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Signs and symptoms:

Dyspnea on exertion (DOE) or at rest, fatigue, decreased exercise tolerance, weakness, orthop- nea (unable to lie flat; may need to sleep on pillows or sitting in a chair), paroxysmal nocturnal dyspnea, wheezing, cough, cyanosis, irregular or rapid HR, sudden weight gain from fluid retention, lower extremity edema, abdominal distention, nausea, early satiety, and nocturia. Associated indicators include chest/anginal pains, palpitations, near-syncope, and syncope. Low-output symptoms include positional lightheaded- ness, weakness, mental status changes, and decreased urine output.

Physical assessment:

Decreased or elevated blood pressure (BP), dysrhythmias, tachycardia, tachypnea, increased venous pulsations, pulsus alternans (alternating strong and weak heartbeats), increased central venous pressure (CVP), jugular venous distention, crackles (rales), wheezes, decreased breath sounds, cardiac gallop and/or murmur, hepatomegaly, ascites, and pitting edema in dependent areas (lower extremities, sacrum).

History/risk factors:

CAD, hypertension, DM, OSA or

other pulmonary disease, recent IV fluid infusions, surgery,

pregnancy, recent/current infectious illness, pneumonia, non-

adherence to medication or diet regimen, obesity, hypercho-

lesterolemia, and recent nonsteroidal antiinflammatory

drug or COX-2 inhibitor use. In addition, see “Other causes

of heart failure,” earlier.

PART I: Medical-Surgical Nursing

Oximetry/arterial blood gas (ABG) values:

Measure oxygen levels in the blood. ABGs assess oxygen, carbon dioxide, bicarbonate, and pH levels. Hypoxemia and metabolic/

respiratory acidosis often occur in acute myocardial ischemia, cardiac arrest, and severe HF. Overnight (sleep) oximetry evaluates obstructive sleep apnea.

Serum blood urea nitrogen (BUN), creatinine:

Elevated in renal insufficiency and chronic kidney disease. It may be ele- vated in poor renal perfusion associated with low cardiac output and hypotension. Treatment with diuretics, angiotensin- converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or aldosterone antagonists also affects these renal markers.

Serum electrolytes:

Altered in multiple cardiac and renal conditions/diseases. Careful monitoring is essential to avoid cardiac arrest due to dysrhythmias caused by alterations in potassium, magnesium, calcium, sodium, and phosphorous.

Cardiac enzymes:

Mild elevation in cardiac troponins (with normal creatinine kinase [CK]) is common in patients

Liver function tests, including serum aspartate amino- transferase and serum bilirubin:

May be elevated in patients with hepatic congestion.

Brain natriuretic peptide (BNP):

Released from the ventri- cles in response to wall stress. This test is useful in differentiat- ing HF from other causes of dyspnea, including pulmonary disease. Negative BNP (less than 100 pg/mL) suggests non-HF etiology. When used in conjunction with standard clinical assessment, elevated BNP may support diagnosis of HF and evaluate the patient’s response to treatment.

Digoxin level:

The goal in patients with HF is a level less than 1.0 ng/mL. Hypokalemia and impaired renal function can predispose patients to digoxin toxicity.

Complete blood count (CBC):

May reveal decreased hemoglobin (Hgb) and hematocrit (Hct) in the presence of anemia.

Thyroid-stimulating hormone level:

To rule out hyperthy- roidism or hypothyroidism, either of which may contribute to HF and dysrhythmias.

Nursing Diagnosis

Impaired Gas Exchange

related to alveolar-capillary membrane changes (fluid accumulation in the alveoli)

Desired Outcome:

Within 30 min of treatment/intervention, the patient has adequate gas exchange as evidenced by normal breath sounds and skin color, presence of eupnea, HR 100 bpm or less, Pa

O2

80 mm Hg or higher, and Pa

CO2

45 mm Hg or less.

ASSESSMENT/INTERVENTIONS RATIONALES

Assessalllungfieldsforbreathsounds. Thepresenceofcrackles(rales)maysignalalveolarfluidcongestionand

systolicdysfunctional(left-sided)HF.Decreasedbreathsoundssignifyfluid

overloadordecreasedventilation.Wheezingmaysignifyassociated

bronchitisorasthma.

MonitoroximetryandABGvaluesandreportsignificantfindings. Oximetryof92%orlessandthepresenceofhypoxemia(decreasedPaO2)and

hypercapnia(increasedPaCO2)signifydecreasedoxygenation.

Assessrespiratoryrate(RR),lungexcursion,useofaccessory

muscles,airhunger,mentalstatuschanges,cyanosis,and

changesinHRorBP.Reportsignificantchanges.

Thesearesignsofincreasingrespiratorydistressthatrequireprompt

intervention.

AssistthepatientintohighFowler’spositionwiththeheadofbed

(HOB)up90degrees.

Thispositiondecreasesworkofbreathing,reducescardiacworkload,and

promotesgasexchange.

Teachthepatienttotakeslow,deepbreaths. Takingdeepbreathsincreasesoxygenationtothemyocardiumandimproves

prognosis.Hypoxiaaddsstresstothealreadydistressedmyocardium.

Administeroxygenasprescribed.Deliveroxygenwithhumidity. InADHF/pulmonaryedema,high-flowO2maybegiveneitherbynon- rebreathingmask,positiveairwaypressuredevices,orendotracheal

intubationandmechanicalventilation.Oncestabilized,O2istitratedto

keeppulseoximetryreadingshigherthan92%.

Humidityhelpspreventoxygen’sconvectivedryingeffectsonoralandnasal

mucosa.

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ASSESSMENT/INTERVENTIONS RATIONALES

Administerdiureticsasprescribed. Diureticspromotenormovolemiabyreducingfluidaccumulationandblood

volume.Fluidoverloaddecreasesperfusioninthelungs,causing

hypoxemia.

MonitorK+levels. Thereispotentialforhypokalemia(K+lessthan3.5mEq/L)inpatientstaking

somediuretics,suchasfurosemideandmetolazone.

Administervasodilatorsasprescribed. Vasodilatorsincreasevenouscapacitance(dilation)anddecreasepulmonary

congestion,whichwillimprovegasexchange.

Hydralazineisanoralvasodilatorandafterloadreducer.Itisusedin

combinationwithnitratesinpatientswhoareACEinhibitor/ARBintolerant

becauseofrenaldysfunction.ItimprovesmortalityandHFsymptomstoa

lesserdegreethanACEinhibitorsandcancausereflextachycardia.

Nitratesarecoronaryvasodilatorsusedinconjunctionwithhydralazine(see

above).Theyarealsousedinischemicheartdiseaseasantianginaldrugs.

ACE inhibitors(enalapril,lisinopril,benazepril,captopril,quinapril,ramipril)

suppresseffectsoftherenin-angiotensinsystembyreducingangiotensinII

andcausingdecreasedaldosteronesecretion.ThesedrugslowerBPand

reducepreloadandafterload,decreasingworkoftheleftventricle.

Angiotensin II receptor antagonists(ARBs—losartan,valsartan,candesartan)

areusedforpatientswhodonottolerateACEinhibitorsbecauseofcough

causedbybradykininrelease.

Asindicated,haveemergencyequipment(e.g.,airway,manual

resuscitationbag)availableandfunctional.

PatientswithseverelydecompensatedHFmaysuffercardiacarrest.

Asindicated,preparetotransferthepatienttoICU. Thepatientmayrequireinvasiveand/orclosermonitoring.

Nursing Diagnosis

Excess Fluid Volume

related to compromised regulatory mechanisms occurring with decreased cardiac output

Desired Outcomes:

Within 1 hr of intervention/treatment, the patient demonstrates less shortness of breath and has output greater than intake on intake and output (I&O) monitor- ing. Within 1 day of treatment/intervention, edema is 1+ or less on a 0-4+ scale. Weight becomes stable within 2-3 days.

ASSESSMENT/INTERVENTIONS RATIONALES

AtfrequentintervalsassessI&O,includinginsensiblelossesfrom

diaphoresisandrespirations.

Decreasingurinaryoutputcansignaldecreasedcardiacoutput,which

decreasesrenalbloodflow.

Assessdailymorningweight;recordandreportsteadylossesorgains. Thisassessmenthelpsidentifyfluidretentionandfluidloss,enabling

titrationofdiuretics.

Assessforedema(interstitialfluids),especiallyindependentareassuch

astheanklesandsacrum.

Thepresenceofweightgainandedemaisakeydeterminantoffluid

retention.Ifdiligentassessmentismaintainedandearlyintervention

ispracticed,theoccurrenceofrehospitalizationcanbedecreased

dramatically.

Assesstherespiratorysystemforindicatorsoffluidextravasation,such

ascrackles(rales)orpink-tinged,frothysputum.

Thesearesignsoffluidvolumeexcessandsystolicdysfunction

(left-sided)HF.

Monitorforjugularveindistention,peripheraledema,andascites. Theseareotherindicatorsoffluidoverload.

Monitorlaboratoryresultsforincreasedurinaryspecificgravity,

decreasedHct,increasedurineosmolality,hyponatremia,

hypokalemia,andhypochloremia.

Thesefindingsareindicatorsoffluidimbalance.

PART I: Medical-Surgical Nursing

MonitorIVrateofflow.Useaninfusioncontroldevice. ThesemeasuresareessentialtopreventvolumeoverloadduringIV

infusion.

Unlesscontraindicated,provideicechipsoricepops.Recordamounton

theI&Orecord.Providefrequentmouthcaretoreducedrymucous

membranes.

Thesemeasureshelpthepatientcontrolthirstwhileprovidingminimal

amountsoffluid.Note:Somecarecentersadvocatesmallamounts

ofroom-temperaturewaterinsteadbecauseitmayrelievethirst

better.

Administerdiureticsasprescribed,andrecordthepatient’sresponse. Diureticspromotenormovolemiabyreducingfluidaccumulationand

bloodvolume.

Loop diuretics(furosemide,bumetanide,torsemide):Theseagents

promoteexcretionofwaterandsodium,reducepreload,andprevent

fluidretention.InADHF,thesediureticsareadministeredviaIVbolus

orindripformuntilstabilizationoccurs.Thesedrugscancause

neurohormonalactivationandaggravatepreexistingrenal

dysfunctionorhypokalemia.

Thiazide diuretics(hydrochlorothiazide,metolazone):Hydrochlorothiazide

maybeusedformildfluidretention.Metolazoneisapotentdrug

that,whengiven12hrbeforeloopdiuretics,markedlypotentiates

diuresisandthereforeisreservedformoreseverevolumeoverload

inADHForlate-stageHF.Hyponatremia,hypokalemia,and

worseningofrenalfunctionmayoccurandnecessitatecareful

assessment.

Administermorphinesulfateifprescribed. Morphineinducesvasodilationanddecreasesvenousreturntothe

heart.

Teachpatientsandfamiliesabouttheimportanceofadheringtoa

low-sodiumdiet.

Hypernatremiacanpromoteexcessfluidretention.A2-g-per-day

sodiumdietisrecommendedformostpatients.

Nursing Diagnosis

Risk for Decreased Cardiac Tissue Perfusion

related to interrupted blood flow occurring with decreased cardiac output

Desired Outcome:

By at least the 24-hr period before hospital discharge, the patient has adequate tissue perfusion as evidenced by BP within 20 mm Hg of baseline BP; HR 100 bpm or less with regular rhythm; RR 20 breaths/min or less with normal depth and pattern (eupnea); brisk capillary refill (less than 2 sec); and significant improvement in mental status or orientation to person, place, and time.

ASSESSMENT/INTERVENTIONS RATIONALES

AssessBPq15minormorefrequentlyifunstable.Bealerttodecreases

greaterthan20mmHgoverpatient’sbaselineorassociated

changessuchasdizzinessandalteredmentation.

HypotensionisasideeffectofmanyHFmedications,aswellasa

consequenceofaggressivediuresis.Carefulmonitoringisessentialto

avoiddecreasedperfusiontovitalorgans.

AssessHRq15-30min.Monitorforirregularities,increasedHR,or

skippedbeats.

Thesesignsmaysignaldecompensationanddecreasedfunctionofthe

heart.

Assesstheextremitiesforpulsepresenceandamplitude,capillaryrefill,

edema,color,andtemperature.

Decreasedpulseamplitude,delayedcapillaryrefill(morethan

2sec),pallor,andcoolnessareindicatorsofperipheral

vasoconstriction(fromSNScompensation).Edemaisevidence

offluidoverload.

Reportanyassessmentchangesimmediatelytothehealthcare

provider.

Significantalterationsmaybelifethreatening.

Assessforrestlessness,anxiety,mentalstatuschanges,confusion,

lethargy,stupor,andcoma.Institutesafetyprecautionsaccordingly.

Theseareindicatorsofdecreasedcerebralperfusionandhypoxiaand

shouldbeaddressedpromptlyforrapidintervention.

PART I

MEDICAL-SURGICALNURSING:Cardiovascular Care Plans DecreasedCardiacOutput

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ASSESSMENT/INTERVENTIONS RATIONALES

Administerinotropicmedicationsandvasodilatorsasprescribed.

Monitoreffectsclosely.Bealerttoproblemssuchashypotension

andirregularheartbeats.

IVinotropicmedications(dobutamine,dopamine,milrinone)increase

strengthofcontractionsandarereservedforuseinADHF-associated

low-cardiacoutputandcardiogenicshockuntilthepatientisstabilized.

Theymaybeusedlongerterminadvanced-stageHFasabridgeto

transplantationorforpalliationofsymptoms.Usemaybeassociated

withincreasedmortalityandventriculardysrhythmias.Administration

ofinotropicmedicationsmayrequiretransfertothecoronarycareunit

(CCU)tomonitorforhemodynamiceffectsanddysrhythmias.

IVvasodilators(nitroglycerin[NTG],nitroprusside,nesiritide)areusedin

ADHFtodecreasecardiacworkloadbyreducingventricularfilling

pressuresandsystemicvascularresistance(SVR,afterload).These

medicationsareavoidedinlow-outputHF,cardiogenicshock,and

systolicbloodpressure(SBP)lessthan90mmHg.

- Nesiritide:Balancedarterialandvenousvasodilator.Thismedication

canalleviateacutedyspneaandreducepulmonarycapillarywedge

pressure(PCWP)withinthefirst30minoftherapy.Itpromotes

diuresisandnatriuresisbutdoesnotreplaceneedfordiuretic

therapy.Itimprovescardiacoutputbyoff-loadingtheheartand

decreasesneurohormonalactivation.ItdoesnotrequireCCU

monitoring.

- NTG:Arterialandvenousvasodilator.ItalsoreducesPCWPandmay

requireICU/CCUmonitoring.Becauseoftachyphylaxis(tolerance),

patientsmayneedescalatingdosestoachievethedesiredeffect.

- Nitroprusside:Potentarterialandvenousvasodilatorandafterload

reducer.Itmustbeadministeredinintensivecareduetotheneedfor

continualhemodynamicmonitoring.

- Morphine sulfate:AcoronaryvasodilatorthatmaybegiveninADHF

oracutepulmonaryedematodecreaseanxietyandworkofbreathing

andtorelieveanginaifischemicheartdiseaseispresent.

Nursing Diagnosis

Decreased Cardiac Output

related to negative inotropic changes in the heart (decreased cardiac contractility)

Desired Outcomes:

By at least the 24-hr period before hospital discharge, the patient exhibits adequate cardiac output as evidenced by SBP at least 90 mm Hg, HR 100 bpm or less, urinary output at least 30 mL/hr (0.5 mL/kg/hr), stable weight, eupnea, normal breath sounds, and edema 1+ or less on a 0-4+ scale. By at least 48 hr before hospital discharge, the patient is free of new dysrhythmias, does not exhibit significant changes in mental status, and remains oriented to person, place, and time.

ASSESSMENT/INTERVENTIONS RATIONALES

Assessforjugularvenousdistention,extraheartsoundssuchasS3,

changesinmentalstatusorlevelofconsciousness,cool

extremities,hypotension,tachycardia,andtachypnea.

Theseareindicatorsofdecreasedcardiacoutput,whichshouldbereported

promptlyfortimelyintervention.

Assesslungsforadventitiousbreathsoundsandshortnessofbreath. Dyspnea,crackles,andshortnessofbreathsignalfluidaccumulationinthe

lungsandmaybeadirectindicatorofventricularfailureanddecreased

cardiacoutput.CardiacoutputdecreasesasHFprogresses.

MonitorI&O;weighthepatientdaily. Decreasingurineoutputandweightgaincanoccurasaresultofdecreased

cardiaccontractility,whichcancausedecreasedrenalperfusionand

fluidretention.

PART I: Medical-Surgical Nursing

Assessforperipheral(sacral,pedal)edema. Edemacanoccurwithdiastolicdysfunction(right-sided)HF/myocardial

infarction.

Assistwithactivitiesofdailylivingandfacilitatecoordinationof

healthcareproviders,allowing90minforundisturbedrest.If

necessary,limitvisitors.

Restdecreasescardiacworkload.

Administermedicationsasprescribed,suchasbeta-blockers,

calciumchannelblockers,andantidysrhythmicagents.

Beta-blockers(metoprololXL)andalpha/beta-adrenergic blockers

(carvedilol):BlockeffectsofSNSandtoxiceffectsofneurohormoneson

themyocardium.ThesemedicationsdecreaseHRandBP,thereby

decreasingcardiacworkload.

Calcium channel blockers:MaybeusedindiastolicHFtoassistwith

relaxationandfillingandreduceoutflowtractobstruction(hypertrophic

cardiomyopathy).Exceptforamlodipineorfelodipine,calciumchannel

blockersareavoidedinLVsystolicdysfunctionbecausetheydecrease

cardiaccontractility.

AmiodaroneisanexampleofanantidysrhythmicgivenforpatientswithHF.

Explainthepotentialfordysrhythmiamanagementunderthe

guidanceofanelectrophysiologist/cardiologist.

Dysrhythmiashavebecomeamajorfactorinquality-of-lifeissuesand

rehospitalizationinpatientswithHF.Manyofthesepatientsrequirean

implantablecardioverter-defibrillator(ICD)becauseofrepeated

life-threateningepisodesofventriculartachycardiafromanirritable

myocardium.Patientswithventricularasynchrony,asseeninbundle

branchblocks,maybenefitfromabiventricularpacer.Pacingeach

ventricleinsynchronymayresultinbettercardiacoutput.

Assistthepatientintoapositionofcomfort,usuallysemi-Fowler’s

position(HOBup30-45degrees).

Thispositiondecreasesworkofbreathingandreducescardiacworkload.

Nursing Diagnosis

Activity Intolerance

related to imbalance between oxygen supply and demand occurring with a decrease in cardiac muscle contractility

Desired Outcome:

During activity, the patient rates perceived exertion at 3 or less on a 0-10 scale and exhibits cardiac tolerance to activity as evidenced by RR 20 breaths/min or less, SBP within 20 mm Hg of resting range, HR within 20 bpm of resting HR, and absence of chest pain and new dysrhythmias.

ASSESSMENT/INTERVENTIONS RATIONALES

Assessthepatient’sphysiologicresponsetoactivityandreport

significantfindings.

Chestpain,newdysrhythmias,increasedshortnessofbreath,HR

increasedgreaterthan20bpmoverrestingHR,andSBPgreaterthan

20mmHgoverrestingSBParesignificantfindingsofdecreased

cardiacoutputorcardiacfailurethatcanmanifestduringactivity.

Askthepatienttorateperceivedexertion(RPE)(seep.62fora

description).

Optimally,patientsshouldnotexperienceRPEofmorethan3.Ifthis

happens,intensityoftheactivityshouldbedecreasedanditsfrequency

increaseduntilRPEof3orlessisachieved.

Assessvitalsignsq4h,andreportsignificantfindings. FindingssuchasirregularHR,HRgreaterthan100bpm,ordecreasingBP

maybesignsofcardiacischemia.

Beforehospitaldischargeteachthepatientself-measurementofHR

forgaugingexercisetolerance.

AnHRthatistoohighincreasesmyocardialO2demand;anHRthatis

toolowmaycausemoreischemia.Patientsshoulduseanexertion

scaleandapainscaletogaugeexercisetoleranceandensurethat

HRislessthan20bpmoverbaselineorasprescribedbythehealth

careprovider.