of
patients, nursing actions that are cen-
26 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 by guest on
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tral to patients outcomes are admin-istration of medications,
evaluationof treatment effectiveness, and edu-cation and ongoing
communicationwith patients, patients families, andthe healthcare
team. If a patientsdyspnea improves but weight loss,urination,
intake and output, orproportional pulse pressure do notimprove,
nurses must be assertive inproviding timely communication ofthese
findings to peers and the physi-cian team because delays can
diminishhigh-quality care, hinder achievementof clinical goals, and
harm the hospi-tal financially. Table 8 outlines nurs-ing actions
and goals that reflectcritical thinking and foster commu-nication
when managing patientswith heart failure.
Nurses often take an active rolein prompting initiation and
adjust-ment of medication therapies. Nursesmust know the actions,
dosing, andeffects of heart failure medicationsand must promote
decisions that willaffect the overall goal of managementof heart
failure (reversal of cardiacremodeling). This goal can beachieved
during the acute hospital-ization by adding, maintaining,
andincreasing dosages of vasodilators(ACE inhibitors) and
maintaining-blocker therapy per consensusrecommendations. Nurses
must notfocus on pharmacological therapiesthat simply improve
symptoms (eg,diuretics), because these therapiesalso increase
cardiac workload, acti-vate adverse neuroendocrine systems,and
increase mortality. When indoubt about therapeutic priorities,it is
always helpful to reassess thepatients clinical status. When
patientshave congestion and inadequate organor peripheral perfusion
(cool/luke-warm to touch), intravenous diuretic
blood pressure unless the patient hasorthostatic hypotension or
othersigns and symptoms reflectinghypoperfusion or
hypovolemia.Nurses must use multiple clinicalparameters, not just
blood pressurevalues, to determine that withhold-ing drugs will
benefit a patients clin-ical status.
Critical evaluation of eachpatients progress involves
ongoingassessment of electrolyte and fluid
and vasodilator therapy (along withmaintenance of prehospital
-blockertherapy) may decrease afterload andpreload to improve
perfusion andcardiac index. When profoundhypoperfusion compromises
organfunction, an intravenous inotropicagent may be the preferred
agent ofchoice (Figure 2). It is especiallyimportant for nurses not
to withholddoses of vasodilators, -blockers, ordiuretics because of
a patients low
CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 27
Table 8 Nursing considerations: critical thinking and
communication
Nursing role
Critically evaluateeffectiveness ofinterventions
Communicate topatient, patientsfamily and teammembers
Actions/goals
Monitor vital signs; maintain systolic blood pressure >80 mm
Hgand 1.8 mg/dL)Sodium >138 and
-
status. Such assessment is especiallyimportant in managing
patientswith heart failure because activationof neuroendocrine
systems, renaldysfunction, and current drug thera-pies may disrupt
the fine balance ofelectrolytes and cause shifts insodium,
potassium, calcium, andmagnesium.53 It is important fornurses to
develop and use advancedmeasurement and cardiac ausculta-tion
skills to monitor fluid status(eg, assessment of jugular
venouspressure and the presence or wors-ening of systolic murmurs
and S3 orS4 heart sounds) because patientsmay still have
intravascular volumeoverload after obvious interstitialfluid
retention (crackles, edema) dissi-pates. Freedom from congestion
inthe early weeks after hospital dis-charge was an independent
predictorof survival in patients hospitalizedwith New York Heart
Associationfunctional class IV symptoms.54 Inorder to prevent
readmission andmaintain clinical stability, patientswho have
evidence of clinical andsubclinical congestion before dis-charge
should be considered foraggressive follow-up
(cardiologistspecializing in heart failure) andinterventions aimed
at promotingeuvolemia (eg, increased restrictionin sodium diet or
fluid intake, diureticself-management program, heartfailure nurse
clinic).
Serum BNP values provideanother mechanism for monitoringfluid
status in the early hours after
hospitalization and for assessingpatients outcomes. In patients
withsymptomatic, functional class III orIV heart failure who were
undergo-ing tailored therapy for their con-gested state, hourly
changes in BNPlevels were significantly correlatedwith hourly
changes in pulmonaryartery occlusive pressure.55 WhenBNP levels at
initial hospital assess-ment and within 24 hours of dischargeor
death were compared as an out-come variable,24 successfully
treatedpatients (as compared with patientswho died during the index
hospital-ization or were readmitted within 30days of discharge) had
a meandecrease in BNP level of 216 pg/mL.Patients who were
readmitted or diedhad levels that increased during thecourse of
hospitalization.
Last, communication betweenhealthcare providers and patientsand
patients families about thepatients clinical status and manage-ment
plan is essential. Proactivelyassessing the knowledge base
ofpatients and their families to promoteunderstanding of the
current plan ofcare and asking if there are questionscan aid
communication and infor-mation sharing. Information sharingand
ongoing communication withpatients and their families
enhancesperceived control, potentially decreas-ing stress.56 This
communication isespecially important because loss offunctional
mobility and role changesthat occur with the progression ofheart
failure lead to a perceived loss
of control57 that can ultimately affectcoping, lifestyle
modifications, andbehaviors. Examples of importantfactors to
address in patients educa-tion are found in the first item inTable
3 and in Table 4. It is well rec-ognized that improving
patientsknowledge of heart failure and pro-viding support,
encouragement, andpositive reinforcement of self-carebehaviors
improves outcomes inpatients with heart failure.58
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Nurses must use multiple clinical parameters,not just blood
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apatients clinical status.
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30 CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004
CE Test Form
Evidence-Based Practice forAcute Decompensated Heart Failure
Objectives:
1. Identify the core drug therapies for decompensated heart
failure
2. Describe the role of B-type natriuretic peptide in
decompensated heart failure
3. Explain the pharmacological management of decompensated heart
failure
Mark your answers clearly in the appropriate box. There is only
1 correct answer. You may photocopy this form.
To receive CE credit for this test (ID C046), mark your answers
on the form below, complete the enroll-ment information, and submit
it with the $12 processing fee (payable in US funds) to the
American Asso-ciation of Critical-Care Nurses (AACN). Answer forms
must be postmarked by December 1, 2006. Within 3to 4 weeks of AACN
receiving your test form, you will receive an AACN CE
certificate.
This continuing education program is provided by AACN, which is
accredited as a provider of continuing education in nursing by
theAmerican Nurses Credentialing Centers Commission on
Accreditation. AACN has been approved as a provider of continuing
educa-tion by the State Boards of Nursing of Alabama (#ABNP0062),
California (01036), Florida (#FBN2464), Iowa (#332),
Louisiana(#ABN12), and Nevada. AACN programming meets the standards
for most other states requiring mandatory continuing
educationcredit for relicensure.
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Mail this entire page to AACN, 101 Columbia, Aliso Viejo, CA
92656, (800) 899-2226
Test ID: C046Test writer: John P. Harper, RN, MSN, BC
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Passing score: 9 correct (75%)Category: A
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CE Test Instructions
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CRITICALCARENURSE Vol 24, No. 6, DECEMBER 2004 31
7. Which of the following is not a direct effect ofnesiritide?a.
Decreased preloadb. Decreased afterloadc. Increased diuresisd.
Increased contractility
8. What is the typical dosage range of nesiritide in
thetreatment of acute decompensated HF?a. 0.001 ug/kg/minb. 0.01
ug/kg/minc. 0.1 ug/kg/mind. 1 ug/kg/min
9. Which of the following drugs inhibits renin releaseand
indirectly decreases proximal reabsorption ofsodium?a. Diureticsb.
-Blockersc. ACE inhibitorsd. Digitalis
10. Which one of the following medications has beenassociated
with increased mortality when used inpatients requiring inotropic
support?a. Dobutamineb. Dopaminec. Digoxind. Levophed
11. Which of the following goals indicates effective
HFmanagement?a. Resting heart rate 4 L/min/m2
c. Pulmonary artery occlusive pressure
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