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Fluids & Electrolytes
Sixth Edition
0 . Wolters Kluwer Phb6clph!a • 8albm0~ • New Yotk • london Buenos A11H • Hong Kong • sydney • Tol<yo
AcquisitionsEditor:ShannonW.MageeProductDevelopmentEditor:MariaM.McAveySeniorMarketingManager:MarkWiraghEditorialAssistant:ZacharyShapiroProductionProjectManager:MarianBellusDesignCoordinator:ElaineKasmerManufacturingCoordinator:KathleenBrownPrepressVendor:AbsoluteService,Inc.
SixthEdition
Copyright©2015WoltersKluwerHealthCopyright©2010LippincottWilliams&Wilkins
Allrightsreserved.Thisbookisprotectedbycopyright.Nopartofthisbookmaybereproducedortransmittedinanyformorbyanymeans,includingasphotocopiesorscanned-inorotherelectroniccopies,orutilizedbyanyinformationstorageandretrievalsystemwithoutwrittenpermissionfromthecopyrightowner,exceptforbriefquotationsembodiedincriticalarticlesandreviews.MaterialsappearinginthisbookpreparedbyindividualsaspartoftheirofficialdutiesasU.S.governmentemployeesarenotcoveredbytheabove-mentionedcopyright.Torequestpermission,pleasecontactWoltersKluwerHealthatTwoCommerceSquare,2001MarketStreet,Philadelphia,PA19103,[email protected],orviaourwebsiteatlww.com(productsandservices).
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Fluids&electrolytesmadeincrediblyeasy!/clinicaleditor,LauraWillis.—Sixthedition.p.;cm.
Fluidsandelectrolytesmadeincrediblyeasy!Includesbibliographicalreferencesandindex.ISBN978-1-4511-9396-1I.Willis,Laura,1969-editor.II.LippincottWilliams&Wilkins,issuingbody.III.Title:Fluidsandelectrolytesmadeincrediblyeasy![DNLM:1.Water-ElectrolyteImbalance—Nurses’Instruction.2.Water-ElectrolyteBalance—Nurses’Instruction.WD220]RC630616.3’9920231—dc23
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considerationof,amongotherthings,age,weight,gender,currentorpriormedicalconditions,medicationhistory,laboratorydata,andotherfactorsuniquetothepatient.Thepublisherdoesnotprovidemedicaladviceorguidanceandthisworkismerelyareferencetool.Healthcareprofessionals,andnotthepublisher,aresolelyresponsiblefortheuseofthisworkincludingallmedicaljudgmentsandforanyresultingdiagnosisandtreatments.Givencontinuous,rapidadvancesinmedicalscienceandhealthinformation,independentprofessionalverificationofmedicaldiagnoses,
indications,appropriatepharmaceuticalselectionsanddosages,andtreatmentoptionsshouldbemadeandhealthcareprofessionalsshouldconsultavarietyofsources.Whenprescribingmedication,healthcareprofessionalsareadvisedtoconsulttheproductinformationsheet(themanufacturer’spackageinsert)accompanyingeachdrugtoverify,amongotherthings,conditionsofuse,warnings,andsideeffectsandidentifyanychangesindosagescheduleorcontradictions,particularlyifthemedicationtobeadministeredisnew,infrequentlyused,orhasanarrowtherapeuticrange.Tothemaximumextentpermittedunderapplicablelaw,noresponsibilityisassumedbythepublisherforanyinjuryand/ordamagetopersonsorproperty,asamatterofproductsliability,negligencelaworotherwise,orfromanyreferencetoorusebyanypersonofthiswork.
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Contents
Contributors
Priorcontributors
Foreword
PartI Balancingbasics
1 Balancingfluids
2 Balancingelectrolytes
3 Balancingacidsandbases
PartII Fluidandelectrolyteimbalances
4 Whenfluidstipthebalance
5 Whensodiumtipsthebalance
6 Whenpotassiumtipsthebalance
7 Whenmagnesiumtipsthebalance
8 Whencalciumtipsthebalance
9 Whenphosphorustipsthebalance
10 Whenchloridetipsthebalance
11 Whenacidsandbasestipthebalance
PartIII Disordersthatcauseimbalances
12 Heat-relatedhealthalterations
13 Heartfailure
14 Respiratoryfailure
15 ExcessiveGIfluidloss
16 Acutepancreatitis
17 Renalfailure
18 Burns
PartIV Treatingimbalances
19 I.V.fluidreplacement
20 Totalparenteralnutrition
Appendicesandindex
Commonfluidandelectrolyteimbalancesinpediatricpatients
Commonfluidandelectrolyteimbalancesinelderlypatients
Transfusingbloodandselectedcomponents
Practicemakesperfect
Glossary
SelectedReferences
Index
Contributors
CherylBrady,MSN,RN,CNE
NursingFacultyKentStateUniversitySalem,OH
ShelbaDurston,MSN,RN,CCRN
NursingInstructorSanJoaquinDeltaCollegeStockton,CA
LauraFavand,MS,RN,CEN
ChiefofPlans,TrainingMobilizationU.S.ArmyMedicalDepartmentActivitiesFortKnox,KY
MargaretGingrich,MSN,RN,CRNP
ProfessorofNursingHarrisburgAreaCommunityCollegeHarrisburg,PA
MaryJones,DNP,CNM,ENP-BC,FNP-BC
FamilyNursePractitionerDoctorofNursingPracticeMedQuestHealthCenter,Inc.Mansfield,OH
RexannPickering,PhD,MS,RN,CIM,CIP
DirectorofContinuingMedicalandNursingEducationMethodistLeBonheurHealthcareMemphis,TN
CherieRebar,PhD,MBA,RN,FNP,COI
Director,DivisionofNursingKetteringCollegeDayton,OH
DonnaScemons,PhD,FNP-BC,CNSAssistantProfessorCaliforniaStateUniversity
LosAngeles,CA
AllisonTerry,PhD,MSN,RN
AssistantDeanofClinicalPracticeAuburnUniversityMontgomery,AL
LeighAnnTrujillo,MSN,RN
PatientCareManagerUniversityofChicagoChicago,IL
PriorContributors
CherylL.Brady,MSN,RN
ShelbaDurston,MSN,RN,CCRN
LauraR.Favand,MS,RN,CEN
MargaretM.Gingrich,MSN,RN
KarlaJones,MS,RN
PatriciaLemelle-Wright,MS,RN
LindaLudwig,BS,RN,MED
RexannG.Pickering,PhD,MS,RN,CIP,CIM
AlexisPuglia,RN
RoseanneHanlonRafter,MSN,RN,GCNS-BC
DonnaScemons,PhD,RN,FNP-C,CNS
VanessaM.Scheidt,RN,TNS,PHRN,FF2
AllisonJ.Terry,PhD,MSN,RN
LeighAnnTrujillo,BSN,RN
Foreword
Ifyouarelikeme,youaretoobusytowadethroughaforewordthatusespretentioustermsandumpsteendullparagraphstogettothepoint.Solet’scutrighttothechase!Hereiswhythisbookissoterrific:1.Itwillteachyoualltheimportantthingsyouneedtoknowaboutfluidsandelectrolytes.(Itwill
leaveoutallthefluffthatwastesyourtime.)2.Itwillhelpyourememberwhatyouhavelearned.3.Itwillmakeyousmileasitenhancesyourknowledgeandskills.Don’tbelieveme?Trythese
recurringlogosonforsize:
Memoryjogger!—helpsyourememberandunderstanddifficultconcepts
CAUTION!—listsdangeroussignsandsymptomsandenablesyoutoquicklyrecognizetrouble
It’snotworking—helpsyoufindalternativeinterventionswhenpatientoutcomesaren’twhatyouexpected
Chartsmart—listscriticaldocumentationelementsthatcankeepyououtoflegaltrouble
Teachingpoints—providesclearpatient-teachingtipsthatyoucanusetohelpyourpatientspreventrecurrenceoftheproblem
Agesandstages—identifiesissuestowatchforinyourpediatricandgeriatricpatients
That’sawrap!—summarizeswhatyou’velearnedinthechapter
See?Itoldyou!Andthat’snotall.Lookformeandmyfriendsinthemarginsthroughoutthisbook.Wewillbetheretoexplainkeyconcepts,provideimportantcarereminders,andofferreassurance.Oh,andifyoudon’tmind,we’llbespicingupthepageswithabitofhumoralongthewaytoteachandentertaininawaythatnootherresourcecan.Ihopeyoufindthisbookhelpful.Bestofluckthroughoutyourcareer!
PartI
Balancingbasics
1 Balancingfluids
2 Balancingelectrolytes
3 Balancingacidsandbases
Chapter1
Balancingfluids
JustthefactsInthischapter,you’lllearn:
♦theprocessoffluiddistributionthroughoutthebody
♦themeaningsofcertainfluid-relatedterms
♦thedifferentwaysfluidmovesthroughthebody
♦therolesthathormonesandkidneysplayinfluidbalance.
AlookatfluidsWherewouldwebewithoutbodyfluids?Fluidsarevitaltoallformsoflife.Theyhelpmaintainbodytemperatureandcellshape,andtheyhelptransportnutrients,gases,andwastes.Let’stakeacloselookatfluidsandthewaythebodybalancesthem.
MakinggainsequallossesJustaboutallmajororgansworktogethertomaintaintheproperbalanceoffluid.Tomaintainthatbalance,theamountoffluidgainedthroughoutthedaymustequaltheamountlost.Someofthoselossescanbemeasured;otherscan’t.
HowinsensibleFluidlossesfromtheskinandlungsarereferredtoasinsensiblelossesbecausetheycan’tbemeasuredorseen.Lossesfromevaporationoffluidthroughtheskinarefairlyconstantbutdependonaperson’stotalbodysurfacearea.Forexample,thebodysurfaceareaofaninfantisgreaterthanthatofanadultrelativetotheirrespectiveweights.Becauseofthisdifferenceinbodysurfacearea—ahighermetabolicrate,alargerpercentageofextracellularbodyfluid,andimmaturekidneyfunction—infantstypicallylosemorewaterthanadultsdo.Changesinenvironmentalhumiditylevelsalsoaffecttheamountoffluidlostthroughtheskin.
Likewise,respiratoryrateanddepthaffecttheamountoffluidlostthroughthelungs.Tachypnea,forexample,causesmorewatertobelost;bradypnea,less.Feverincreasesinsensiblelossesoffluidfromboththeskinandlungs.
Nowthat’ssensibleFluidlossesfromurination,defecation,wounds,andothermeansarereferredtoassensiblelossesbecausetheycanbemeasured.Atypicaladultlosesabout150to200ml/dayoffluidthroughdefecation.Incasesofsevere
diarrhea,lossesmayexceed5,000ml/day(Wait&Alouidor,2011).(Formoreinformationaboutinsensibleandsensiblelosses,seeSitesinvolvedinfluidloss.)
SitesinvolvedinfluidlossEachday,thebodygainsandlosesfluidthroughseveraldifferentprocesses.Thisillustrationshowstheprimarysitesoffluidlossesandgainsaswellastheiraverageamounts.Gastric,intestinal,pancreatic,andbiliarysecretionsarealmostcompletelyreabsorbedandaren’tusuallycountedindailyfluidlossesandgains.
FollowingthefluidThebodyholdsfluidintwobasicareas,orcompartments—insidethecellsandoutsidethecells.Fluidfoundinsidethecellsiscalledintracellularfluid(ICF);fluidfoundoutsidethecells,extracellularfluid(ECF).Capillarywallsandcellmembranesseparatetheintracellularandextracellularcompartments.(SeeFluidcompartments.)
FluidcompartmentsThisillustrationshowstheprimaryfluidcompartmentsinthebody:intracellularandextracellular.Extracellularisfurtherdividedintointerstitialandintravascular.CapillarywallsandcellmembranesseparateICFsfromECFs.
Memoryjogger
Tohelpyourememberwhichfluidbelongsinwhichcompartment,keepinmindthatintermeansbetween(asininterval—betweentwoevents)andintrameanswithinorinside(asinintravenous—insideavein).
Tomaintainproperfluidbalance,thedistributionoffluidbetweenthetwocompartmentsmustremainrelativelyconstant.Inanaverageadult,thetotalamountoffluidis42L,withthetotalamountofICFaveraging40%oftheperson’sbodyweight,orabout28L(Seager&Slaubaugh,2011).ThetotalamountofECFaverages20%oftheperson’sbodyweight,orabout14L.ECFcanbebrokendownfurtherintointerstitialfluid,whichsurroundsthecells,and
intravascularfluidorplasma,whichistheliquidportionofblood.Inanadult,interstitialfluidaccountsforabout75%oftheECF.Plasmaaccountsfortheremaining25%.Thebodycontainsotherfluids,calledtranscellularfluids,inthecerebrospinalcolumn,pleural
cavity,lymphsystem,joints,andeyes.Transcellularfluidsgenerallyaren’tsubjecttosignificantgainsandlossesthroughoutthedaysotheyaren’tdiscussedindetailhere.
Waterhere,waterthereThedistributionoffluidwithinthebody’scompartmentsvarieswithage.Comparedwithadults,infantshaveagreaterpercentageofbodywaterstoredinsideinterstitialspaces.About75%to80%(40%ECF,35%ICF)ofthebodyweightofafull-termneonateiswater.About90%(60%ECFand30%ICF)ofthebodyweightofapremature(23weeksgestation)infantiswater
(Ambalavanan&Rosenkrantz,2012).Theamountofwaterasapercentageofbodyweightdecreaseswithageuntilpuberty.Inatypical154-lb(70kg)leanadultmale,about60%(93lb[42kg])ofbodyweightiswater.(SeeTheevaporationoftime.)
Agesandstages
TheevaporationoftimeTheriskofsufferingafluidimbalanceincreaseswithage.Why?Skeletalmusclemassdeclines,andtheproportionoffatwithinthebodyincreases.Afterage60years,watercontentdropstoabout45%.Likewise,thedistributionoffluidwithinthebodychangeswithage.Forinstance,about15%ofa
typicalyoungadult’stotalbodyweightismadeupofinterstitialfluid.Thatpercentageprogressivelydecreaseswithage.About5%ofthebody’stotalfluidvolumeismadeupofplasma.Plasmavolumeremainsstable
throughoutlife.
Skeletalmusclecellsholdmuchofthatwater;fatcellscontainlittleofit.Women,whonormallyhaveahigherratiooffattoskeletalmusclethanmen,typicallyhaveasomewhatlowerrelativewatercontent.Likewise,anobesepersonmayhavearelativewatercontentlevelaslowas45%.Accumulatedbodyfatintheseindividualsincreasesweightwithoutboostingthebody’swatercontent.
FluidtypesFluidsinthebodygenerallyaren’tfoundinpureforms.They’reusuallyfoundinthreetypesofsolutions:isotonic,hypotonic,andhypertonic.
Isotonic:AlreadyatmatchpointAnisotonicsolutionhasthesamesolute(matterdissolvedinsolution)concentrationasanothersolution.Forinstance,iftwofluidsinadjacentcompartmentsareequallyconcentrated,they’realreadyinbalance,sothefluidinsideeachcompartmentstaysput.Noimbalancemeansnonetfluidshift.(SeeUnderstandingisotonicfluids.)
UnderstandingisotonicfluidsNonetfluidshiftsoccurbetweenisotonicsolutionsbecausethesolutionsareequallyconcentrated.
Forexample,normalsalinesolutionisconsideredisotonicbecausetheconcentrationofsodiuminthesolutionnearlyequalstheconcentrationofsodiumintheblood.
Hypotonic:GetthelowdownAhypotonicsolutionhasalowersoluteconcentrationthananothersolution.Forinstance,sayonesolutioncontainsonlyonepartsodiumandanothersolutioncontainstwoparts.Thefirstsolutionishypotoniccomparedwiththesecondsolution.Asaresult,fluidfromthehypotonicsolutionwouldshiftintothesecondsolutionuntilthetwosolutionshadequalconcentrationsofsodium.Rememberthatthebodyconstantlystrivestomaintainastateofbalance,orequilibrium(alsoknownashomeostasis).(SeeUnderstandinghypotonicfluids.)
UnderstandinghypotonicfluidsWhenalessconcentrated,orhypotonic,solutionisplacednexttoamoreconcentratedsolution,fluidshiftsfromthehypotonicsolutionintothemoreconcentratedcompartmenttoequalizeconcentrations.
Half-normalsalinesolutionisconsideredhypotonicbecausetheconcentrationofsodiuminthesolutionislessthantheconcentrationofsodiuminthepatient’sblood.
Hypertonic:JustthehighlightsAhypertonicsolutionhasahighersoluteconcentrationthananothersolution.Forinstance,sayonesolutioncontainsalargeamountofsodiumandasecondsolutioncontainshardlyany.Thefirstsolutionishypertoniccomparedwiththesecondsolution.Asaresult,fluidfromthesecondsolutionwouldshiftintothehypertonicsolutionuntilthetwosolutionshadequalconcentrations.Again,thebodyconstantlystrivestomaintainastateofequilibrium(homeostasis).(SeeUnderstandinghypertonicfluids.)
UnderstandinghypertonicfluidsIfonesolutionhasmoresolutesthananadjacentsolution,ithaslessfluidrelativetotheadjacentsolution.Fluidwillmoveoutofthelessconcentratedsolutionintothemoreconcentrated,orhypertonic,solutionuntilbothsolutionshavethesameamountofsolutesandfluid.
Forexample,asolutionofdextrose5%innormalsalinesolutionisconsideredhypertonicbecausetheconcentrationofsolutesinthesolutionisgreaterthantheconcentrationofsolutesinthepatient’sblood.
FluidmovementJustastheheartconstantlybeats,fluidsandsolutesconstantlymovewithinthebody.Thatmovementallowsthebodytomaintainhomeostasis,theconstantstateofbalancethebodyseeks.(SeeFluidtips.)
FluidtipsFluids,nutrients,andwasteproductsconstantlyshiftwithinthebody’scompartments—fromthecellstotheinterstitialspaces,tothebloodvessels,andbackagain.Achangeinonecompartmentcanaffectalloftheothers.
KeepingtrackoftheshiftsThatcontinuousshiftingoffluidscanhaveimportantimplicationsforpatientcare.Forinstance,ifahypotonicfluid,suchashalf-normalsalinesolution,isgiventoapatient,itmaycausetoomuchfluidtomovefromtheveinsintothecells,andthecellscanswell.Ontheotherhand,ifahypertonicsolution,suchasdextrose5%innormalsalinesolution,isgiventoapatient,itmaycausetoomuchfluidtobepulledfromcellsintothebloodstream,andthecellsshrink.FormoreinformationaboutI.V.solutions,seechapter19,I.V.fluidreplacement.
WithinthecellsSoluteswithintheintracellular,interstitial,andintravascularcompartmentsofthebodymovethroughthemembranes,separatingthosecompartmentsindifferentways.Themembranesaresemipermeable,meaningthattheyallowsomesolutestopassthroughbutnotothers.Inthissection,you’lllearnthedifferentwaysfluidsandsolutesmovethroughmembranesatthecellularlevel.
GoingwiththeflowIndiffusion,solutesmovefromanareaofhigherconcentrationtoanareaoflowerconcentration,whicheventuallyresultsinanequaldistributionofsoluteswithinthetwoareas.Diffusionisaformofpassivetransportbecausenoenergyisrequiredtomakeithappen;itjusthappens.Likefishswimmingwiththecurrent,thesolutessimplygowiththeflow.(SeeUnderstandingdiffusion.)
UnderstandingdiffusionIndiffusion,solutesmovefromareasofhigherconcentrationtoareasoflowerconcentrationuntiltheconcentrationisequalinbothareas.
GivingthatextrapushInactivetransport,solutesmovefromanareaoflowerconcentrationtoanareaofhigherconcentration.Likeswimmingagainstthecurrent,activetransportrequiresenergytomakeithappen.Theenergyrequiredforasolutetomoveagainstaconcentrationgradientcomesfroma
substancecalledadenosinetriphosphateorATP.Storedinallcells,ATPsuppliesenergyforsolutemovementinandoutofcells.(SeeUnderstandingactivetransport.)
UnderstandingactivetransportDuringactivetransport,energyfromamoleculecalledadenosinetriphosphate(ATP)movessolutesfromanareaoflowerconcentrationtoanareaofhigherconcentration.
Somesolutes,suchassodiumandpotassium,useATPtomoveinandoutofcellsinaformofactivetransportcalledthesodium-potassiumpump.(Formoreinformationonthisphysiologicpump,seechapter5,Whensodiumtipsthebalance.)Othersolutesthatrequireactivetransporttocrosscellmembranesincludecalciumions,hydrogenions,aminoacids,andcertainsugars.
LettingfluidsthroughOsmosisreferstothepassivemovementoffluidacrossamembranefromanareaoflowersoluteconcentrationandcomparativelymorefluidintoanareaofhighersoluteconcentrationandcomparativelylessfluid.Osmosisstopswhenenoughfluidhasmovedthroughthemembranetoequalizethesoluteconcentrationonbothsidesofthemembrane.(SeeUnderstandingosmosis.)
UnderstandingosmosisInosmosis,fluidmovespassivelyfromareaswithmorefluid(andfewersolutes)toareaswithlessfluid(andmoresolutes).Rememberthatinosmosis,fluidmoves,whereasindiffusion,solutesmove.
WithinthevascularsystemWithinthevascularsystem,onlycapillarieshavewallsthinenoughtoletsolutespassthrough.Themovementoffluidsandsolutesthroughcapillarywallsplaysacriticalroleinthebody’sfluidbalance.
ThepressureisonThemovementoffluidsthroughcapillaries—aprocesscalledcapillaryfiltration—resultsfrombloodpushingagainstthewallsofthecapillary.Thatpressure,calledhydrostaticpressure,forcesfluidsandsolutesthroughthecapillarywall.Whenthehydrostaticpressureinsideacapillaryisgreaterthanthepressureinthesurrounding
interstitialspace,fluidsandsolutesinsidethecapillaryareforcedoutintotheinterstitialspace.Whenthepressureinsidethecapillaryislessthanthepressureoutsideofit,fluidsandsolutesmovebackintothecapillary.(SeeFluidmovementthroughcapillaries.)
FluidmovementthroughcapillariesWhenhydrostaticpressurebuildsinsideacapillary,itforcesfluidsandsolutesoutthroughthecapillarywallsintotheinterstitialfluid,asshownbelow.
KeepingthefluidinAprocesscalledreabsorptionpreventstoomuchfluidfromleavingthecapillariesnomatterhowmuchhydrostaticpressureexistswithinthecapillaries.Whenfluidfiltersthroughacapillary,theproteinalbuminremainsbehindinthediminishingvolumeofwater.Albuminisalargemoleculethatnormallycan’tpassthroughcapillarymembranes.Astheconcentrationofalbumininsideacapillaryincreases,fluidbeginstomovebackintothecapillariesthroughosmosis.
Thinkofalbuminasawatermagnet.Theosmotic,orpulling,forceofalbuminintheintravascularspaceiscalledtheplasmacolloidosmoticpressure.Theplasmacolloidosmoticpressureincapillariesaveragesabout25mmHg.(SeeAlbuminmagnetism.)
AlbuminmagnetismAlbumin,alargeproteinmolecule,actslikeamagnettoattractwaterandholditinsidethebloodvessel.
Aslongascapillarybloodpressure(thehydrostaticpressure)exceedsplasmacolloidosmoticpressure,waterandsolutescanleavethecapillariesandentertheinterstitialfluid.Whencapillarybloodpressurefallsbelowplasmacolloidosmoticpressure,wateranddiffusiblesolutesreturntothecapillaries.Normally,bloodpressureinacapillaryexceedsplasmacolloidosmoticpressureinthe
arterioleendandfallsbelowitinthevenuleend.Asaresult,capillaryfiltrationoccursalongthefirsthalfofthevessel;reabsorption,alongthesecond.Aslongascapillarybloodpressureandplasmaalbuminlevelsremainnormal,theamountofwaterthatmovesintothevesselequalstheamountthatmovesout.
ComingaroundagainOccasionally,extrafluidfiltersoutofthecapillary.Whenthathappens,theexcessfluidshiftsintothelymphaticvesselslocatedjustoutsidethecapillariesandeventuallyreturnstotheheartforrecirculation.
MaintainingthebalanceManymechanismsinthebodyworktogethertomaintainfluidbalance.Becauseoneproblemcanaffecttheentirefluid-maintenancesystem,it’simportanttokeepallmechanismsincheck.Here’sacloserlookatwhatmakesthisbalancingactpossible.
ThekidneysThekidneysplayavitalroleinfluidbalance.Ifthekidneysdon’tworkproperly,thebodyhasahardtimecontrollingfluidbalance.Theworkhorseofthekidneyisthenephron.Thebodyputsthenephronstoworkeveryday.Anephronconsistsofaglomerulusandatubule.Thetubule,sometimesconvoluted,endsina
collectingduct.Theglomerulusisaclusterofcapillariesthatfiltersblood.Likeavascularcradle,Bowman’scapsulesurroundstheglomerulus.CapillarybloodpressureforcesfluidthroughthecapillarywallsandintoBowman’scapsuleat
theproximalendofthetubule.Alongthelengthofthetubule,waterandelectrolytesareeitherexcretedorretaineddependingonthebody’sneeds.Ifthebodyneedsmorefluid,forinstance,itretainsmore.Ifitneedslessfluid,lessisreabsorbedandmoreisexcreted.Electrolytes,suchassodiumandpotassium,areeitherfilteredorreabsorbedthroughoutthesamearea.Theresultingfiltrate,whicheventuallybecomesurine,flowsthroughthetubuleintothecollectingductsandeventuallyintothebladderasurine.
SuperabsorbentNephronsfilterabout125mlofbloodeveryminute,orabout180L/day.Thatrate,calledtheglomerularfiltrationrate,usuallyleadstotheproductionof1to2Lofurineperday.Thenephronsreabsorbtheremaining178Lormoreoffluid,anamountequivalenttomorethan30oilchangesforthefamilycar!
AstrictconservationistIfthebodyloseseven1%to2%ofitsfluid,thekidneystakestepstoconservewater.Perhapsthemostimportantstepinvolvesreabsorbingmorewaterfromthefiltrate,whichproducesamoreconcentratedurine.Thekidneysmustcontinuetoexcreteatleast20mlofurineeveryhour(about500ml/day)to
eliminatebodywastes.Aurineexcretionratethat’slessthan20ml/hourusuallyindicatesrenaldiseaseandimpendingrenalfailure.Theminimumexcretionratevarieswithage.(SeeThehighertherate,thegreaterthewaste.)
Agesandstages
Thehighertherate,thegreaterthewasteInfantsandyoungchildrenexcreteurineatahigherratethanadultsbecausetheirhighermetabolicratesproducemorewaste.Also,aninfant’skidneyscan’tconcentrateurineuntilaboutage3months,andtheyremainlessefficientthananadult’skidneysuntilaboutage2years.
Thekidneysrespondtofluidexcessesbyexcretingurinethatismoredilute,whichridsthebodyoffluidandconserveselectrolytes.
AntidiuretichormoneSeveralhormonesaffectfluidbalance,amongthemawaterretainercalledantidiuretichormone(ADH).(Youmayalsohearthishormonecalledvasopressin.)ThehypothalamusproducesADH,buttheposteriorpituitaryglandstoresandreleasesit.(SeeHowantidiuretichormoneworks.)
HowantidiuretichormoneworksADHregulatesfluidbalanceinfoursteps.
AdaptableabsorptionIncreasedserumosmolality,ordecreasedbloodvolume,canstimulatethereleaseofADH,whichinturnincreasesthekidneys’reabsorptionofwater.Theincreasedreabsorptionofwaterresultsinmoreconcentratedurine.Likewise,decreasedserumosmolality,orincreasedbloodvolume,inhibitsthereleaseofADH
andcauseslesswatertobereabsorbed,makingtheurinelessconcentrated.TheamountofADHreleasedvariesthroughouttheday,dependingonthebody’sneeds.Thisup-and-downcycleofADHreleasekeepsfluidlevelsinbalancealldaylong.Likeadam
inariver,thebodyholdswaterwhenfluidlevelsdropandreleasesitwhenfluidlevelsrise.
Memoryjogger
RememberwhatADHstandsfor—antiduretichormone—andyou’llrememberitsjob:restoringbloodvolumebyreducingdiuresisandincreasingwaterretention.
Renin-angiotensin-aldosteronesystemTohelpthebodymaintainabalanceofsodiumandwateraswellasahealthybloodvolumeandbloodpressure,specialcells(calledjuxtaglomerularcells)neareachglomerulussecreteanenzymecalledrenin.Throughacomplexseriesofsteps,reninleadstotheproductionofangiotensinII,apowerfulvasoconstrictor.
AngiotensinIIcausesperipheralvasoconstrictionandstimulatestheproductionofaldosterone.Bothactionsraisebloodpressure.(SeeAldosteroneproduction,page14.)
AldosteroneproductionThisillustrationshowsthestepsinvolvedintheproductionofaldosterone(ahormonethathelpstoregulatefluidbalance)throughtherenin-angiotensin-aldosteronesystem.
Usually,assoonasthebloodpressurereachesanormallevel,thebodystopsreleasingrenin,andthisfeedbackcycleofrenintoangiotensintoaldosteronestops.
TheupsanddownsofreninTheamountofreninsecreteddependsonbloodflowandthelevelofsodiuminthebloodstream.Ifbloodflowtothekidneysdiminishes,ashappensinapatientwhoishemorrhaging,oriftheamountofsodiumreachingtheglomerulusdrops,thejuxtaglomerularcellssecretemorerenin.Therenincausesvasoconstrictionandasubsequentincreaseinbloodpressure.
Conversely,ifbloodflowtothekidneysincreases,oriftheamountofsodiumreachingtheglomerulusincreases,juxtaglomerularcellssecretelessrenin.Adrop-offinreninsecretion
reducesvasoconstrictionandhelpstonormalizebloodpressure.
SodiumandwaterregulatorThehormonealdosteronealsoplaysaroleinmaintainingbloodpressureandfluidbalance.Secretedbytheadrenalcortex,aldosteroneregulatesthereabsorptionofsodiumandwaterwithinthenephron.(SeeHowaldosteroneworks.)
HowaldosteroneworksAldosterone,producedasaresultoftherenin-angiotensinmechanism,actstoregulatefluidvolumeasdescribedbelow.
TriggeringactivetransportWhenbloodvolumedrops,aldosteroneinitiatestheactivetransportofsodiumfromthedistaltubulesandthecollectingductsintothebloodstream.Whensodiumisforcedintothebloodstream,morewaterisreabsorbedandbloodvolumeexpands.
AtrialnatriureticpeptideTherenin-angiotensin-aldosteronesystemisn’ttheonlyfactoratworkbalancingfluidsinthebody.Acardiachormonecalledatrialnatriureticpeptide(ANP)alsohelpskeepthatbalance.Storedinthecellsoftheatria,ANPisreleasedwhenatrialpressureincreases.Thehormonecounteractstheeffectsoftherenin-angiotensin-aldosteronesystembydecreasingbloodpressureandreducingintravascularbloodvolume.(SeeHowatrialnatriureticpeptideworks.)
HowatrialnatriureticpeptideworksWhenbloodvolumeandbloodpressureriseandbegintostretchtheatria,theheart’sANPshutsofftherenin-angiotensin-aldosteronesystem,whichstabilizesbloodvolumeandbloodpressure.
Thispowerfulhormone:•suppressesserumreninlevels•decreasesaldosteronereleasefromtheadrenalglands•increasesglomerularfiltration,whichincreasesurineexcretionofsodiumandwater•decreasesADHreleasefromtheposteriorpituitarygland•reducesvascularresistancebycausingvasodilation.
StretchthatatriumTheamountofANPthattheatriareleaserisesinresponsetoanumberofconditions;forexample,chronicrenalfailureandheartfailure.
AnythingthatcausesatrialstretchingcanalsoleadtoincreasesintheamountofANPreleased,includingorthostaticchanges,atrialtachycardia,highsodiumintake,sodiumchlorideinfusions,anduseofdrugsthatcausevasoconstriction.
ThirstPerhapsthesimplestmechanismformaintainingfluidbalanceisthethirstmechanism.Thirstoccursasaresultofevensmalllossesoffluid.LosingbodyfluidsoreatinghighlysaltyfoodsleadstoanincreaseinECFosmolality.Thisincreaseleadstodryingofthemucousmembranesinthemouth,whichinturnstimulatesthethirstcenterinthehypothalamus.Inanelderlyperson,thethirstmechanismislesseffectivethanitisinayoungerperson,leavingtheolderpersonmorepronetodehydration.(SeeDehydrationinelderlypeople.)
Agesandstages
DehydrationinelderlypeopleThesignsandsymptomsofdehydrationmaybedifferentinolderadults.Forexample,theymightinclude:•
confusion•
subnormaltemperature•
tachycardia•
pinchedfacialexpression.
QuenchthatthirstNormally,whenapersonisthirsty,hedrinksfluid.Theingestedfluidisabsorbedfromtheintestineintothebloodstream,whereitmovesfreelybetweenfluidcompartments.Thismovementleadstoanincreaseintheamountoffluidinthebodyandadecreaseintheconcentrationofsolutes,thusbalancingfluidlevelsthroughoutthebody.
That’sawrap!
That’sawrap!
Balancingfluidsreview
Fluidbalancebasics•
Fluidmovementthroughoutthebodyhelpsmaintainbodytemperatureandcellshape.•
Fluidshelptransportnutrients,gases,andwastes.•
Mostofthebody’smajororgansworktogethertomaintainfluidbalance.•
Theamountoffluidsgainedthroughintakemustequaltheamountlost.
Fluidlosses•
Insensiblelosses–
Immeasurable–
Examples:throughtheskin(affectedbyhumidityandbodysurfacearea)andlungs(affectedbyrespiratoryrateanddepth)•
Sensiblelosses–
Measurable–
Examples:fromurination,defecation,andwounds
Understandingbodyfluids•
Differenttypesoffluidsarelocatedindifferentcompartments.•
Fluidsmovethroughoutthebodybygoingbackandforthacrossacell’ssemipermeablemembrane.•
Distributionoffluidsvarieswithage.
Fluidcompartments•
ICF—fluidinsidethecell;mustbebalancedwithECF
•ECF—fluidoutsidethecell;mustbebalancedwithICF;madeupof75%interstitialfluid(fluidsurroundingthecell)and25%plasma(liquidportionofblood)•
Transcellularfluid—inthecerebrospinalcolumn,pleuralcavity,lymphsystem,joints,andeyes;remainsrelativelyconstant
Fluidtypes•
Isotonic—equallyconcentratedwithothersolutions•
Hypotonic—lessconcentratedthanothersolutions•
Hypertonic—moreconcentratedthanothersolutions
Fluidmovement•
Diffusion—formofpassivetransport(noenergyisrequired)thatmovessolutesfromanareaofhigherconcentrationtoanareaoflowerconcentration,resultinginanequaldistributionofsolutesbetweenthetwoareas•
Activetransport—usesATPtomovesolutesfromanareaoflowconcentrationtoanareaofhigherconcentration;example:sodium-potassiumpump•
Osmosis—passivemovementoffluidacrossamembranefromanareaoflowersoluteconcentrationtoanareaofhighersoluteconcentration;stopswhenbothsideshaveanequalsoluteconcentration•
Capillaryfiltration—movementoffluidthroughcapillarywallsthroughhydrostaticpressure;balancedbyplasmacolloidosmoticpressurefromalbuminthatcausesreabsorptionoffluidandsolutes
MaintainingfluidbalanceKidneys•
Nephronsformurinebyfilteringblood.•
Ifthebodyneedsmorefluid,nephrontubulesretainorreabsorbwaterandelectrolytes.•
Ifthebodyneedslessfluid,tubulesabsorbless,causingmorefluidsandelectrolytestobeexcreted.•
Kidneysalsosecreterenin,anenzymethatactivatestherenin-angiotensin-aldosteronesystem.•
Aldosteronesecretedbytheadrenalcortexregulatessodiumandwaterreabsorptionbythekidneys.
Hormones•
ADH—Alsoknownasvasopressin,ADHisproducedbythehypothalamustoreducediuresisandincreasewaterretentionifserumosmolalityincreasesorbloodvolumedecreases.•
Renin-angiotensin-aldosteronesystem—Ifbloodflowdecreases,thejuxtaglomerularcellsinthekidneyssecreterenin,whichleadstotheproductionofangiotensinII,apowerfulvasoconstrictor;angiotensinIIstimulatestheproductionofaldosterone;aldosteroneregulatesthereabsorptionofsodiumandwaterinthenephron.•
ANP—Thishormone,producedandstoredintheatriaoftheheart,stopstheactionoftherenin-angiotensin-aldosteronesystem;ANPdecreasesbloodpressurebycausingvasodilationandreducesfluidvolumebyincreasingexcretionofsodiumandwater.
Thirst•
Regulatedbythehypothalamus•
StimulatedbyanincreaseinECFanddryingofthemucousmembranes•
Causesapersontodrinkfluids,whichareabsorbedbytheintestines,movedtothebloodstream,anddistributedbetweenthecompartments
Quickquiz
1.IfyouwerewalkingacrosstheSaharaDesertwithanemptycanteen,theamountofADHsecretedwouldmostlikely:
A.increase.B.decrease.C.staythesame.D.havenoeffect.
Answer:A.Becauseyourbodywouldprobablybedehydrated,itwouldtrytoretainasmuchfluidaspossible.Toretainfluid,ADHsecretionincreases.
2.Ifyouplacedtwocontainersnexttoeachother,separatedonlybyasemipermeablemembrane,andthesolutioninonecontainerwashypotonicrelativetotheother,fluidin
thehypotoniccontainerwould:A.moveoutofthehypotoniccontainerintotheother.B.pullfluidfromtheothercontainerintothehypotoniccontainer.C.causeosmosistooccur.D.stayunchangedwithinthehypotoniccontainer.
Answer:A.Fluidwouldmoveoutofthehypotoniccontainerintotheothercontainertoequalizetheconcentrationoffluidwithinthetwocontainers.Osmosisoccurswhenfluidmovesfromanareawithmorefluidtoanareawithlessfluid.
3.Hydrostaticpressure,whichpushesfluidoutofthecapillaries,isopposedbycolloidosmoticpressure,whichinvolves:
A.reducedreninsecretion.B.adecreaseinaldosterone.C.thepullingpowerofalbumintoreabsorbwater.D.anincreaseinADHsecretion.
Answer:C.Albuminincapillariesdrawswatertowardit,aprocesscalledreabsorption.
4.Whenaperson’sbloodpressuredrops,thekidneysrespondby:A.secretingrenin.B.producingaldosterone.C.slowingthereleaseofADH.D.secretingANP.
Answer:A.Juxtaglomerularcellsinthekidneyssecreterenininresponsetolowbloodfloworalowsodiumlevel.Theeventualeffectofreninsecretionisanincreaseinbloodpressure.
5.GivingahypertonicI.V.solutiontoapatientmaycausetoomuchfluidtobe:A.pulledfromthecellsintothebloodstream,whichmaycausethecellstoshrink.B.pulledoutofthebloodstreamintothecells.C.pushedoutofthebloodstreamintotheextravascularspaces.D.pulledfromthecellsintothebloodstream,whichmaycausethecellstoincreasein
size.Answer:A.BecausetheconcentrationofsolutesintheI.V.solutionisgreaterthantheconcentrationofsolutesinthepatient’sblood,ahypertonicsolutionmaycausefluidtobepulledfromthecellsintothebloodstream,causingthecellstoshrink.
ScoringIfyouansweredallfivequestionscorrectly,congratulations!You’reafluidwhiz.Ifyouansweredfourcorrectly,takeaswigofwater;you’rejustalittledry.Ifyouansweredfewerthanfourcorrectly,pouryourselfaglassofsportsdrinkandenjoyaninvigoratingburstoffluidrefreshment!
ReferencesAmbalavanan,N.,&Rosenkrantz,T.(Eds.).(2012).Fluid,electrolyte,andnutritionmanagementofthe
newborn.Retrievedfromhttp://emedicine.medscape.com/article/976386-overview#aw2aab6b3Seager,S.L.,&Slaubaugh,M.L.(2011).Organicandbiochemistryfortoday(7thed.,p.412).Belmont,
CA:Brooks/ColeCentageLearning.Wait,R.B.,&Alouidor,R.(2011).Fluids,electrolytes,andacid–basebalance.InM.Mulhollandetal.
(Eds.),Greenfield’ssurgery:Scientificprinciples&practice(5thed.).Philadelphia,PA:LippincottWilliams&Wilkins.Retrievedfromhttp://books.google.com/books?id=KkJc0XYVc0IC&pg=PT483&lpg=PT483&dq=normal+24+hour+water+loss+in+stool&source=bl&ots=pIic8DvQj2&sig=65EaVLjtk2O5l0gNL6Wqav6-g4M&hl=en&sa=X&ei=z_XOUrXfFNTBoASSioGgCQ&ved=0CE0Q6AEwBzgK#v=onepage&q=normal%2024%20hour%20water%20loss%20in%20stool&f=false
Chapter2
Balancingelectrolytes
JustthefactsInthischapter,you’lllearn:
♦thedifferencebetweencationsandanions
♦theinterpretationofnormalandabnormalserumelectrolyteresults
♦therolenephronsplayinelectrolytebalance
♦theeffectdiureticshaveonelectrolytesinthekidneys
♦theelectrolyteconcentrationofselectedI.V.fluids.
AlookatelectrolytesElectrolytesworkwithfluidstomaintainhealthandwell-being.They’refoundinvariousconcentrations,dependingonwhetherthey’reinsideoroutsidethecells.Electrolytesarecrucialfornearlyallcellularreactionsandfunctions.Let’stakealookatwhatelectrolytesare,howtheyfunction,andwhatupsetstheirbalance.
IonsElectrolytesaresubstancesthat,wheninsolution,separate(ordissociate)intoelectricallychargedparticlescalledions.Someionsarepositivelychargedandothersarenegativelycharged.Severalpairsofoppositelychargedionsaresocloselylinkedthataproblemwithoneioncausesaproblemwiththeother.Sodiumandchloridearelinkedthatway,asarecalciumandphosphorus.
Avarietyofdiseasescandisruptthenormalbalanceofelectrolytesinthebody.Understandingelectrolytesandrecognizingimbalancescanmakeyourpatientassessmentmoreaccurate.
AnionsandcationsAnionsareelectrolytesthatgenerateanegativecharge;cationsareelectrolytesthatproduceapositivecharge.Anelectricalchargemakescellsfunctionnormally.(SeeLookingontheplusandminussides.)
LookingontheplusandminussidesElectrolytescanbeeitheranionsorcations.Here’salistofanions(thenegativecharges)andcations(thepositivecharges).
•Bicarbonate•
Chloride•
Phosphorus
•Calcium•
Magnesium•
Potassium•
Sodium
Theaniongapisausefultestfordistinguishingtypesandcausesofacid-baseimbalancesbecauseitreflectsserumanion-cationbalance.(Theaniongapisdiscussedinchapter3,Balancingacidsandbases.)
Memoryjogger
Toremindyourselfaboutthedifferencebetweenanionsandcations,rememberthattheTin“cation”lookslikethepositivesymbol,“+.”
BalancingtheplusesandminusesElectrolytesoperateoutsidethecellinextracellularfluidcompartmentsandinsidethecellinintracellularfluidcompartments.Individualelectrolytesdifferinconcentration,butelectrolytetotalsbalancetoachieveaneutralelectricalcharge(positivesandnegativesbalanceeachother).Thisbalanceiscalledelectroneutrality.
HookingupwithhydrogenMostelectrolytesinteractwithhydrogenionstomaintainacid-basebalance.Themajorelectrolyteshavespecializedfunctionsthatcontributetometabolismandfluidandelectrolytebalance.
MajorelectrolytesoutsidethecellSodiumandchloride,themajorelectrolytesinextracellularfluid,exertmostoftheirinfluenceoutsidethecell.Sodiumconcentrationaffectsserumosmolality(soluteconcentrationin1Lofwater)andextracellularfluidvolume.Sodiumalsohelpsnerveandmusclecellsinteract.Chloridehelpsmaintainosmoticpressure(water-pullingpressure).Gastricmucosalcellsneedchloridetoproducehydrochloricacid,whichbreaksdownfoodintoabsorbablecomponents.
MoreoutsidersCalciumandbicarbonatearetwootherelectrolytesfoundinextracellularfluid.Calciumisthemajorcationinvolvedinthestructureandfunctionofbonesandteeth.Calciumisneededto:•stabilizethecellmembraneandreduceitspermeabilitytosodium•transmitnerveimpulses•contractmuscles•coagulateblood•formboneandteeth.Bicarbonateplaysavitalroleinacid-basebalance.
Majorelectrolytesinsidethecell
Potassium,phosphorus,andmagnesiumareamongthemostabundantelectrolytesinsidethecell.
PotentpotassiumPotassiumplaysanimportantrolein:•cellexcitabilityregulation•nerveimpulseconduction•restingmembranepotential•musclecontractionandmyocardialmembraneresponsiveness•intracellularosmolalitycontrol.
FundamentalphosphorusThebodycontainsphosphorusintheformofphosphatesalts.Sometimes,thewordsphosphorusandphosphateareusedinterchangeably.Phosphateisessentialforenergymetabolism.Combinedwithcalcium,phosphateplaysakeyroleinboneandtoothmineralization.Italsohelpsmaintainacid-basebalance.
MagnificentmagnesiumMagnesiumactsasacatalystforenzymereactions.Itregulatesneuromuscularcontraction,promotesnormalfunctioningofthenervousandcardiovascularsystems,andaidsinproteinsynthesisandsodiumandpotassiumiontransportation.
ElectrolytemovementWhencellsdie(e.g.,fromtraumaorchemotherapy),theircontentsspillintotheextracellularareaandupsettheelectrolytebalance.Inthiscase,elevatedlevelsofintracellularelectrolytesare
foundinplasma.Althoughelectrolytesaregenerallyconcentratedinaspecificcompartment,theyaren’tconfined
totheseareas.Likefluids,theymovearoundtryingtomaintainbalanceandelectroneutrality.
ElectrolytebalanceFluidintakeandoutput,acid-basebalance,hormonesecretion,andnormalcellfunctionallinfluenceelectrolytebalance.Becauseelectrolytesfunctionbothcollaboratively,withotherelectrolytes,andindividually,imbalancesinoneelectrolytecanaffectbalanceinothers.(SeeUnderstandingelectrolytes.)
UnderstandingelectrolytesElectrolyteshelpregulatewaterdistribution,governacid-basebalance,andtransmitnerveimpulses.Theyalsocontributetoenergygenerationandbloodclotting.Thistablesummarizesthefunctionsofeachofthebody’smajorelectrolytes.Checktheillustrationbelowtoseehowelectrolytesaredistributedinandaroundthecell.
Potassium(K)•
Mainintracellularfluid(ICF)cation•
Regulatescellexcitability•
Permeatescellmembranes,therebyaffectingthecell’selectricalstatus•
HelpstocontrolICFosmolalityand,consequently,ICFosmoticpressure
Magnesium(Mg)•
AleadingICFcation•
Contributestomanyenzymaticandmetabolicprocesses,particularlyproteinsynthesis•
Modifiesnerveimpulsetransmissionandskeletalmuscleresponse(unbalancedMgconcentrationsdramaticallyaffectneuromuscularprocesses)•
Maintainscellmembranestability(Lobo,Lewington,&Allison,2013)
Phosphorus(P)•
MainICFanion•
Promotesenergystorageandcarbohydrate,protein,andfatmetabolism•
Actsasahydrogenbuffer
Sodium(Na)•
Mainextracellularfluid(ECF)cation•
HelpsgovernnormalECFosmolality(ashiftinNaconcentrationstriggersafluidvolumechangetorestorenormalsoluteandwaterratios)•
Helpsmaintainacid-basebalance•
Activatesnerveandmusclecells•
Influenceswaterdistribution(withchloride)
Chloride(Cl)•
MainECFanion•
HelpsmaintainnormalECFosmolality•
AffectsbodypH•
Playsavitalroleinmaintainingacid-basebalance;combineswithhydrogenionstoproducehydrochloricacid
Calcium(Ca)•
Amajorcationinteethandbones;foundinfairlyequalconcentrationsinICFandECF•
Alsofoundincellmembranes,whereithelpscellsadheretooneanotherandmaintaintheirshape•
Actsasanenzymeactivatorwithincells(musclesmusthaveCatocontract)•
Aidscoagulation•
Affectscellmembranepermeabilityandfiringlevel
Bicarbonate(HCO3−)
•PresentinECF•
Regulatesacid-basebalance
ElectrolytelevelsEventhoughelectrolytesexistinsideandoutsidethecell,onlythelevelsoutsidethecellinthebloodstreamaremeasured.Althoughserumlevelsremainfairlystablethroughoutaperson’slifespan,understandingwhichlevelsarenormalandwhichareabnormaliscriticaltoreactingquicklyandappropriatelytoapatient’selectrolyteimbalance.Thepatient’sconditiondetermineshowoftenelectrolytelevelsarechecked.Resultsformany
laboratorytestsarereportedinmilliequivalentsperliter(mEq/L),whichisameasureoftheion’schemicalactivity,oritspower.(SeeInterpretingserumelectrolytetestresults,page26,foralookatnormalandabnormalelectrolytelevelsintheblood.)
SeethewholepictureWhenyouseeanabnormallaboratorytestresult,considerwhatyouknowaboutthepatient.Forinstance,aserumpotassiumlevelof7mEq/Lforapatientwithpreviouslynormalserumpotassiumlevelsandnoapparentreasonfortheincreasemaybeaninaccurateresult.Perhapsthepatient’sbloodsamplewashemolyzedfromtraumatothecells,whichcanoccurwhendrawingthebloodorduringtransporttothelab.
Withthatsaid,lookatthewholepicturebeforeyouact,includingwhatyouknowaboutthepatient,hissignsandsymptoms,andhiselectrolytelevels.(SeeDocumentingelectrolyteimbalances,page27.)
Chartsmart
DocumentingelectrolyteimbalancesBesuretoincludethefollowinginformationinyourdocumentationofapatient’selectrolyteimbalance:•
assessmentfindings•
laboratoryresultspertainingtotheimbalance•
relatednursingdiagnoses•
notificationandresponseofthepractitioner•
interventionsandtreatmentfortheelectrolyteimbalance,includingsafetymeasures•
patientteaching•
patient’sresponsetointerventions.
FluidregulationManyactivitiesandfactorsareinvolvedinregulatingfluidandelectrolytebalance.Aquickreviewofsomeofthebasicswillhelpyouunderstandthisregulationbetter.
FluidandsolutemovementAsdiscussedinchapter1,activetransportmovessolutesupstreamandrequirespumpswithinthebodytomovethesubstancesfromareasoflowerconcentrationtoareasofhigherconcentration—againstaconcentrationgradient.Adenosinetriphosphate(ATP)istheenergythatmovessolutesupstream.
Pushingfluids
Thesodium-potassiumpump,anexampleofanactivetransportmechanism,movessodiumionsfromintracellularfluid(anareaoflowerconcentration)toextracellularfluid(anareaofhigherconcentration).Withpotassium,thereversehappens:Alargeamountofpotassiuminintracellularfluidcausesanelectricalpotentialatthecellmembrane.Asionsrapidlyshiftinandoutofthecell,electricalimpulsesareconducted.Theseimpulsesareessentialformaintaininglife.
OrganandglandinvolvementMostmajororgansandglandsinthebody—thelungs,liver,adrenalglands,kidneys,heart,hypothalamus,pituitarygland,skin,gastrointestinal(GI)tract,andparathyroidandthyroidglands—helptoregulatefluidandelectrolytebalance.
Aspartoftherenin-angiotensin-aldosteronesystem,thelungsandliverhelpregulatesodiumandwaterbalanceaswellasbloodpressure.Theadrenalglandssecretealdosterone,whichinfluencessodiumandpotassiumbalanceinthekidneys.Theselevelsareaffectedbecausethekidneysexcretepotassium,orhydrogenions,inexchangeforretainedsodium.
TheheartsaysnoTheheartcounteractstherenin-angiotensin-aldosteronesystemwhenitsecretesatrialnatriureticpeptide(ANP),causingsodiumexcretion.Thehypothalamusandposteriorpituitaryglandproduceandsecreteanantidiuretichormonethatcausesthebodytoretainwaterwhich,inturn,affectssoluteconcentrationintheblood.
WhereelectrolytesarelostSodium,potassium,chloride,andwaterarelostinsweatandfromtheGItract;however,electrolytesarealsoabsorbedfromtheGItract.DiscussionsofindividualelectrolytesinupcomingchaptersexplainhowGIabsorptionoffoodsandfluidsaffectstheirbalance.
TheglandsplayonTheparathyroidglandsalsoplayaroleinelectrolytebalance,specificallythebalanceofcalciumandphosphorus.Theparathyroidglands(usuallytwopairs)arelocatedbehindandtothesideofthethyroidgland.Theysecreteparathyroidhormone,whichdrawscalciumintothebloodfromthebones,intestines,andkidneysandhelpsmovephosphorusfromthebloodtothekidneys,whereit’sexcretedinurine.Thethyroidglandisalsoinvolvedinelectrolytebalancebysecretingcalcitonin.Thishormone
lowersanelevatedcalciumlevelbypreventingcalciumreleasefrombone.Calcitoninalsodecreasesintestinalabsorptionandkidneyreabsorptionofcalcium.
KidneyinvolvementRememberfiltration?It’stheprocessofremovingparticlesfromasolutionbyallowingtheliquidportiontopassthroughamembrane.Filtrationoccursinthenephron(theanatomicandfunctionalunitofthekidneys).Asbloodcirculatesthroughtheglomerulus(atuftofcapillaries),fluidsandelectrolytesarefilteredandcollectedinthenephron’stubule.Somefluidsandelectrolytesarereabsorbedthroughcapillariesatvariouspointsalongthe
nephron;othersaresecreted.Agecanplayanimportantroleinthewaykidneysfunction—ormalfunction.(SeeWho’satrisk?)
Agesandstages
Who’satrisk?Theimmaturekidneysofaninfantcan’tconcentrateurineorreabsorbelectrolytesthewaythekidneysofanadultcan,soinfantsareatahigherriskforelectrolyteimbalances.Olderadultsarealsoatriskforelectrolyteimbalances.Theirkidneyshavefewerfunctional
nephrons,adecreasedglomerularfiltrationrate,andadiminishedabilitytoconcentrateurine.
AjugglingactAvitalpartofthekidneys’jobistoregulateelectrolytelevelsinthebody.Normallyfunctioningkidneysmaintainthecorrectfluidlevelinthebody.Sodiumandfluidbalancearecloselyrelated.Whentoomuchsodiumisreleased,thebody’sfluidleveldrops.
Thekidneysalsoridthebodyofexcesspotassium.Whenthekidneysfail,potassiumbuildsupinthebody.Highlevelsofpotassiuminthebloodcanbefatal.(Formoreinformationaboutwhichareasofthenephroncontrolfluidandelectrolytebalance,seeHowthenephronregulatesfluidandelectrolytebalance.)
HowthenephronregulatesfluidandelectrolytebalanceInthisillustration,thenephronhasbeenstretchedtoshowwhereandhowfluidsandelectrolytesareregulated.
HowdiureticsaffectbalanceManypatients—whetherinamedicalfacilityorathome—takeadiuretictoincreaseurineproduction.Diureticsareusedtotreatmanydisorders,suchashypertension,heartfailure,electrolyteimbalances,andkidneydisease.
KeepingaclosewatchThehealthcareteammonitorstheeffectsofadiuretic,includingitseffectonelectrolytebalance.Adiureticmaycauseelectrolyteloss,whereasanI.V.fluidcauseselectrolytegain.Olderadults,whoareatriskforfluidandelectrolyteimbalances,needcarefulmonitoringbecauseadiureticcanworsenanexistingimbalance.Whenyouknowhowthenephronfunctionsnormally,youcanpredictadiuretic’seffectson
yourpatientbyknowingwherealongthenephronthedrugacts.Thisknowledgeandunderstanding
canhelpyouprovideoptimalcareforapatienttakingadiuretic.(SeeHowdrugsaffectnephronactivity.)
HowdrugsaffectnephronactivityHere’salookathowcertaindiureticsandotherdrugsaffectthenephron’sregulationoffluidandelectrolytebalance.
I.V.fluidsLikediuretics,I.V.fluidsaffectelectrolytebalanceinthebody.WhenprovidingI.V.fluid,keepinmindthepatient’snormalelectrolyterequirements.Forinstance,thepatientmayrequire:•1to2mEq/kg/dayofsodium•0.5to1mEq/kg/dayofpotassium•1to2mEq/kg/dayofchloride.
ImprovingyourI.V.IQToevaluateI.V.fluidtreatment,ask:•IstheI.V.fluidprovidingthecorrectamountofelectrolytes?•HowlonghasthepatientbeenreceivingI.V.fluids?•Isthepatientreceivingoralsupplementationofelectrolytes?FormoreaboutI.V.fluids,seechapter19,I.V.fluidreplacement.(Fortheelectrolytecontentof
somecommonlyusedI.V.fluids,seeI.V.fluidcomponents,page32.)
That’sawrap!
Balancingelectrolytesreview
Electrolytebasics•
Foundthroughoutthebodyinvariousconcentrations•
Criticaltocellfunction
Ions,anions,cations•
Ions—electricallychargedparticlescreatedwhenelectrolytesseparateinasolution;maybepositivelyornegativelycharged•
Anions—negativelychargedelectrolytes;includechloride,phosphorus,andbicarbonate•
Cations—positivelychargedelectrolytes;includesodium,potassium,calcium,andmagnesium•
Electroneutrality—positiveandnegativeionsbalanceeachotherout,achievinganeutralelectricalcharge
Majorextracellularelectrolytes•
Sodium—helpsnervecellsandmusclecellsinteract•
Chloride—maintainsosmoticpressureandhelpsgastricmucosalcellsproducehydrochloricacid•
Calcium—stabilizescellmembrane,reducingitspermeability;transmitsnerveimpulses;contractsmuscles;coagulatesblood;andformsbonesandteeth•
Bicarbonate—regulatesacid-basebalance
Majorintracellularelectrolytes•
Potassium—regulatescellexcitability,nerveimpulseconduction,restingmembranepotential,musclecontraction,myocardialmembraneresponsiveness,andintracellularosmolality•
Phosphate—controlsenergymetabolism•
Magnesium—influencesenzymereactions,neuromuscularcontractions,normalfunctioningofnervousandcardiovascularsystem,proteinsynthesis,andsodiumandpotassiumiontransportation
Influencesonelectrolytebalance•
Normalcellfunction•
Fluidintakeandoutput•
Acid-basebalance•
Hormonesecretion
Maintainingelectrolytebalance•
Mostmajororgansandglandsinthebodyhelpregulatefluidandelectrolytebalance.
Theroleoforgansandglands•
Kidneys—regulatesodiumandpotassiumbalance(excretepotassiuminexchangeforsodiumretention)•
Lungsandliver—regulatesodiumandwaterbalanceandbloodpressure•
Heart—secretesANP,causingsodiumexcretion•
Sweatglands—excretesodium,potassium,chloride,andwaterinsweat•
GItract—absorbsandexcretesfluidsandelectrolytes•
Parathyroidglands—secreteparathyroidhormone,whichdrawscalciumintothebloodandhelpsmovephosphoroustothekidneysforexcretion•
Thyroidgland—secretescalcitonin,whichpreventscalciumreleasefromthebone•
Hypothalamusandposteriorpituitary—produceandsecreteantidiuretichormonecausingwaterretention,whichaffectssoluteconcentration•
Adrenalglands—secretealdosterone,whichinfluencessodiumandpotassiumbalanceinthekidneys
Theeffectofdiuretics•
Treathypertension,heartfailure,electrolyteimbalances,andkidneydisease•
Increaseurineproduction•
Causelossofelectrolytes,particularlypotassium•
Requirecarefulmonitoringofelectrolytes
KeyissuesinI.V.fluidtreatment•
Patient’snormalelectrolyterequirements•
Correctamountofelectrolytesprescribedandgiven•
Lengthoftreatment•
Concomitantoralelectrolytesupplementation
Quickquiz
1.Whenaburndamagescells,youwouldexpectthecellstoreleasethemajorelectrolyte:
A.potassium.B.chloride.C.calcium.D.sodium.
Answer:A.Potassiumisoneofthemajorelectrolytesinsidethecellthatleaksoutintoextracellularfluidafteramajortrauma,suchasaburn.Thisputsthepatientatriskforhyperkalemia.
2.Diureticsaffectthekidneysbyalteringthereabsorptionandexcretionof:A.wateronly.B.electrolytesonly.C.waterandelectrolytes.D.otherdrugs.
Answer:C.Diureticsgenerallyaffecthowmuchwaterandsodiumthebodyexcretes.Atthesametime,otherelectrolytessuchaspotassiumcanalsobeexcretedinurine.
3.Themainextracellularcationis:A.calcium.B.potassium.C.bicarbonate.D.sodium.
Answer:D.Sodiumisthemainextracellularcation.Inadditiontootherfunctions,ithelpsregulatefluidbalanceinthebody.
4.Inthenephron,mostelectrolytesarereabsorbedinthe:A.proximaltubule.B.glomerulus.C.loopofHenle.D.distaltubule.
Answer:A.Theproximaltubulereabsorbsmostelectrolytesfromthefiltrate.Italsoreabsorbsglucose,urea,aminoacids,andwater.
5.Potassiumisessentialforconductingelectricalimpulsesbecauseitcausesionsto:A.clumptogethertogenerateacurrent.B.shiftinandoutofthecelltoconductacurrent.C.trapsodiuminsidethecelltomaintainacurrent.D.adheretoeachothertocreateacurrent.
Answer:B.Potassiumintheintracellularfluidcausesionstoshiftinandoutofthecell,whichallowselectricalimpulsestobeconductedfromcelltocell.
6.Olderadultsareatincreasedriskforelectrolyteimbalancesbecause,withage,thekidneyshave:
A.increasedglomerularfiltrationrate.
B.fewerfunctioningnephrons.C.increasedabilitytoconcentrateurine.D.increasedbloodflow.
Answer:B.Olderadultsareatincreasedriskforelectrolyteimbalancesbecausetheirkidneyshavefewerfunctioningnephrons,adecreasedglomerularfiltrationrate,andadiminishedabilitytoconcentrateurine.
ScoringIfyouansweredallsixquestionscorrectly,congratulations!Youunderstandbalancesowell,you’rereadytowalkthehighwire.Ifyouansweredfourorfivecorrectly,great!Youstillhaveallthequalitiesofawell-balancedindividual!Ifyouansweredfewerthanfourcorrectly,noneedtofeeltoounbalanced!Justreviewthechapterandyou’llbefine.
ReferenceLobo,D.N.,Lewington,A.J.P.,&Allison,S.P.(2013).Disordersofsodium,potassium,calcium,
magnesium,andphosphate.InBasicconceptsoffluidandelectrolytetherapy(pp.105,110).Melsungen,Germany:MedizinischeVerlagsgesellschaft.
Chapter3
Balancingacidsandbases
JustthefactsInthischapter,you’lllearn:
♦thedefinitionsofacidsandbases
♦therolepHplaysinmetabolism
♦regulationofacid-basebalanceinthebody
♦essentialdiagnostictestsforassessingacid-basebalance.
AlookatacidsandbasesThechemicalreactionsthatsustainlifedependonadelicatebalance—orhomeostasis—betweenacidsandbasesinthebody.Evenaslightimbalancecanprofoundlyaffectmetabolismandessentialbodyfunctions.Severalconditions,suchasinfectionortrauma,andmedicationscanaffectacid-basebalance.However,tounderstandthisbalance,youneedtounderstandsomebasicchemistry.
UnderstandingpHUnderstandingacidsandbasesrequiresanunderstandingofpH,acalculationbasedonthepercentageofhydrogenionsinasolutionaswellastheamountofacidsandbases.
Acidsconsistofmoleculesthatcangiveup,ordonate,hydrogenionstoothermolecules.Carbonicacidisanacidthatoccursnaturallyinthebody.Basesconsistofmoleculesthatcanaccepthydrogenions;bicarbonateisoneexampleofabase.Asolutionthatcontainsmorebasethanacidhasfewerhydrogenions,soithasahigherpH.A
solutionwithapHabove7isabase,oralkaline.Asolutionthatcontainsmoreacidthanbasehasmorehydrogenions,soithasalowerpH.AsolutionwithapHbelow7isanacid,oracidotic.
GettingyourPhDinpHYoucanassessapatient’sacid-basebalanceifyouknowthepHofhisblood.BecausearterialbloodisusuallyusedtomeasurepH,thisdiscussionfocusesonarterialsamples.Arterialbloodisnormallyslightlyalkaline,rangingfrom7.35to7.45.ApHlevelwithinthat
rangerepresentsabalancebetweenthepercentageofhydrogenionsandbicarbonateions.Generally,pHismaintainedinaratioof20partsbicarbonateto1partcarbonicacid.ApHbelow6.8orabove7.8isusuallyfatal.(SeeUnderstandingnormalpH.)
UnderstandingnormalpHThisillustrationshowsthatbloodpHnormallystaysslightlyalkaline,between7.35and7.45.Atthatpoint,theamountofacid(H+)isbalancedwiththeamountofbase(representedhereasbicarbonate).ApHbelow7.35isabnormallyacidic;apHabove7.45isabnormallyalkaline.
ToolowUndercertainconditions,thepHofarterialbloodmaydeviatesignificantlyfromitsnormalnarrowrange.Iftheblood’shydrogenionconcentrationincreasesorbicarbonateleveldecreases,pHmaydecrease.Ineithercase,adecreaseinpHbelow7.35signalsacidosis.(SeeUnderstandingacidosis.)
UnderstandingacidosisAcidosis,aconditioninwhichpHisbelow7.35,occurswhenacids(H+)accumulateorbases,suchasbicarbonate,arelost.
ToohighIftheblood’sbicarbonatelevelincreasesorhydrogenionconcentrationdecreases—theoppositeeffectofalowpH—pHmayincrease.Ineithercase,anincreaseinpHabove7.45signalsalkalosis.(SeeUnderstandingalkalosis,page40.)
UnderstandingalkalosisAlkalosis,aconditioninwhichpHishigherthan7.45,occurswhenbases,suchasbicarbonate,accumulateoracids(H+)arelost.
RegulatingacidsandbasesAperson’swell-beingdependsonhisabilitytomaintainanormalpH.AdeviationinpHcancompromiseessentialbodyprocesses,includingelectrolytebalance,activityofcriticalenzymes,musclecontraction,andbasiccellularfunction.ThebodynormallymaintainspHwithinanarrowrangebycarefullybalancingacidicandalkalineelements.Whenoneaspectofthatbalancingactbreaksdown,thebodycan’tmaintainahealthypHaseasily,andproblemsarise.
ThebigthreeThebodyregulatesacidsandbasestoavoidpotentiallyseriousconsequences.Therefore,whenpHrisesorfalls,threeregulatorysystemscomeintoplay:•Chemicalbuffersactimmediatelytoprotecttissuesandcells.Thesebuffersinstantlycombine
withtheoffendingacidorbase,neutralizingharmfuleffectsuntilotherregulatorstakeover.•Therespiratorysystemuseshypoventilationorhyperventilationasneededtoregulate
excretionorretentionofacidswithinminutesofachangeinpH.•Thekidneyskickinbyexcretingorretainingacidsandbasesasneeded.Renalcompensation
kicksinaftertheaforementionedsystemsfailtorestorenormalpHlevels,typicallyafterapproximately6hoursofalkalosisoracidosis(Appel&Downs,2008).Renalregulationcantakehoursordaystorestorenormalhydrogenionconcentration.
Regulationsystem1:BuffersThebodymaintainsahealthypHinpartthroughchemicalbuffers,substancesthatminimizechangesinpHbycombiningwithexcessacidsorbases.Chemicalbuffersintheblood,intracellularfluid,andinterstitialfluidserveasthebody’smostefficientpH-balancingweapon.Themainchemicalbuffersarebicarbonate,phosphate,andprotein.
BringonthebicarbonateThebicarbonatebuffersystemisthebody’sprimarybuffersystem.It’smainlyresponsibleforbufferingbloodandinterstitialfluid.Thissystemreliesonaseriesofchemicalreactionsinwhichpairsofweakacidsandbases(suchascarbonicacidandbicarbonate)combinewithstrongeracids(suchashydrochloricacid)andbasestoweakenthem.Decreasingthestrengthofpotentiallydamagingacidsandbasesreducesthedangerthose
chemicalsposetopHbalance.Thekidneysassistthebicarbonatebuffersystembyregulatingproductionofbicarbonate.Thelungsassistbyregulatingtheproductionofcarbonicacid,which
resultsfromcombiningcarbondioxideandwater.
FeelingbetterwithphosphateLikethebicarbonatebuffersystem,thephosphatebuffersystemdependsonaseriesofchemicalreactionstominimizepHchanges.PhosphatebuffersreactwitheitheracidsorbasestoformcompoundsthatslightlyalterpH,whichcanprovideextremelyeffectivebuffering.Thissystemprovesespeciallyeffectiveinrenaltubules,wherephosphatesexistingreaterconcentrations.
PlentyofproteinProteinbuffers,themostplentifulbuffersinthebody,workinsideandoutsidecells.They’remadeupofhemoglobinaswellasotherproteins.Behavingchemicallylikebicarbonatebuffers,proteinbuffersbindwithacidsandbasestoneutralizethem.Inredbloodcells,forinstance,hemoglobincombineswithhydrogenionstoactasabuffer.
Regulationsystem2:RespirationTherespiratorysystemservesasthesecondlineofdefenseagainstacid-baseimbalances.Thelungsregulatebloodlevelsofcarbondioxide(CO2),agasthatcombineswithwatertoformcarbonicacid.IncreasedlevelsofcarbonicacidleadtoadecreaseinpH.
ChemoreceptorsinthemedullaofthebrainsensethosepHchangesandvarytherateanddepthofbreathingtocompensate.Breathingfasterordeepereliminatesmorecarbondioxidefromthelungs.Themorecarbondioxidethatislost,thelesscarbonicacidthatismadeand,asaresult,pHrises.ThebodydetectsthatpHchangeandreducescarbondioxideexcretionbybreathingslowerorlessdeeply.(SeeCarbondioxideandhyperventilation,page42.)
CarbondioxideandhyperventilationWhenapatient’srateofbreathingincreases,thebodyblowsoffcarbondioxide,andcarbondioxideleveldrops.
CheckforsuccessToassesstheeffectivenessofventilation,lookatthepartialpressureofcarbondioxideinarterialblood(PaCO2).AnormalPaCO2levelinthebodyis35to45mmHg.PaCO2valuesreflectcarbondioxidelevelsintheblood.Asthoselevelsincrease,sodoesPaCO2.
TwiceasgoodAsabuffer,therespiratorysystemcanmaintainacid-basebalancetwiceaseffectivelyaschemicalbuffersbecauseitcanhandletwicetheamountofacidsandbases.AlthoughtherespiratorysystemrespondstopHchangeswithinminutes,itcanrestorenormalpHonlytemporarily.Thekidneysareresponsibleforlong-termadjustmentstopH.
Regulationsystem3:KidneysThekidneysserveasyetanothermechanismformaintainingacid-basebalanceinthebody.Theycanreabsorbacidsandbasesorexcretethemintourine.Theycanalsoproducebicarbonatetoreplenishlostsupplies.SuchadjustmentstopHcantakethekidneyshoursordaystocomplete.Aswithotheracid-baseregulatorysystems,theeffectivenessofthekidneyschangeswithage.(SeeAcid-basebalanceacrossthelifespan.)
Agesandstages
Agesandstages
Acid-basebalanceacrossthelifespanTheeffectivenessofthesystemsthatregulateacid-basebalancevarywithage.Forexample,aninfant’skidneyscan’tacidifyurineaswellasanadult’scan.Also,therespiratorysystemofanolderadultmaybecompromisedand,therefore,lessabletoregulateacid-basebalance.Inaddition,becauseammoniaproductiondecreaseswithage,thekidneysofanolderadultcan’thandleexcessacidaswellasthekidneysofayoungeradult.
Thekidneysalsohaveapartintheregulationofthebicarbonatelevel,whichisareflectionofthemetaboliccomponentofacid-basebalance.Normally,thebicarbonatelevelisreportedwitharterialbloodgas(ABG)results.Thenormalbicarbonatelevelis22to26mEq/L.
ThekidneyskeepworkingIfthebloodcontainstoomuchacidornotenoughbase,pHdropsandthekidneysreabsorbsodiumbicarbonate.Thekidneysalsoexcretehydrogenalongwithphosphateorammonia.Althoughurinetendstobeacidicbecausethebodyusuallyproducesslightlymoreacidsthanbases,insuchsituations,urinebecomesmoreacidicthannormal.Thereabsorptionofbicarbonateandtheincreasedexcretionofhydrogencausesmore
bicarbonatetobeformedintherenaltubulesandeventuallyretainedinthebody.Thebicarbonatelevelinthebloodthenrisestoamorenormallevel,increasingpH.
UpsanddownsofacidsandbasesIfthebloodcontainsmorebaseandlessacid,pHrises.Thekidneyscompensatebyexcretingbicarbonateandretainingmorehydrogenions.Asaresult,urinebecomesmorealkalineandbloodbicarbonateleveldrops.Conversely,ifthebloodcontainslessbicarbonateandmoreacid,pHdrops.
AltogethernowThebodyrespondstoacid-baseimbalancesbyactivatingcompensatorymechanismsthatminimizepHchanges.ReturningthepHtoanormalornear-normallevelmainlyinvolveschangesinthecomponent—metabolicorrespiratory—notprimarilyaffectedbytheimbalance.Ifthebodycompensatesonlypartiallyforanimbalance,pHremainsoutsidethenormalrange.
Ifthebodycompensatesfullyorcompletely,pHreturnstonormal.
Respiratoryhelpsmetabolic...
Ifmetabolicdisturbanceistheprimarycauseofanacid-baseimbalance,thelungscompensateinoneoftwoways.Whenalackofbicarbonatecausesacidosis,thelungsincreasetherateofbreathing,whichblowsoffcarbondioxideandhelpsraisethepHtonormal.Whenanexcessofbicarbonatecausesalkalosis,thelungsdecreasetherateofbreathing,whichretainscarbondioxideandhelpslowerpH.
...AndviceversaIftherespiratorysystemdisturbstheacid-basebalance,thekidneyscompensatebyalteringlevelsofbicarbonateandhydrogenions.WhenPaCO2ishigh(astateofacidosis),thekidneysretainbicarbonateandexcretemoreacidtoraisethepH.WhenPaCO2islow(astateofalkalosis),thekidneysexcretebicarbonateandholdontomoreacidtolowerthepH.
Memoryjogger
Remember,PaCO2andpHmoveinoppositedirections.IfPaCO2rises,thenpHfalls,andviceversa.
DiagnosingimbalancesAnumberoftestsareusedtodiagnoseacid-basedisturbances.Here’salookatthemost
commonlyusedtests.
ArterialbloodgasanalysisAnABGanalysisisadiagnostictestinwhichasampleofbloodobtainedfromanarterialpuncturecanbeusedtoassesstheeffectivenessofbreathingandoverallacid-basebalance.Inadditiontohelpingyouidentifyproblemswithoxygenationandacid-baseimbalances,thetestcanhelpyoumonitorapatient’sresponsetotreatment.(SeeTakinganABGsample.)
TakinganABGsampleWhenaneedlepunctureisneededtoobtainanABGsample,theradial,brachial,orfemoralarteriesmaybeused.However,theangleofpenetrationvaries.Fortheradialartery(thearterymostcommonlyused),theneedleshouldenterbevelupata45-
degreeangle,asshownbelow.Forthebrachialartery,theangleshouldbe60degrees;forthefemoralartery,90degrees.
KeepinmindthatABGanalysisshouldbeusedonlyinconjunctionwithafullpatientassessment.Onlybyassessingallinformationcanyougainaclearpictureofwhat’shappening.AnABGanalysisinvolvesseveralseparatetestresults,onlythreeofwhichrelatetoacid-base
balance:pH,PaCO2,andbicarbonatelevel.Thenormalrangesforadultsare:•pH—7.35to7.45•PaCO2—35to45mmHg•bicarbonate—22to26mEq/L.
TheABCsofABGsRecallthatpHisameasureofthehydrogenionconcentrationofblood;PaCO2isameasureofthepartialpressureofcarbondioxideinarterialblood,whichindicatestheeffectivenessofbreathing.PaCO2levelsmoveintheoppositedirectionofpHlevels.Bicarbonate,whichmovesin
thesamedirectionofpH,representsthemetaboliccomponentofthebody’sacid-basebalance.OtherinformationroutinelyreportedwithABGresultsincludespartialpressureofoxygen
dissolvedinarterialblood(PaO2)andarterialoxygensaturation(SaO2).ThenormalPaO2rangeis80to100mmHg;however,PaO2varieswithage.Afterage60years,thePaO2maydropbelow80mmHgwithoutsignsandsymptomsofhypoxia.ThenormalSaO2rangeis95%to100%.
InterpretingABGresultsWheninterpretingresultsfromanABGanalysis,followaconsistentsequencetoanalyzetheinformation.Here’sonestep-by-stepprocessyoucanuse.(SeeQuicklookatABGresults.)
QuicklookatABGresultsHere’saquicklookathowtointerpretABGresults:•
CheckthepH.Isitnormal(7.35to7.45),acidotic(below7.35),oralkalotic(above7.45)?•
CheckPaCO2.Isitnormal(35to45mmHg),low,orhigh?•
Checkthebicarbonatelevel.Isitnormal(22to26mEq/L),low,orhigh?•
Checkforsignsofcompensation.Whichvalue(PaCO2orbicarbonate)morecloselycorrespondstothechangeinpH?•
CheckPaO2andSaO2.IsthePaO2normal(80to100mmHg),low,orhigh?IstheSaO2normal(95%to100%),low,orhigh?
Step1:CheckthepHFirst,checkthepHlevel.Thisfigureformsthebasisforunderstandingmostotherfigures.IfpHisabnormal,determinewhetheritreflectsacidosis(below7.35)oralkalosis(above
7.45).Thenfigureoutwhetherthecauseisrespiratoryormetabolic.
Step2:DeterminethePaCO2RememberthatthePaCO2levelprovidesinformationabouttherespiratorycomponentofacid-basebalance.IfPaCO2isabnormal,determinewhetherit’slow(lessthan35mmHg)orhigh(greaterthan
45mmHg).ThendeterminewhethertheabnormalresultcorrespondswithachangeinpH.Forexample,ifthepHishigh,youwouldexpectthePaCO2tobelow(hypocapnia),indicatingthattheproblemisrespiratoryalkalosis.Respiratoryalkalosisiscausedbyhyperventilation,mechanicaloverventilation,pregnancy,stroke,highaltitudes,andsepticemia(Appel&Downs,2008;Rogers&McCutcheon,2013).Conversely,ifthepHislow,youwouldexpectthePaCO2tobehigh(hypercapnia),indicatingthattheproblemisrespiratoryacidosiscausedbyhypoventilation.Causesofrespiratoryacidosismaybeacuteorchronicandarelinkedtochronicdiseasessuchaschronicbronchitis,asthma,pneumonia,andairwayobstruction(Rogers&McCutcheon,2013).
Step3:WatchthebicarbonateNext,examinethebicarbonatelevel.Thisvalueprovidesinformationaboutthemetabolicaspectofacid-basebalance.Ifthebicarbonatelevelisabnormal,determinewhetherit’slow(lessthan22mEq/L)orhigh
(greaterthan26mEq/L).ThendeterminewhethertheabnormalresultcorrespondswiththechangeinpH.Forexample,ifpHishigh,youwouldexpectthebicarbonateleveltobehigh,indicatingthattheproblemismetabolicalkalosis.Causesofmetabolicalkalosisincludetheuseofdiuretics,vomiting,hyperaldosteronism,excessiveuseofalkalinemedicationssuchasantacids,andCushing’ssyndrome(Appel&Downs,2008;Rogers&McCutcheon,2013).Conversely,ifpHislow,youwouldexpectthebicarbonateleveltobelow,indicatingthattheproblemismetabolicacidosis.Causesofmetabolicacidosisincludediabeticketoacidosis,lacticacidosis,andseverediarrheathatleadtoalossofbicarbonate(Appel&Downs,2008;Rogers&McCutcheon,2013).
Memoryjogger
Remember,bicarbonateandpHincreaseordecreasetogether.Whenonerisesorfalls,sodoestheother.
Step4:LookforcompensationSometimesyou’llseeachangeinboththePaCO2andthebicarbonatelevel.OnevalueindicatestheprimarysourceofthepHchange;theother,thebody’sefforttocompensateforthedisturbance.Completecompensationoccurswhenthebody’sabilitytocompensateissoeffectivethatpH
fallswithinthenormalrange.Partialcompendethenormalrange.Compensationinvolvesopposites.Forinstance,ifresultsindicateprimarymetabolic
acidosis,csation,ontheotherhand,occurswhenpHremainsoutsiompensationwillcomeintheform
ofrespiratoryalkalosis.Forexample,thefollowingABGresultsindicatemetabolicacidosiswithcompensatoryrespiratoryalkalosis:•pH—7.29•PaCO2—17mmHg•bicarbonate—19mEq/L.ThelowpHindicatesacidosis.However,thePaCO2islow,whichnormallyleadsto
alkalosis,andthebicarbonatelevelislow,whichnormallyleadstoacidosis.Thebicarbonatelevel,then,morecloselycorrespondswiththepH,makingtheprimarycauseoftheproblemmetabolic.TheresultantdecreaseinPaCO2reflectspartialrespiratorycompensation.NormalvaluesforpH,PaCO2,andbicarbonatewouldindicatethatthepatient’sacid-base
balanceisnormal.
Step5:DeterminePaO2andSaO2Last,checkPaO2andSaO2,whichyieldinformationaboutthepatient’soxygenationstatus.Ifthevaluesareabnormal,determinewhetherthey’rehigh(PaO2greaterthan100mmHg)orlow(PaO2lessthan80mmHgandSaO2lessthan95%).RememberthatPaO2reflectsthebody’sabilitytopickupoxygenfromthelungs.AlowPaO2
representshypoxemiaandcancausehyperventilation.ThePaO2valuealsoindicateswhentomakeadjustmentsintheconcentrationofoxygenbeingadministeredtoapatient.(SeeInaccurateABGresults.)
InaccurateABGresultsToavoidalteringABGresults,besuretousepropertechniquewhendrawingasampleofarterialblood.Remember:•
AdelayingettingthesampletothelaboratoryordrawingbloodforABGanalysiswithin15to20minutesofaprocedure,suchassuctioningoradministeringarespiratorytreatment,couldalterresults.•
Airbubblesinthesyringecouldaffecttheoxygenlevel.•
VenousbloodinthesyringecouldaltercarbondioxideandoxygenlevelsandpH.
AniongapYoumayalsocomeacrossatestresultcalledtheaniongap.(SeeCrossingthegreataniongap.)Earlierchaptersdiscusshowthestrengthofcations(positivelychargedions)andanions(negativelychargedions)mustbeequalinthebloodtomaintainaproperbalanceofelectricalcharges.Theaniongapresulthelpsyoudifferentiateamongvariousacidoticconditions.
CrossingthegreataniongapThisillustrationrepresentsthenormalaniongap.Thegapiscalculatedbyaddingthechloridelevelandthebicarbonatelevelandthensubtractingthattotalfromthesodiumlevel.Thevaluenormallyrangesfrom8to14mEq/Landrepresentsthelevelofunmeasuredanionsinextracellularfluid.Intheexamplebelow,thechloridelevelis105mEq/L,thebicarbonatelevelis25mEq/L,andthe
sodiumlevelis140mEq/L.Tofindtheaniongap,firstaddthechlorideandbicarbonatelevelstogetatotalof130mEq/L.Thensubtractthattotalfromthesodiumlevelof140mEq/L,whichleaves10mEq/L—theaniongap.
Identifyingthegap
Theaniongapreferstotherelationshipamongthebody’scationsandanions.Sodiumaccountsformorethan90%ofthecirculatingcations.Chlorideandbicarbonatetogetheraccountfor85%ofthecounterbalancinganions.(Potassiumisgenerallyomittedbecauseitoccursinsuchlow,stableamounts.)Thegapbetweenthetwomeasurementsrepresentstheanionsnotroutinelymeasured,including
sulfates,phosphates,proteins,andorganicacidssuchaslacticacidandketoneacids.Becausetheseanionsaren’tmeasuredinroutinelaboratorytests,theaniongapisawayofdeterminingtheirpresence.
GazingintothegapAnincreaseintheaniongapthat’sgreaterthan14mEq/Lindicatesanincreaseinthepercentageofoneormoreunmeasuredanionsinthebloodstream.Increasescanoccurwithacidoticconditionscharacterizedbyhigherthannormalamountsoforganicacids.Suchconditionsincludelacticacidosisandketoacidosis.Theaniongapremainsnormalforcertainotherconditions,includinghyperchloremicacidosis,
renaltubularacidosis,andseverebicarbonate-wastingconditions,suchasbiliaryorpancreaticfistulasandpoorlyfunctioningilealloops.Adecreasedaniongapisrarebutmayoccurwithhypermagnesemiaandparaproteinanemia
states,suchasmultiplemyelomaandWaldenström’smacroglobulinemia.
That’sawrap!
Balancingacidsandbasesreview
Acid-basebasics•
Acids—moleculesthatcangivehydrogenmoleculestoothermolecules;includesolutionswithapHbelow7•
Bases—moleculesthatcanaccepthydrogenmolecules;includesolutionswithapHabove7•
Mustmaintainadelicatebalanceforthebodytoworkproperly•
Metabolismandbodyfunctionsaffectedbyslightimbalances•
Imbalancecausedbyinfection,trauma,andmedications
UnderstandingpH
•pH—calculationbasedonthepercentageofhydrogenionsandtheamountofacidsandbasesinasolution•
NormalbloodpH—7.35to7.45,whichrepresentsthebalancebetweenhydrogenionsandbicarbonateions
DeviationfromnormalpH•
Acidosis—bloodpHisbelow7.35andeitherthehydrogenionconcentrationhasincreasedorthebicarbonatelevelhasdecreased.•
Alkalosis—bloodpHisabove7.45andeitherthehydrogenionconcentrationhasdecreasedorthebicarbonatelevelhasincreased.•
ApHbelow6.8orabove7.8isgenerallyfatal.•
Deviationcompromiseswell-being,electrolytebalance,activityofcriticalenzymes,musclecontraction,andbasiccellularfunction.
Maintainingacid-basebalanceThreesystemsregulateacidsandbases:•
Chemicalbuffers—neutralizetheoffendingacidorbase•
Respiratorysystem—regulatesretentionandexcretionofacids•
Kidneys—excreteorretainacidsorbases
Chemicalbuffersystems•
Bicarbonatebuffersystem—buffersbloodandinterstitialfluid•
Phosphatebuffersystem—reactswithacidsandbasestoformcompoundsthatalterpH;especiallyeffectiveintherenaltubules•
Proteinbuffersystem—actsinsideandoutsidethecell;bindswithacidsandbasestoneutralizethem
Respiratorysystem•
Functionsasthesecondlineofdefense•
RespondstopHchangesinminutes•
MakestemporaryadjustmentstopH•
Regulatescarbondioxidelevelsinthebloodbyvaryingtherateanddepthofbreathing•
Compensateswithquickanddeepbreathingsomorecarbondioxideislostwhenbicarbonatelevelsarelow•
Compensateswithslow,shallowbreathingsomorecarbondioxideisretainedwhenbicarbonatelevelsarehigh•
Regulatescarbonicacidproduction
Kidneys•
Kickinwhenthefirsttwosystemsfailtoreversetheacidosisoralkalosis•
Makelong-termadjustmentstopH•
Reabsorbacidsandbasesorexcretethemintourine•
Producebicarbonatetoreplenishlostsupply•
Regulatebicarbonateproduction•
CompensatewithbicarbonateretentionandincreasedacidexcretionwhenPaCO2levelishigh•
RespondwithbicarbonateexcretionandincreasedacidretentionwhenPaCO2levelislow
Aniongap•
Representsthelevelofunmeasuredanionsinextracellularfluid•
Normallyrangesfrom8to14mEq/L•
Helpsdifferentiateacidoticconditions
Interpretingacid-baseimbalances•
Step1:CheckpH.Acidosisoralkalosis?•
Step2:DeterminePaCO2.Isitnormal,high,orlow?•
Step3:Watchbicarbonateforinformationaboutmetaboliccondition.•
Step4:Lookforcompensation.Forexample,metabolicacidosiscanleadtocompensationbyrespiratoryalkalosis.•
Step5:DeterminePaO2andSaO2.Togethertheyyieldinformationaboutoxygenstatus.
Quickquiz
1.PaCO2levelindicatestheeffectivenessof:A.kidneyfunction.B.lungventilation.C.phosphatebuffers.D.bicarbonatebuffers.
Answer:B.PaCO2reflectshowwelltherespiratorysystemishelpingtomaintainacid-basebalance.
2.Thekidneysrespondtoacid-basedisturbancesby:A.adjustingPaCO2levels.B.producingphosphatebuffers.C.producingproteinbuffers.D.excretingorreabsorbinghydrogenorbicarbonate.
Answer:D.Thekidneysrespondtoparticularacid-baseimbalancesbyexcretingorreabsorbinghydrogenorbicarbonate,accordingtothebody’sneeds.
3.Ifyourpatientisbreathingrapidly,hisbodyisattemptingto:A.retaincarbondioxide.B.getridofexcesscarbondioxide.C.improvethebufferingabilityofbicarbonate.D.producemorecarbonicacid.
Answer:B.Highcarbondioxidelevelsintheblood,measuredasPaCO2,causeadropinpH.Chemoreceptorsinthebrainsensethisdecreaseandstimulatethelungstohyperventilate,causingthebodytoeliminatemorecarbondioxide.
4.IfyourpatienthasahigherthannormalpH(alkalosis),youwouldexpecttoalsosee:
A.highPaCO2andhighbicarbonate.B.lowPaCO2andhighbicarbonate.C.lowbicarbonateandhighPaCO2.D.lowPaCO2andlowbicarbonate.
Answer:B.AlowPaCO2meanslesscarbondioxide(acid)isintheblood,whichraisespH.WhenpHisraised,thebicarbonatelevelalsoincreases.
5.ThelaboratoryreportsthefollowingABGresultsforyourpatient:pH,7.33;PaCO2,40mmHg;andbicarbonate,20mEq/L.Youinterprettheseresultsas:
A.respiratoryacidosis.B.metabolicacidosis.C.respiratoryalkalosis.D.metabolicalkalosis.
Answer:B.Thepatient’spHislow,whichindicatesacidosis.BecausePaCO2isnormalandbicarbonateislow(matchingthepH),theprimarycauseoftheproblemismetabolic.
6.AcolleaguehandsyoutheseABGresults:pH,7.52;PaCO2,47mmHg;andbicarbonate,36mEq/L.Youinterprettheseresultsas:
A.normal.B.respiratoryacidosis.C.respiratoryalkalosiswithrespiratorycompensation.D.metabolicalkalosiswithrespiratorycompensation.
Answer:D.ThepHisalkalotic.AlthoughbothPaCO2andbicarbonatehavechanged,thebicarbonatematchesthepH.TheelevatedPaCO2representstheeffortsoftherespiratorysystemtocompensateforthealkalosisbyretainingcarbondioxide.
ScoringIfyouansweredallsixquestionscorrectly,congratulations!Youdidagreatjobcoveringallthebases(andacids)!Ifyouansweredfourorfivecorrectly,great!Youcertainlydidn’thydrogenbomb!Ifyouansweredfewerthanfourcorrectly,don’tworry!It’snevertoolatetogetyourPhDinpH!
ReferencesAppel,S.J.,&Downs,C.A.(2008).Understandingacid-basebalance.Findouthowtointerpretvalues
andsteadyadisturbedequilibriuminanacutelyillpatient.Nursing2014,38,9–11.Rogers,K.M.,&McCutcheon,K.(2013).Understandingarterialbloodgases.JournalofPerioperative
Practice,23(9),191–197.
PartII
Fluidandelectrolyteimbalances
4 Whenfluidstipthebalance
5 Whensodiumtipsthebalance
6 Whenpotassiumtipsthebalance
7 Whenmagnesiumtipsthebalance
8 Whencalciumtipsthebalance
9 When
9 Whenphosphorustipsthebalance
10 Whenchloridetipsthebalance
11 Whenacidsandbasestipthebalance
Chapter4
Whenfluidstipthebalance
JustthefactsInthischapter,you’lllearn:
♦waystoassessapatient’sfluidstatus
♦waystoidentifypatientsatriskforfluidimbalances
♦signsandsymptomsoffluidimbalances
♦teachingtipsforpatientswithfluidimbalances
♦tipsforensuringproperdocumentationoffluidimbalances.
AlookatfluidvolumeBloodpressureisrelatedtotheamountofbloodtheheartpumpsandtheextentofvasoconstrictionpresent.Fluidvolumeaffectstheseelements,makingbloodpressuremeasurementkeyinassessingapatient’sfluidstatus.Certaintypesofpressure,suchaspulmonaryarterypressure(PAP)andcentralvenouspressure(CVP),aremeasuredthroughspecializedcatheters.Thesemeasurementsalsohelpassessfluidvolumestatus.Tomaintaintheaccuracyofwhateverbloodpressuremeasurementsystemyouuse,periodically
comparethereadingsofautomatedanddirectmeasurementsystemswithmanualreadings.
CuffmeasurementsAsimplebloodpressuremeasurement,takenwithastethoscopeandasphygmomanometer,isstilloneofthebesttoolsforassessingfluidvolume.It’squickandeasyandcarrieslittleriskforthepatient.Directandindirectbloodpressuremeasurementsaregenerallyrelatedtotheamountofbloodflowingthroughthepatient’scirculatorysystem.
AsizeabletaskTomeasurebloodpressureaccurately,youmustfirstmakesurethecuffisthecorrectsize.Thebladderofthecuffshouldhavealengththat’s80%andawidththat’satleast40%oftheupperarmcircumference.
InpositionPositionthearmsothatthebrachialarteryisatheartlevel.Topositionthebloodpressurecuffproperly,wrapitsnuglyaroundtheupperarm.Foradults,placethelowerborderofthecuffabout1″(2.5cm)abovetheantecubitalfossa.Forchildren,placethelowerborderclosertotheantecubitalfossa.Placethecenterofthecuff’sbladderdirectlyoverthemedialaspectofthearm,overthe
brachialartery.Mostcuffshaveareferencemarktohelpyoupositionthebladder.Afterpositioningthecuff,palpatethebrachialarteryusingyourindexfinger,andplacethebellofthestethoscopedirectlyoverthepointwhereyoucanfeelthestrongestpulsations.(SeePositioningabloodpressurecuff.)Oncethepatientisproperlypositioned,heorsheshouldbealloweda5-minuterestperiodbeforebloodpressuremeasurement(Garcia,Ang,Ahmad,&Lim,2012).
PositioningabloodpressurecuffThisphotographshowshowtoproperlypositionabloodpressurecuffandstethoscopebell.
ListenupOnceyouhavethestethoscopeandcuffinplace,usethethumbandindexfingerofyourotherhandtoturnthescrewontherubberbulboftheairpumpandclosethevalve.Thenpumpairintothecuffwhileauscultatingoverthebrachialarteryandcontinuepumpingairuntilthegaugeregistersatleast10mmHgabovethelevelofthelastaudiblesound.Next,carefullyopentheairpumpvalveandslowlydeflatethecuff.Whilereleasingair,watchthegaugeandauscultateovertheartery.Whenyouhearthefirstbeat,notethepressureonthegauge;thisisthesystolicpressure.Continuegraduallyreleasingair,watchingthegauge,andauscultating.Notethediastolicreadingwhenthetonebecomessoftandmuffled.Ifyoususpectafalse-highorfalse-lowreading,takestepstocorrecttheproblem.(SeeCorrectingproblemsofbloodpressuremeasurement.)
It’snotworking
CorrectingproblemsofbloodpressuremeasurementUsethischarttofigureoutwhattodoforeachpossiblecauseofafalse-highorfalse-lowbloodpressurereading.
Problemandpossiblecause WhattodoFalse-highreadingCufftoosmall Makesurethecuffbladderislongenoughto
completelyencircletheextremity.Cuffwrappedtooloosely,reducingitseffectivewidth
Tightenthecuff.
Slowcuffdeflation,causingvenouscongestioninthearmorleg
Neverdeflatethecuffslowerthan2mmHgperheartbeat.
Poorlytimedmeasurement(afterthepatienthaseaten,ambulated,appearedanxious,orflexedhisarmmuscles)
Postponebloodpressuremeasurementorhelpthepatientrelaxbeforetakingpressures.
Multipleattemptsatreadingbloodpressureinthesamearm,causingvenouscongestion
Don’tattempttomeasurebloodpressuremorethantwiceinthesamearm;waitseveralminutesbetweenattempts.
False-lowreadingIncorrectpositionofthearmorleg Makesurethearmorlegislevelwiththe
patient’sheart.Failuretonoticeauscultatorygap(soundfadesoutfor10to15mmHg,thenreturns)
Estimatesystolicpressureusingpalpationbeforeactuallymeasuringit.Thencheckthepalpablepressureagainstthemeasuredpressure.
Inaudibleorlow-volumesounds Beforereinflatingthecuff,instructthepatienttoraisehisarmorlegtodecreasevenouspressureandamplifylow-volumesounds.Afterinflatingthecuff,tellthepatienttolowerhisarmorleg.Thendeflatethecuffandlisten.Ifyoustillfailtodetectlow-volumesounds,chartthepalpablesystolicpressure.
It’sallautomaticYoumayalsohaveaccesstoanautomatedbloodpressureunit.Thisunitisdesignedtotakebloodpressuremeasurementsrepeatedly,whichishelpfulwhenyou’recaringforapatientwhosebloodpressureisexpectedtochangefrequently(forexample,apatientwithafluidimbalance).Theunitautomaticallycomputesanddigitallyrecordsbloodpressurereadings.Thecuffautomaticallyinflatestocheckthebloodpressureanddeflatesimmediatelyafterward.
Youcanprogramthemonitortoinflatethecuffasoftenasneededandsetalarmsforhigh,low,andmeanbloodpressures.Mostmonitorsdisplayeachbloodpressurereadinguntilthenextreadingistaken.
PalpablepressuresIfyouhavetroublehearingthepatient’sbloodpressure,whichiscommonwhenapatientishypotensive,palpatethebloodpressuretoestimatesystolicpressure.Topalpatebloodpressure,placeacuffontheupperarmandpalpatethebrachialpulseorthe
radialpulse.Inflatethecuffuntilyounolongerfeelthepulse.Thenslowlydeflatethecuff,notingthepointatwhichyoufeelthepulseagain—thesystolicpressure.Ifyoupalpateapatient’sbloodpressureat90mmHg,forexample,chartitas“90/P”(thePstandsforpalpable).
TheDopplerdifferenceWhatshouldyoudoifyourpatient’sarmisswollenorhisbloodpressureissolowyoucan’tfeelhispulse?First,palpatehiscarotidarterytomakesurehehasapulse.Then,useaDopplerdevicetoobtainareadingofhissystolicpressure.(SeeHowtotakeaDopplerbloodpressure.)
HowtotakeaDopplerbloodpressureWhenyoucan’thearorfeelapatient’sbloodpressure,tryusingaDopplerultrasounddevice,asshownbelow.
TheDopplerprobeusesultrasoundwavesdirectedatthebloodvesseltodetectbloodflow.ThroughtheDopplerunit,you’llbeabletohearthepatient’sbloodflowwitheachpulse.ToobtainaDopplerbloodpressure,takethesesteps:
•Placeabloodpressurecuffonthearmasyounormallywould.•Applylubricanttotheantecubitalareawhereyouwouldexpecttofindthebrachialpulse.•Turntheunitonandplacetheprobelightlyonthearmoverthebrachialartery.•Adjustthevolumecontrolandtheplacementoftheprobeuntilyouhearthepulseclearly.•Inflatethebloodpressurecuffuntilthepulsesounddisappears.•Slowlydeflatethecuffandnotethepointatwhichthepulsesoundreturns—thesystolic
pressure.Ifyouhearthepulseat80mmHg,forinstance,recorditas“80/D”(theDstandsforDoppler).
DirectmeasurementsDirectmeasurementisaninvasivemethodofobtainingbloodpressurereadingsusingarterialcatheters.Directmeasurementisusedwhenhighlyaccurateorfrequentbloodpressuremeasurementsarerequired,suchaswithseverefluidimbalances.
ArteriallinesArteriallines,orA-lines,areinsertedintotheradialorthebrachialartery(orthefemoralartery,ifneeded).A-linescontinuouslymonitorbloodpressureandcanalsobeusedtosamplearterial
bloodforbloodgasanalysisorotherlaboratorytests.BecauseA-linesrequireacertainleveloftechnologyandstafftraining,patientswhohavethemareusuallyplacedinintermediateorcriticalcareunits.
LinesunderpressureThecatheterisconnectedtoacontinuousflushsystem—abagofnormalsalinesolution(whichmaycontainheparin)insideapressurizedcuff.ThissystemmaintainsthepatencyoftheA-line.TheA-lineisconnectedtoatransducerandthentoabedsidemonitor.Thetransducerconverts
fluid-pressurewavesfromthecatheterintoanelectronicsignalthatcanbeanalyzedanddisplayedonthemonitor.Becausethepatient’sbloodpressureisdisplayedcontinuously,youcaninstantlynotechangesinthemeasurementsandrespondquickly.
PulmonaryarterycathetersAnA-linedirectlymeasuresbloodpressure,whereasapulmonaryartery(PA)catheterdirectlymeasuresotherpressures.PAcathetersareusuallyinsertedintothesubclavianveinortheinternaljugularvein,althoughthelinesaresometimesinsertedintoaveininthearm(brachialvein)ortheleg(femoralvein).
Thetipofthecatheterisadvancedthroughtheveinintotherightatrium,thenintotherightventricle,andfinallyintothepulmonaryartery.Thehubsofthecatheterarethenconnectedtoapressurizedtransducersystemthat’ssimilartothesystemusedforanA-line.(SeePulmonaryarterycatheterports,page60.)
PulmonaryarterycatheterportsTheportsonaPAcatheter(shownhere)canbeusedforpacing;infusingsolutions;ormonitoringoxygensaturation,bodytemperature,cardiacoutput,orvariousintraluminalpressures,suchasCVP(throughtheproximallumen)orPAWP(throughthedistallumen).
GettingaclearerpictureAPAcatheterprovidesaclearerpictureofthepatient’sfluidvolumestatusthanothermeasurementtechniques.ThecatheterallowsformeasurementofPAP,pulmonaryarterywedgepressure(PAWP),cardiacoutput,andCVP—allofwhichprovideinformationabouthowtheleftsideoftheheartisfunctioning,includingitspumpingability,fillingpressures,andvascularvolume.ThePAPisthepressureroutinelydisplayedonthemonitor.AnormalsystolicPAPis15to25
mmHgandreflectspressurefromcontractionoftherightatrium(Muralidhar,2002).AnormaldiastolicPAPis8to15mmHgandreflectsthelowestpressureinthepulmonaryvessels,andthemeanPAPis10to20mmHg(Muralidhar,2002).
WedgedinWhenyouinflatethesmallballoonatthecathetertip,bloodcarriesthecathetertipfartherintothepulmonaryartery.Thetipfloatsinsidethearteryuntilitstops—orbecomeswedged—inasmallerbranch.Whenthetipiswedgedinabranchofthepulmonaryartery,thecathetermeasurespressures
comingfromtheleftsideoftheheart,whichisameasurementthatmayproveusefulingaugingchangesinbloodvolume.AnormalPAWPis4to12mmHg(Muralidhar,2002).PAPandPAWParegenerallyincreasedincasesoffluidoverloadanddecreasedincasesof
fluidvolumedeficit,explainingwhyaPAcatheterisusefulwhenassessingandtreatinganacutely
illpatientwithafluidimbalance(Muralidhar,2002).
MultiplemeasurementsPAcathetersalsomeasurecardiacoutput,eithercontinuouslyorafterinjectionsofI.V.fluidthroughtheproximallumen.Cardiacoutputistheamountofbloodthattheheartpumpsin1minuteandiscalculatedbymultiplyingtheheartratebythestrokevolume.(Conveniently,themonitormakesthatcalculationforyou.)Thestrokevolumeistheamountofbloodtheventriclepumpsoutwitheachbeat,andit’salso
calculatedbythebedsidemonitor.Normalcardiacoutputis4to8L/minute.Ifapersonlacksadequatebloodvolume,cardiacoutputislow(assumingtheheartcanpumpnormallyotherwise).Ifthepersonisoverloadedwithfluid,cardiacoutputishigh.
CentralvenouspressureAcentralvenouscathetercanmeasureCVP,anotherusefulindicationofapatient’sfluidstatus.ThetermCVPreferstothepressureofthebloodinsidethecentralvenouscirculation.TheCVPcatheteristypicallyinsertedinoneofthejugularveinsintheneckorinasubclavianveininthechest,withthetipofthecatheterpositionedabovetherightatriuminthesuperiorvenacava.NormalCVPrangesfrom2to8mmHg(2to6cmH2O).IfCVPishigh,itusuallymeansthe
patientisoverloadedwithfluid.Ifit’slow,itusuallymeansthepatientislowonfluid.(TocalculateCVPbyyourself,seeEstimatingCVP,page62.)
EstimatingCVPToestimateapatient’sCVP,followthesesteps:1.Placethepatientata45-to60-degreeangle.2.Usetangentiallightingtoobservetheinternaljugularvein.3.Notethehighestlevelofvisiblepulsation.4.Next,locatetheangleofLouisorsternalnotch.Todothis,firstpalpatethepointatwhichtheclaviclesjointhesternumtofindthesuprasternalnotch.5.Thenplacetwofingersonthepatient’ssuprasternalnotchandslidethemdownthesternumuntiltheyreachabonyprotuberance—theangleofLouis.Therightatriumliesabout2″(5cm)belowthispoint.6.MeasurethedistancebetweentheangleofLouisandthehighestlevelofvisiblepulsation.Normally,thisdistanceislessthan1.2″(3cm).7.Add2″tothisfiguretoestimatethedistancebetweenthehighestlevelofpulsationandtherightatrium.Adistancegreaterthan4″(10cm)mayindicateelevatedCVP.
MaintainingbalanceMostofthetime,thebodyadequatelycompensatesforminorfluidimbalancesandkeepsbloodpressurereadingsandothermeasurementsfairlynormal.Sometimes,however,thebodycan’tcompensateforfluiddeficitsorexcesses.Whenthathappens,anyofseveralproblemsmayresult,includingdehydration,hypovolemia,hypervolemia,andwaterintoxication.
DehydrationThebodyloseswaterallthetime.Apersonrespondstothethirstreflexbydrinkingfluidsandeatingfoodsthatcontainwater.However,ifwaterisn’tadequatelyreplaced,thebody’scellscanlosewater,aconditioncalleddehydration.Dehydrationcanbeclassifiedasisotonic,hypertonic,andhypotonic(Ashford,2008).Isotonicdehydrationisaresultofhypovolemiaorfluidvolumeloss(Ashford,2008).Hypertonicdehydrationisaresultofdeprivationoffluidsoftenseenintheelderlyandveryyoung(Ashford,2008).Hypotonicdehydrationisaresultofsodiumlossingreateramountsthanfreewateroftenseenasaresultofalow-sodiumdietordiureticoveruse(Ashford,2008).
HowithappensLossofbodyfluidscausesbloodsoluteconcentrationtoincrease(increasedosmolality)andserumsodiumlevelstorise.Inanattempttoregainfluidbalancebetweenintracellularandextracellularspaces,watermoleculesshiftoutofcellsintomoreconcentratedblood.Thisprocess,combinedwithincreasedwaterintakeandincreasedwaterretentioninthekidneys,usuallyrestoresthebody’sfluidvolume.
IncrediblyshrinkingcellsWithoutanadequatesupplyofwaterintheextracellularspace,fluidcontinuestoshiftoutofthecellsintothatspace.Thecellsbegintoshrinkastheprocesscontinues.Becausewaterisessentialforobtainingnutrients,expellingwastes,andmaintainingcellshape,cellscan’tfunctionproperlywithoutadequatefluid.
Whoisatrisk?Failuretorespondadequatelytothethirststimulusincreasestheriskofdehydration.Confused,comatose,andbedriddenpatientsareparticularlyvulnerable,asareinfants,whocan’tdrinkfluidontheirownandwhohaveimmaturekidneysthatcan’tconcentrateurineefficiently.Olderpatientsarealsopronetodehydrationbecausetheyhavealowerbodywatercontent,
diminishedkidneyfunction,andareducedabilitytosensethirst,sotheycan’tcorrectfluidvolumedeficitsaseasilyasyoungeradults.Apatientmayalsobecomedehydratedifhe’sreceivinghighlyconcentratedtubefeedingswithoutenoughsupplementalwater.(SeeDifferentbutthesame.)
Agesandstages
Agesandstages
DifferentbutthesameElderlyandveryyoungpatientsarehighlysusceptibletofluidandelectrolyteimbalances.Despitethesignificantagedifference,thecontributingfactorsfortheseimbalancesarethesameinmanycases:•
inabilitytoobtainfluidwithouthelp•
inabilitytoexpressfeelingsofthirst•
inaccurateassessmentofoutput—forexample,ifthepatientmustwearadiaper•
lossoffluidthroughperspirationbecauseoffever•
lossoffluidthroughdiarrheaandvomiting.
Whatbringsiton?Anysituationthatacceleratesfluidlosscanleadtodehydration.Forinstance,indiabetesinsipidus,thebrainfailstosecreteantidiuretichormone(ADH).Ifthebraindoesn’tsecreteenoughADH,theresultisgreater-than-normaldiuresis.Apatientwithdiabetesinsipidusproduceslargeamountsofhighlydilutedurine—asmuchas30L/day.Thepatientisalsothirstyandtendstodrinklargeamountsoffluids,althoughhegenerallycan’tkeepupwiththediuresis.Othercausesofdehydrationincludeprolongedfever,waterydiarrhea,renalfailure,and
hyperglycemia(whichcausesthepersontoproducelargeamountsofdilutedurine).
WhattolookforAsdehydrationprogresses,watchforchangesinmentalstatus.Thepatientmaycomplainofdizziness,weakness,orextremethirst.Hemayhaveafever(becauselessfluidisavailableforperspiration,whichlowersbodytemperature),dryskin,ordrymucousmembranes.Skinturgormaybepoor.Becauseanolderpatient’sskinmaylackelasticity,checkingskinturgormaybeanunreliableindicatorofdehydration.Thepatient’sheartratemaygoup,andhisbloodpressuremayfall.Inseverecases,seizures
andcomamayresult.Also,urineoutputmayfallbecauselessfluidiscirculatinginthebody.Thepatient’surinewillbemoreconcentratedunlesshehasdiabetesinsipidus,inwhichcasetheurinewillprobablybepaleandproducedinlargevolume.(SeeDangersignsofdehydration.)
CAUTION!
DangersignsofdehydrationBeginemergencytreatmentfordehydrationifapatientwithasuspectedfluidimbalancedevelopsanyoftheseconditions:•
impairedmentalstatus•
seizure•
coma.
WhattestsshowDiagnostictestresultsmayinclude:•elevatedhematocrit(HCT)•elevatedserumosmolality(above300mOsm/kg)•elevatedserumsodiumlevel(above145mEq/L)•urinespecificgravityabove1.030.Becausepatientswithdiabetesinsipidushavemoredilutedurine,specificgravityisusually
lessthan1.005;osmolality,50to200mOsm/kg.
Howit’streatedTreatmentfordehydrationaimstoreplacemissingfluids.Becauseadehydratedpatient’sbloodisconcentrated,avoidhypertonicsolutions.Ifthepatientcanhandleoralfluids,encouragethem;however,becausetheserumsodiumleveliselevated,makesurethefluidsgivenaresalt-free.AseverelydehydratedpatientshouldreceiveI.V.fluidstoreplacelostfluids.Mostpatients
receivehypotonic,low-sodiumfluids,suchasdextrose5%inwater(D5W).Remember,ifyougiveahypotonicsolutiontooquickly,thefluidmovesfromtheveinsintothecells,causingthemtobecomeedematous.Swellingofcellsinthebraincancreatecerebraledema.Toavoidsuchpotentiallydevastatingproblems,givefluidsgradually,overaperiodofabout48hours.
HowyouinterveneMonitorat-riskpatientscloselytodetectimpendingdehydration.Ifapatientbecomesdehydrated,herearesomestepsyou’llwanttotake:•Monitorsymptomsandvitalsignscloselysoyoucanintervenequickly.•Accuratelyrecordthepatient’sintakeandoutput,includingurineandstool.•MaintainI.V.accessasordered.MonitorI.V.infusions.Watchforsignsandsymptomsof
cerebraledemawhenyourpatientisreceivinghypotonicfluids.Theseincludeheadache,confusion,irritability,lethargy,nausea,vomiting,wideningpulsepressure,decreasedpulserate,andseizures.(SeeTeachingaboutdehydration.)
Teachingpoints
TeachingaboutdehydrationWhenteachingapatientwithdehydration,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
explanationofdehydrationanditstreatment•
warningsignsandsymptoms•
prescribedmedications•
importanceofcomplyingwiththerapy.
•Keepinmindthatvasopressinmaybeorderedforpatientswithdiabetesinsipidus.•Monitorserumsodiumlevels,urineosmolality,andurinespecificgravitytoassessfluid
balance.•Insertaurinarycatheterasorderedtoaccuratelymonitoroutput.•Provideasafeenvironmentforanypatientwhoisconfused,dizzy,oratriskforaseizure,and
teachhisfamilytodothesame.•Obtaindailyweights(samescale,sametimeofday)toevaluatetreatmentprogress.(SeeDocumentingdehydration,page66.)
•Provideskinandmouthcaretomaintaintheintegrityoftheskinsurfaceandoralmucousmembranes.
•Assessthepatientfordiaphoresis—itcanbethesourceofmajorwaterloss.
Chartsmart
DocumentingdehydrationWhenyourpatientisdehydrated,youshoulddocument:•
assessmentfindings•
intake,output,anddailyweight•
I.V.therapy•
patient’sresponsetointerventions•
associateddiagnostictestresults•
patientteachingperformedandthepatient’sunderstanding.
HypovolemiaHypovolemiareferstoisotonicfluidloss(whichincludeslossoffluidsandsolutes)fromtheextracellularspace.Childrenandolderpatientsareespeciallyvulnerabletohypovolemia.Someoftheinitialsignsandsymptomsofhypovolemiacanbesubtleasthebodytriestocompensateforthelossofcirculatingbloodvolume.Subtlesignscanbecomemoreseriousand,ifnotdetectedearlyandtreatedproperly,canprogresstohypovolemicshock,acommonformofshock.
HowithappensExcessivefluidloss(bleeding,forinstance)isariskfactorforhypovolemia,especiallywhencombinedwithreducedfluidintake.Anotherriskfactorisathird-spacefluidshift,whichoccurswhenfluidmovesoutofintravascularspacesbutnotintointracellularspaces.Forinstance,fluidmayshiftintotheabdominalcavity(ascites),thepleuralcavity,orthepericardialsac.Thesethird-spacefluidshiftsmayoccurasaresultofincreasedpermeabilityofthecapillarymembraneordecreasedplasmacolloidosmoticpressure.
AclusterofcausesFluidlossfromtheextracellularcompartmentcanresultfrommanydifferentcauses,including:•abdominalsurgery•diabetesmellitus(withincreasedurination)•excessivediuretictherapy•excessivelaxativeuse•excessivesweating•fever•fistulas•hemorrhage(bleedingmaybefrank[obvious]oroccult[hidden])•nasogastricdrainage•renalfailurewithincreasedurination•vomitinganddiarrhea.
TradingspacesThird-spacefluidshiftsalsocanresultfromanynumberofconditions,including:
•acuteintestinalobstruction•acuteperitonitis•burns(duringtheinitialphase)•crushinjuries•heartfailure•hipfracture•hypoalbuminemia•liverfailure•pleuraleffusion.
WhattolookforIfvolumelossisminimal(10%to15%oftotalcirculatingbloodvolume),thebodytriestocompensateforitslackofcirculatingvolumebyincreasingitsheartrate.Youmayalsonoteorthostatichypotension,restlessness,oranxiety.Thepatientwillprobablyproducemorethan30mlofurineperhour,buthemayhavedelayedcapillaryrefillandcool,paleskinoverthearmsandlegs.(SeeDangersignsofhypovolemia,page68.)
CAUTION!
DangersignsofhypovolemiaAvoidsurprises.Watchforthesesignsandsymptomsofhypovolemiaandimpendinghypovolemicshock:•
deteriorationinmentalstatus(fromrestlessnessandanxietytounconsciousness)•
thirst•
dizziness•
nausea•
tachycardia•
delayedcapillaryrefill•
orthostatichypotensionprogressingtomarkedhypotension•
urineoutputinitiallymorethan30ml/hour,thenurineoutputdropsbelow10ml/hour•
cool,paleskinoverthearmsandlegs•
weightloss•
flatjugularveins•
decreasedCVP•
weakorabsentperipheralpulses.
WeightyevidenceApatientwithhypovolemiamayalsoloseweight.Acuteweightlosscanindicaterapidfluid
changes.Adropinweightof5%to10%canindicatemildtomoderateloss;morethan10%,severeloss.Ashypovolemiaprogresses,thepatient’ssignsandsymptomsworsen.CVPandPAWPmayfallaswell.Monitoryourpatientforsubtlesigns,includingorthostatichypotension.
DazedandconfusedWithmoderateintravascularvolumeloss(about25%),thepatientmaybecomemoreconfusedandirritableandmaycomplainofdizziness,nausea,orextremethirst.Thepulseusuallybecomesrapidandthready,andthebloodpressuredrops.Thepatient’sskinmayfeelcoolandclammy,andurineoutputmaydropto10to30ml/hour.
Shock!Severehypovolemia(40%ormoreofintravascularvolumeloss)mayleadtohypovolemicshock.Inapatientwiththiscondition,cardiacoutputdropsandmentalstatuscandeterioratetounconsciousness.Signsmayprogresstomarkedtachycardiaandhypotensionwithweakorabsentperipheralpulses.Theskinmaybecomecoolandmottledorevencyanotic.Urineoutputdropstolessthan10ml/hour.
WhattestsshowNosinglediagnosticfindingcanconfirmhypovolemia.Laboratorytestvaluescanvary,dependingontheunderlyingcauseandotherfactors.Laboratoryvaluesusuallysuggestanincreasedconcentrationofblood.Typicallaboratoryfindingsinclude:•normalorhighserumsodiumlevel(>145mEq/L),dependingontheamountoffluidandsodium
lost•decreasedhemoglobinlevelsandHCTwithhemorrhage•elevatedbloodureanitrogen(BUN)andcreatinineratio•increasedurinespecificgravity,asthekidneystrytoconservefluid•increasedserumosmolality.
Howit’streatedTreatmentforhypovolemiaincludesreplacinglostfluidswithfluidsofthesameconcentration.Suchreplacementhelpsnormalizebloodpressureandrestorebloodvolume.Oralfluidsgenerallyaren’tenoughtoadequatelytreathypovolemia.Isotonicfluids,suchasnormalsalinesolutionorlactatedRinger’ssolution,aregivenI.V.toexpandcirculatingvolume.
AfloodoffluidFluidsmayinitiallybeadministeredasafluidbolusinwhichthepatientreceiveslargeamountsofI.V.fluidsinashortamountoftime.Forhypovolemicshock,anemergencycondition,multiplefluidbolusesareessential.NumerousI.V.infusionsshouldbestartedwiththeshortest,largestborecatheterspossiblebecausetheyofferlessresistancetofluidflowthanlong,skinnycatheters.
PumpingitinInfusionsofnormalsalinesolutionorlactatedRinger’ssolutionaregivenrapidly,commonlyfollowedbyaninfusionofplasmaproteinssuchasalbumin.Ifapatientishemorrhaging,he’llneedabloodtransfusion.Hemayalsoneedavasopressor,suchasdopamine,tosupporthisbloodpressureuntilhisfluidlevelsarebacktonormal.Oxygentherapyshouldbeinitiatedtoensuresufficienttissueperfusion.Surgerymaybe
requiredtocontrolbleeding.
HowyouinterveneNursingresponsibilitiesforahypovolemicpatientincludethoselistedhere:•Makesurethepatienthasapatentairway.•Applyandadjustoxygentherapyasordered.•Lowertheheadofthebedtoslowadecliningbloodpressure.•Ifthepatientisbleeding,applydirect,continuouspressuretotheareaandelevateitifpossible.
Assistwithotherinterventionstostopbleeding.•Ifthepatient’sbloodpressuredoesn’trespondtointerventionsasexpected,lookagainfora
siteofbleedingthatmighthavebeenmissed.Remember,apatientcanlosealargeamountofbloodinternallyfromafracturedhiporpelvis.Furthermore,fluidsalonemaynotbeenoughtocorrecthypotensionassociatedwithahypovolemiccondition.Avasopressormaybeneededto
raisebloodpressure.•MaintainpatentI.V.access.Useshort,large-borecatheterstoallowforfasterinfusionrates.
Typically,thispatientshouldhavetwolarge-boreI.V.catheters.•AdministerI.V.fluid,avasopressor,andbloodasprescribed.Anautotransfuser,whichallows
forreinfusionofthepatient’sownblood,mayberequired.•Drawbloodfortypingandcrossmatchingasorderedtopreparefortransfusion.
•Closelymonitorthepatient’smentalstatusandvitalsigns,includingorthostaticbloodpressuremeasurements,whenappropriate.Watchforarrhythmias.
•Ifavailable,monitorhemodynamics(cardiacoutput,CVP,PAP,andPAWP)usingaPAcathetertojudgehowwellthepatientisrespondingtotreatment.(SeeHemodynamicvaluesinhypovolemicshock.)
CAUTION!
HemodynamicvaluesinhypovolemicshockHemodynamicmonitoringhelpsyouevaluatethepatient’scardiovascularstatusinhypovolemicshock.Lookforthesevalues:•
CVPbelowthenormalrangeof2to6cmH2O•
PAPbelowthenormalmeanof10to20mmHg•
PAWPbelowthenormalmeanof4to12mmHg•
cardiacoutputbelowthenormalrangeof4to8L/minute.
•Monitorthequalityofperipheralpulsesandskintemperatureandappearancetoassessforcontinuedperipheralvascularconstriction.
•Obtainandrecordresultsfromdiagnostictests,suchasacompletebloodcount,electrolytelevels,arterialbloodgas(ABG)analyses,a12-leadelectrocardiogram,andchestX-rays.
•Offeremotionalsupporttothepatientandhisfamily.(SeeTeachingabouthypovolemia.)
Teachingpoints
Teachingpoints
TeachingabouthypovolemiaWhenteachingapatientwithhypovolemia,besuretocoverthefollowingtopicsandthenevaluatethepatient’slearning:•
natureoftheconditionanditscauses•
warningsignsandsymptomsandwhentheyshouldbereported•
treatmentandtheimportanceofcompliance•
importanceofchangingpositionsslowly,especiallywhengoingfromasupinepositiontoastandingposition,toavoidorthostatichypotension•
measuringbloodpressureandpulserate•
prescribedmedications.
•Encouragethepatienttodrinkfluidsasappropriate.•Insertaurinarycatheterasordered,andmeasureurineoutputhourlyifindicated.(SeeDocumentinghypovolemia.)
Chartsmart
DocumentinghypovolemiaForapatientwhoishypovolemic,youshoulddocument:•
mentalstatus•
vitalsigns•
strengthofperipheralpulses•
appearanceandtemperatureofskin•
I.V.therapyadministered•
bloodproductsinfused•
dosesofvasopressors(ifnecessary)•
breathsoundsandoxygentherapyused•
hourlyurineoutput•
laboratoryresults•
dailyweight•
interventionsandthepatient’sresponse•
patientteaching.
•Auscultatethepatient’sbreathsoundstomonitorforsignsoffluidoverload,apotentialcomplicationofI.V.therapy.Excessfluidinthelungsmaycausecracklesonauscultation.
•Monitorthepatientforincreasedoxygenrequirements,asignoffluidoverload.•Observethepatientfordevelopmentofsuchcomplicationsasdisseminatedintravascular
coagulation,myocardialinfarction,oradultrespiratorydistresssyndrome.•Weighthepatientdailytomonitortheprogressoftreatment.•Provideeffectiveskincaretopreventskinbreakdown.
HypervolemiaHypervolemiaisanexcessofisotonicfluid(waterandsodium)intheextracellularcompartment.Osmolalityisusuallyunaffectedbecausefluidandsolutesaregainedinequalproportion.Thebodyhascompensatorymechanismstodealwithhypervolemia,butwhentheyfail,signsandsymptomsofhypervolemiadevelop.
HowithappensExtracellularfluidvolumemayincreaseineithertheinterstitialorintravascularcompartments.Usually,thebodycancompensateandrestorefluidbalancebyfine-tuningcirculatinglevelsofaldosterone,ADH,andatrialnatriureticpeptide(ahormoneproducedbytheatrialmuscleoftheheart),causingthekidneystoreleaseadditionalwaterandsodium.However,ifhypervolemiaisprolongedorsevereorthepatienthaspoorheartfunction,the
bodycan’tcompensatefortheextravolume.Heartfailureandpulmonaryedemamayresult.Fluidisforcedoutofthebloodvesselsandmovesintotheinterstitialspace,causingedemaofthetissues.Elderlypatientsandpatientswithimpairedrenalorcardiovascularfunctionareespecially
pronetodevelopinghypervolemia.
TherisingtideHypervolemiaresultsfromexcessivesodiumorfluidintake,fluidorsodiumretention,orashiftinfluidfromtheinterstitialspaceintotheintravascularspace.Itmayalsoresultfromacuteorchronicrenalfailurewithlowurineoutput.Factorsthatcauseexcessivesodiumorfluidintakeinclude:
•I.V.replacementtherapyusingnormalsalinesolutionorlactatedRinger’ssolution•bloodorplasmareplacement•highintakeofdietarysodium.Factorsthatcausefluidandsodiumretentioninclude:
•heartfailure•cirrhosisoftheliver•nephroticsyndrome•corticosteroidtherapy•hyperaldosteronism•lowintakeofdietaryprotein.
Factorsthatcausefluidstoshiftintotheintravascularspaceinclude:•remobilizationoffluidsafterburntreatment•administrationofhypertonicfluids,suchasmannitolorhypertonicsalinesolution•useofplasmaproteinssuchasalbumin.
WhattolookforBecausenosinglediagnostictestconfirmshypervolemia,signsandsymptomsarekeytodiagnosis.Cardiacoutputincreasesasthebodytriestocompensatefortheexcessvolume.Thepulsebecomesrapidandbounding.Bloodpressure,CVP,PAP,andPAWPrise.Astheheartfails,bloodpressureandcardiacoutputdrop.Athirdheartsound(S3)gallopdevelopswithheartfailure.You’llseedistendedveins,especiallyinthehandsandneck.Whenthepatientraiseshishandabovethelevelofhisheart,hishandveinsremaindistendedformorethan5seconds.
Edema’smanyfacesEdemaresultsashydrostatic(fluid-pushing)pressurebuildsinthevessels,forcingfluidintothetissues.Edemamayfirstbevisibleonlyindependentareas,suchasthesacrumandbuttockswhenthepatientislyingdownorinthelegsandfeetwhenthepatientisstanding.(SeeEvaluatingpittingedema.)Later,theedemamaybecomegeneralized.Anasarcareferstosevere,generalizededema.Edematousskinlookspuffy,evenaroundtheeyes,andfeelscoolandpitswhentouched.Thepatientgainsweightasaresultoffluidretention(each17oz[0.5L]offluidgainedtranslatestoa1-lb[0.45kg]weightgain).Anincreaseinweightof5%to10%indicatesmildtomoderatefluidgain;anincreaseofmorethan10%,amoreseverefluidgain.
EvaluatingpittingedemaYoucanevaluateedemausingascaleof+1to+4.Pressyourfingertipfirmlyintotheskinoverabonysurfaceforafewseconds.Thennotethedepthoftheimprintyourfingerleavesontheskin.Theimprintshoulddisappearwithin10to30secondsdependingontheseverityoftheedema.AccordingtoDix(2012),1+edemaischaracterizedbya2-mmindentationintotheswollentissue,2+edemaischaracterizedbya4-mmindentation,3+edemaischaracterizedbya6-mmindentation,and4+edemaischaracterizedbyan8-mmindentationintotheswollentissue.
Aslightimprintindicates+1pittingedema.
Adeepimprint,withtheskinslowtoreturntoitsoriginalcontour,indicates+4pittingedema.
Whentheskinresistspressurebutappearsdistended,theconditioniscalledbrawnyedema.Inbrawnyedema,theskinswellssomuchthatfluidcan’tbedisplaced.
Overload!Edemamayalsooccurinthelungs.Astheleftsideoftheheartbecomesoverloadedandpumpefficiencydeclines,fluidbacksupintothelungs.Hydrostaticpressureforcesfluidoutofthepulmonarybloodvessels(justasinotherblood
vessels)andintotheinterstitialandalveolarareas.Pulmonaryedemaresults.Inapatientwiththiscondition,you’llhearcracklesonauscultation.Thepatientbecomesshortofbreathandtachypneicwithafrequent,sometimesfrothy,cough.Pink,frothysputumisahallmarkofpulmonaryedema.(SeeHowpulmonaryedemadevelops,page74.)
HowpulmonaryedemadevelopsExcessfluidvolumethatlastsalongtimecancausepulmonaryedema.Theseillustrationsshowhowthatprocessoccurs.
WhattestsshowTypicallaboratoryfindingsforapatientwithhypervolemiainclude:•lowHCTduetohemodilution•normalserumsodiumlevel•lowserumpotassiumandBUNlevelsduetohemodilution(higherlevelsmayindicaterenal
failureorimpairedrenalperfusion)•decreasedserumosmolality•lowoxygenlevel(withearlytachypnea,partialpressureofarterialcarbondioxidemaybelow,
causingadropinpHandrespiratoryalkalosis)•pulmonarycongestiononchestX-rays.
Howit’streatedTreatmentforhypervolemiaincludesrestrictionofsodiumandfluidintakeandadministrationofmedicationstopreventsuchcomplicationsasheartfailureandpulmonaryedema.Thecauseofthehypervolemiashouldalsobetreated.Thepatientreceivesdiureticstopromotethelossofexcessfluid.Ifthepatienthaspulmonaryedema,hemayreceiveadditionaldrugs,suchasmorphineand
nitroglycerin,todilatebloodvessels,whichinturnreducespulmonarycongestionandtheamount
ofbloodreturningtotheheart.Heartfailureistreatedwithdigoxin,whichstrengthenscardiaccontractionsandslowstheheartrate.Oxygenandbedresthelpsupportthepatient.Whenthekidneysaren’tworkingproperly,diureticsmaynotbeenoughtoridthebodyofextra
fluid.Thepatientmayrequirehemodialysisorcontinuousrenalreplacementtherapy(CRRT).(SeeUnderstandingCRRT.)
UnderstandingCRRTCRRTisusedtomanagefluidandelectrolyteimbalancesinhemodynamicallyunstablepatientswithmultipleorganfailureorrenalfailurewhocan’ttoleratehemodialysis(Gaspar,Moreira,Moutinho,Pinto,&Lima,2002).InCRRT,adual-lumenvenouscatheterprovidesaccesstothepatient’sbloodandpropelsitthroughatubingcircuit.
HowitworksTheillustrationattherightshowsthestandardsetupforonetypeofCRRTcalledcontinuousvenovenoushemofiltration.Thepatient’sbloodentersthehemofilterfromalineconnectedtoonelumenofthevenouscatheter,flowsthroughthehemofilter,andreturnstothepatientthroughthesecondlumenofthecatheter.Atthefirstpump,ananticoagulantmaybeaddedtotheblood.Asecondpumpmovesdialysate
throughthehemofilter.Athirdpumpaddsreplacementfluidifneeded.Theultrafiltrate(plasmawaterandtoxins)removedfromtheblooddrainsintoacollectionbag.
Advantages•
Allowsimmediateaccesstothepatient’sbloodviaadual-lumenvenouscatheter•
Conservescellularandproteincomponentsofblood•
Doesn’tcreatedramaticchangesinthepatient’sbloodpressure,whichoftenoccurswithhemodialysis•
Offersprecisecontroloffluidvolume
Disadvantages•
Mustbeperformedbyaspeciallytrainedcriticalcareornephrologynurse•
Musttakeplaceonacriticalcareunit•
RequiresCRRTequipmentandsupplies•
MayposeissuesofstaffcompetencyifCRRTisrarelyused•
Istimeconsumingandexpensive•
Maycausehypothermia
HowyouinterveneCaringforapatientwithhypervolemiarequiresanumberofnursingactions.Herearesomeofthem:•Assessthepatient’svitalsignsandhemodynamicstatus,notinghisresponsetotherapy.Watch
forsignsofhypovolemiaduetoovercorrection.Rememberthatelderly,pediatric,andotherwisecompromisedpatientsareathigherriskforcomplications.
•Monitorrespiratorypatternsforworseningdistress,suchasincreasedtachypneaordyspnea.•Watchfordistendedveinsinthehandsorneck.•Recordintakeandoutputhourly.•Listentobreathsoundsregularlytoassessforpulmonaryedema.Notecracklesorrhonchi.•FollowABGresultsandwatchforadropinoxygenlevelorchangesinacid-basebalance.•Monitorotherlaboratorytestresultsforchanges,includingpotassiumlevels(decreasedwith
useofmostdiuretics)andHCT.•Raisetheheadofthebed(ifbloodpressureallows)tohelpthepatient’sbreathing,and
administeroxygenasordered.•Makesurethepatientrestrictsfluidsifnecessary.Alertthefamilyandstafftoensure
compliance.(SeeTeachingabouthypervolemia.)
Teachingpoints
Teachingpoints
TeachingabouthypervolemiaWhenteachingapatientwithhypervolemia,besuretocoverthefollowingtopicsandthenevaluatethepatient’slearning:•
natureoftheconditionanditscauses•
warningsignsandsymptomsandwhentheyshouldbereported•
treatmentandtheimportanceofcompliance•
measurementofbloodpressureandpulserate•
restrictionofsodiumandfluids•
importanceofbeingweighedregularly•
prescribedmedications•
referraltodietitian,ifappropriate.
•Insertaurinarycatheterasorderedtomoreaccuratelymonitoroutputbeforestartingdiuretictherapy.
•MaintainI.V.accessasorderedfortheadministrationofmedicationssuchasdiuretics.Ifthepatientispronetohypervolemia,useaninfusionpumpwithanyinfusionstopreventadministeringtoomuchfluid.
•Giveprescribeddiureticsandothermedicationsandmonitorthepatientforeffectivenessandadversereactions.
•Watchforedema,especiallyindependentareas.•CheckforanS3,audiblewhentheventriclesarevolumeoverloaded.S3isbestheardoverthe
heart’sapexoverthemitralarea.•Providefrequentmouthcare.•Obtaindailyweightandevaluatetrends.•Provideskincarebecauseedematousskinispronetobreakdown.•Offeremotionalsupporttothepatientandhisfamily.•Documentyourassessmentfindingsandinterventions.(SeeDocumentinghypervolemia.)
Chartsmart
DocumentinghypervolemiaForapatientwhoishypervolemic,youshoulddocument:•
yourassessmentfindings,includingvitalsigns,hemodynamicstatus,pulmonarystatus,andedema•
oxygentherapyinuse•
intakeandoutput•
interventions,suchasadministrationofadiuretic,andthepatient’sresponse•
dailyweightandthetypeofscaleused•
pertinentlaboratoryresults•
dietaryorfluidrestrictions•
safetymeasuresimplemented•
patientteaching.
WaterintoxicationWaterintoxicationoccurswhenexcessfluidmovesfromtheextracellularspacetotheintracellularspace.Here’sthelowdownonthiscondition.
HowithappensExcessivelow-sodiumfluidintheextracellularspaceishypotonictothecells;thecellsarehypertonictothefluid.Becauseofthisimbalance,fluidshifts—byosmosis—intothecells,whichhavecomparativelylessfluidandmoresolutes.Thatfluidshift,whichcausesthecellstoswell,
occursasameansofbalancingtheconcentrationoffluidbetweenthetwospaces,aconditioncalledwaterintoxication.
Water,watereverywhereBycausingthebodytoholdontoelectrolyte-freewater(despitelowplasmaosmolality[diluteplasma]andhighfluidvolume),syndromeofinappropriateantidiuretichormone(SIADH)secretioncancausewaterintoxication.SIADHcanresultfromcentralnervoussystemorpulmonarydisorders,headtrauma,certainmedications,tumors,andsomesurgeries.(You’lllearnmoreaboutSIADHwhenyoureadthediscussiononsodiumimbalancesinchapter5.)WaterintoxicationcanalsooccurwithrapidinfusionsofhypotonicsolutionssuchasD5W.
Excessiveuseoftapwaterasanasogastrictubeirrigantorenemaalsoincreaseswaterintake.Psychogenicpolydipsia,apsychologicalcondition,isanothercause.Itoccurswhenaperson
continuestodrinkwaterorotherfluidsinlargeamounts,evenwhentheyaren’tneeded.Theconditionisespeciallydangerousiftheperson’skidneysdon’tfunctionwell.
WhattolookforIndicationsofwaterintoxicationincludelowsodiumlevelsandincreasedintracranialpressure(ICP),whichoccursasbraincellsswell.Althoughheadacheandpersonalitychangesarethefirstsymptoms,suspectanychangeinbehaviororlevelofconsciousness,suchasconfusion,irritability,orlethargy.Thepatientmayalsoexperiencenausea,vomiting,cramping,muscleweakness,twitching,thirst,dyspneaonexertion,anddulledsensorium.LatesignsofincreasedICPincludepupillaryandvitalsignchanges,suchasbradycardiaand
widenedpulsepressure.Apatientwithwaterintoxicationmaydevelopseizuresandcoma.Anyweightgainreflectsadditionalcellularfluid.
Whattestsshow
Typicallaboratoryfindingsforapatientwithwaterintoxicationinclude:•serumsodiumlevellessthan125mEq/L•serumosmolalitylessthan280mOsm/kg.
Howit’streatedTreatmentforwaterintoxicationincludescorrectingtheunderlyingcause,restrictingbothoralandparenteralfluidintake,andavoidingtheuseofhypotonicI.V.solutions,suchasD5W,untilserumsodiumlevelsrise.Hypertonicsolutionsareusedonlyinseveresituationstodrawfluidoutofthecellsandrequireclosepatientmonitoring.Theoriginalcauseoftheintoxicationshouldalsobeaddressed.
HowyouinterveneThebesttreatmentforwaterintoxicationisprevention.However,ifyourpatientdevelopswaterintoxication,you’llwanttoimplementthefollowingnursingactions:•Closelyassesshisneurologicstatus;watchfordeterioration,especiallychangesinpersonality
orlevelofconsciousness.•Monitorvitalsignsandintakeandoutputtoevaluatethepatient’sprogress.•MaintainoralandI.V.fluidrestrictionsasprescribed.•Alertthedietitianandthepatient’sfamilyabouttherestrictions,andpostasigninthepatient’s
roomtoletstaffmembersknow.(SeeTeachingaboutwaterintoxication.)
Teachingpoints
Teachingpoints
TeachingaboutwaterintoxicationWhenteachingapatientwithwaterintoxication,besuretocoverthefollowingtopicsandthenevaluatethepatient’slearning:•
natureoftheconditionanditscauses•
needforfluidrestriction•
warningsignsandsymptomsandwhentheyshouldbereported•
prescribedmedications•
importanceofbeingweighedregularly.
•InsertanI.V.catheterandmaintainitasordered;infusehypertonicsolutionswithcareusinganinfusionpump.
•Closelyobservethepatient’sresponsetotherapy.•Weighthepatientdailytodetectretentionofexcesswater.•Monitorlaboratorytestresultssuchasserumsodiumlevels.•Provideasafeenvironmentforthepatientwithanalteredneurologicstatusandteachhisfamily
todothesame.•Instituteseizureprecautionsinseverecases.•Documentyourassessmentfindingsandinterventions.(SeeDocumentingwaterintoxication.)
Chartsmart
DocumentingwaterintoxicationForapatientwithwaterintoxication,youshoulddocument:•
allassessmentfindings•
intakeandoutput,notingfluidrestrictions•
safetymeasures•
typesofseizureactivityandtreatment•
laboratoryresults•
dailyweight•
nursinginterventionsandpatient’sresponse•
patientteaching.
That’sawrap!
Fluidimbalancesreview
Fluidvolumebasics•
Bloodpressureisrelatedtotheamountofbloodtheheartpumps.•
Fluidvolumeaffectstheamountofbloodtotheheart;therefore,assessingbloodpressurealsoassessesapatient’sfluidstatus.
Measuringbloodpressureandfluidvolumestatus•
Sphygmomanometerandstethoscope–
Providesimpleandnoninvasivemethodformeasuringbloodpressure–
Requireuseofpropersizecuff–
Requirecufftobeplacedoverthemedialaspectofthearm,overthebrachialartery•
Arteriallines–
Aretypicallyinsertedintotheradialorthebrachialartery–
Areusedtocontinuouslymonitorbloodpressure–
Canalsobeusedtosamplearterialbloodforlaboratorytests•
PAcatheters–
Areinsertedintothesubclavianortheinternaljugularvein–
MeasurePAP,PAWP,CVP,andcardiacoutput–
Helpassessleft-sidedheartfunction,includingpumpingability,fillingpressures,andvascularvolume–
Giveclearestpictureoffluidvolumestatus
Dehydration•
Lackofwaterinextracellularspacesthatcausesfluidtoshiftoutofthecells,whichthenshrink•
Maybecausedbyanysituationthatacceleratesfluidloss,includingdiabetesinsipidus,prolongedfever,waterydiarrhea,renalfailure,andhyperglycemia•
Patientswhoaremorepronetodehydration:–
Comatose,confused,orbedriddenpatients–
Infants–
Elderlypatients–
Patientsreceivinghighlyconcentratedtubefeedingswithoutenoughsupplementalwater•
Assessmentfindings:irritability,confusion,dizziness,weakness,extremethirst,fever,dryskin,drymucousmembranes,sunkeneyeballs,poorskinturgor,decreasedurineoutput(withdiabetesinsipidus,urineispaleandplentiful),andincreasedheartratewithfallingbloodpressure
Hypovolemia•
Hypotonicfluidlossfromextracellularspace•
Mayprogresstohypovolemicshockifnotdetectedearlyandtreatedproperly•
Iscausedbyexcessivefluidlossorthird-spacefluidshift
Signsandsymptomsoffluidloss•
Mildfluidloss–
Orthostatichypotension–
Restlessness–
Anxiety–
Weightloss–
Increasedheartrate•
Moderatefluidloss–
Confusion–
Dizziness–
Irritability–
Extremethirst–
Nausea–
Cool,clammyskin–
Rapidpulse–
Decreasedurineoutput(10to30ml/hour)•
Severefluidloss–
Decreasedcardiacoutput–
Unconsciousness–
Markedtachycardia–
Hypotension–
Weakorabsentperipheralpulses–
Cool,mottledskin–
Decreasedurineoutput(<10ml/hour)
Hypervolemia•
Excessisotonicfluidinextracellularspaces•
Canleadtoheartfailureandpulmonaryedema,especiallyinprolongedorseverehypervolemiaorinpatientswithpoorheartfunction•
Mildtomoderatefluidgainequalinga5%to10%weightgain•
Severefluidgainequalingmorethana10%weightgain•
Causesinclude:–
excessivesodiumorfluidintake–
fluidorsodiumretention–
shiftinfluidfromtheinterstitialspaceintotheintravascularspace–
acuteorchronicrenalfailurewithlowurineoutput
•Assessmentfindings:tachypnea;dyspnea;crackles;rapidorboundingpulse;hypertension(unlessinheartfailure);increasedCVP,PAP,andPAWP;distendedneckandhandveins;acuteweightgain;edemaandS3gallop
Waterintoxication•
Excessfluidintheintracellularspacefromtheextracellularspace•
CausesincreasedICP•
Mayleadtoseizuresandcoma•
Causesinclude:–
SIADH–
rapidinfusionofahypotonicsolution–
excessiveuseoftapwaterasanasogastrictubeirrigantoranenema–
psychogenicpolydipsia•
Testresults:lowserumsodiumlevelsandlowserumosmolality
Quickquiz
1.Populationsatriskfordehydrationinclude:A.infants.B.adolescents.C.patientswithSIADH.D.youngadults.
Answer:A.Patientsatriskfordehydrationarethosewhoeitherhaveanimpairedthirstmechanismorcan’trespondtothethirstreflex.Infantsfallintothiscategory.
2.Checkingfororthostatichypotensionallowsthenursetodetectearlysignsof:A.hypovolemia.
B.lowserumosmolality.C.highserumosmolality.D.hypervolemia.
Answer:A.Changesinbloodpressure—whichcanresultinorthostatichypotension—andpulsearetwoinitialchangesseenwithhypovolemia.
3.Ofthefollowingoptions,thefirststepyoushouldtakeforapatientwithhypovolemicshockisto:
A.assessfordehydration.B.administerI.V.fluids.C.insertaurinarycatheter.D.prepareforsurgery.
Answer:B.HypovolemicshockisanemergencythatrequiresrapidinfusionofI.V.fluids.
4.Onesignofhypervolemiais:A.increasedurineoutput.B.clear,waterysputum.C.severehypertension.D.arapid,boundingpulse.
Answer:D.Excessfluidintheintravascularspacecausesarapid,boundingpulse.Whenhypervolemiaprogresses,itcanfillthelungswithfluidandcausepulmonaryedema,asindicatedbythepresenceofpink,frothysputum.
5.Waterintoxicationcanbecausedby:A.administeringtoomuchhypertonicfluid.B.administeringtoomuchhypotonicfluid.C.encouragingfluidintake.D.administeringtoomuchisotonicfluid.
Answer:B.Administeringtoomuchhypotonicfluidcancausewatertoshiftfromthebloodvesselsintothecells,leadingtowaterintoxicationandcellularedema.
ScoringIfyouansweredallfivequestionscorrectly,waytogo!Yourfluidityleavesusbreathless!Ifyouansweredfourcorrectly,greatgoing!Youcertainlyknowhowtogowiththeflowofunderstandingfluidimbalances.Ifyouansweredfewerthanfourcorrectly,that’sokay.Splashalittlewateronyourfaceandcheckoverthechapteragain!
References
Ashford,J.R.(2008).Hydrationanddysphagiamanagement:Water:Understandinganecessityoflife.ASHALeader,13(14),10–12.
Dix,D.(2012).Hypertensivedisordersinpregnancy.InD.L.Lowdermilk,S.E.Perry,K.Cashion,&K.R.Alden(Eds.),Maternity&women’shealthcare(10thed.,pp.654–669).St.Louis,MO:Mosby.
Garcia,M.G.,Ang,E.,Ahmad,M.N.,&Lim,C.C.(2012).Correctplacementofbloodpressurecuffduringbloodpressuremeasurement.InternationalJournalofEvidence-BasedHealthcare,10(3),191–196.
Gaspar,L.J.,Moreira,N.M.,Moutinho,A.A.,Pinto,P.J.,&Lima,H.B.(2002).Continuousrenalreplacementtherapies.JournalofRenalCare,28(S2),19–22.
Muralidhar,K.(2002).Centralvenouspressureandpulmonarycapillarywedgepressuremonitoring.IndianJournalofAnaesthesia,46(4),298–303.
Chapter5
Whensodiumtipsthebalance
JustthefactsInthischapter,you’lllearn:
♦waysthatsodiumcontributestofluidandelectrolytebalance
♦thebody’smechanismsforregulatingsodiumbalance
♦causes,signsandsymptoms,andtreatmentsassociatedwithsodiumimbalances
♦propercareforthepatientwithasodiumimbalance.
AlookatsodiumSodiumisoneofthemostimportantelementsinthebody.Itaccountsfor90%ofextracellularfluidcations(positivelychargedions)andisthemostabundantsoluteinextracellularfluid.Inthebody’snormalstate,almostallsodiuminthebodyisfoundinthisfluid.
Whyit’simportantThebodyneedssodiumtomaintainproperextracellularfluidosmolality(concentration).Sodiumattractsfluidandhelpspreservetheextracellularfluidvolumeandfluiddistributioninthebody.Italsohelpstransmitimpulsesinnerveandmusclefibersandcombineswithchlorideandbicarbonatetoregulateacid-basebalance.Becausetheelectrolytecompositionsofserumandinterstitialfluidareessentiallyequal,sodiumconcentrationinextracellularfluidismeasuredinserumlevels.Thenormalrangeforserumsodiumlevelis135to145mEq/L.Asacomparison,theamountofsodiuminsideacellis10mEq/L(Deglin,Vallerand,&Sanoski,2013;Smeltzer,Bare,Hinkle,&Cheever,2010).
HowthebodyregulatessodiumWhatapersoneatsandhowtheintestinesabsorbitdetermineabody’ssodiumlevel.Sodiumrequirementsvaryaccordingtotheindividual’ssizeandage.Theminimumdailyrequirementis0.5to2.7g;however,asaltydietprovidesatleast6g/day.TheU.S.DepartmentofAgriculture(2013)hasreleasednewguidelinessuggestingnooneshouldconsumemorethan2,300mgofsaltperday.Theyalsosuggestthatpeopleage51yearsandolderandthosewhoareAfricanAmericanorhavehighbloodpressure,diabetes,orchronickidneydiseaseshouldrestrictsaltintaketo1,500mgdaily.Oneteaspoonoftablesalthas2,325mgofsodium(U.S.DepartmentofAgriculture,2013).Kidneysnaturallybalancetheamountofsodiumstoredinthebodyforoptimalhealth.When
sodiumlevelsarelow,kidneysessentiallyholdontothesodium.Whensodiumlevelsarehigh,kidneysexcretetheexcessinurine.Ifthekidneyscan’teliminateenoughsodium,thesodiumstartstoaccumulateinthe
bloodstream.Becausesodiumattractsandholdswater,bloodvolumeincreases,whichinturnincreasesworkloadoftheheartandcontributestohighbloodpressure.(SeeDietarysourcesofsodium.)
DietarysourcesofsodiumMajordietarysourcesofsodiuminclude:•
cannedsoupsandvegetables•
cheese•
ketchup•
processedmeats•
tablesalt•
saltysnackfoods•
seafood•
pickledfoods•
seasoningssuchasmonosodiumglutamate,seasonedsalt,andsoysauce•
bakedgoodswithbakingpowderandbakingsoda.
Sodiumisalsoexcretedthroughthegastrointestinal(GI)tractandthroughtheskininsweat.Whenyouthinksodium,youshouldautomaticallythinkwateraswell—thetwoarethatcloselyrelatedinthebody.Thenormalrangeofserumsodiumlevelsreflectsthiscloserelationship.Ifsodiumintakesuddenlyincreases,extracellularfluidconcentrationalsorisesandviceversa(Smeltzeretal.,2010).
Nottoomuch!Thebodymakesadjustmentswhenthesodiumlevelrises.Increasedserumsodiumlevelscausetheindividualtofeelthirstyandtheposteriorpituitaryglandtoreleaseantidiuretichormone(ADH).(FormoreinformationaboutADH,seechapter1,Balancingfluids.)ADHcausesthekidneystoretainwater,whichdilutesthebloodandnormalizesserumosmolality.Whensodiumlevelsdecreaseandserumosmolalitydecreases,thirstandADHsecretionare
suppressed,andthekidneysexcretemorewatertorestorenormalosmolality.(SeeRegulatingsodiumandwater,page86.)
RegulatingsodiumandwaterThisflowchartshowstwoofthebody’scompensatorymechanismsforrestoringsodiumandwaterbalance.
Aldosteronealsoregulatesextracellularsodiumbalanceviaafeedbackloop.Theadrenalcortexsecretesaldosterone,whichstimulatestherenaltubulestoconservewaterandsodiumwhenthebody’ssodiumlevelislow,thushelpingtonormalizeextracellularfluidsodiumlevels(George,Majeed,Mackenzie,MacDonald,&Wei,2013;Smeltzeretal.,2010).
ThepowerofthepumpNormally,extracellularsodiumlevelsareveryhighcomparedwithintracellularsodiumlevels.Thebodycontainsanactivetransportmechanism,calledthesodium-potassiumpump,thathelpsmaintainnormalsodiumlevels.Thisishowthepumpworks:Indiffusion(aformofpassivetransport),asubstancemovesfromanareaofhigher
concentrationtooneoflowerconcentration.Sodiumions,normallymostabundantoutsidethecells,tendtodiffuseinward,andpotassium(K)ions,normallymostabundantinsidethecells,tendtodiffuseoutward.Tocombatthisionicdiffusionandmaintainnormalsodiumandpotassiumlevels,thesodium-potassiumpumpisconstantlyatworkineverycell.However,movingsodiumoutofthecellandpotassiumbackincan’thappenwithoutsomehelp.
Eachionlinkswithacarrierbecauseitcan’tgetthroughthecellwallalone.Thismovementrequiresenergy(aformofactivetransport),whichcomesfromadenosinetriphosphate(ATP)—madeupofphosphorus,anotherelectrolyte—magnesium,andanenzyme.Thesesubstanceshelpmovesodiumoutofthecellandforcepotassiumbackintothecell.
Thesodium-potassiumpumpallowsthebodytocarryoutitsessentialfunctionsandhelpspreventcellularswellingcausedbytoomanyionsinsidethecellattractingexcessiveamountsofwater.Thepumpalsocreatesanelectricalchargeinthecellfromthemovementofions,permittingtransmissionofneuromuscularimpulses.(SeeSodium-potassiumpump.)
Sodium-potassiumpumpThisillustrationshowshowthesodium-potassiumpumpcarriesionswhentheirconcentrationschange.
NormalplacementNormally,moresodium(Na)ionsexistoutsidecellsthaninside.Morepotassium(K)ionsexistinsidecellsthanoutside.
IncreasedpermeabilityCertainstimuliincreasethemembrane’spermeability.Whenthisoccurs,sodiumionsdiffuseinward;potassiumionsdiffuseoutward.
EnergysourceThecelllinkseachionwithacarriermoleculethathelpstheionreturnthroughthecellwall.Energyfortheion’sreturntripcomesfromATP,magnesium(Mg),andanenzymecommonlyfoundincells.
Hyponatremia
Acommonelectrolyteimbalance,hyponatremiaisatermthatdescribesastatewhensodiumconcentrationintheplasma(outsidethecell)islowerthannormal.Inotherwords,bodyfluidsaredilutedandcellsswellfromdecreasedextracellularfluidosmolality.Severehyponatremiacanleadtoseizures,coma,andpermanentneurologicdamage.
HowithappensNormally,thebodygetsridofexcesswaterbysecretinglessADH;lessADHcausesdiuresis.Forthattohappen,thenephronsmustbefunctioningnormally,receivingandexcretingexcesswaterandreabsorbingsodium.Hyponatremiadevelopswhenthisregulatoryfunctiongoeshaywire.Serumsodiumlevels
decrease,andfluidshiftsoccur.Whenthebloodvesselscontainmorewaterandlesssodium,fluidmovesbyosmosisfromtheextracellularareaintothemoreconcentratedintracellulararea.Withmorefluidinthecellsandlessinthebloodvessels,cerebraledemaandhypovolemia(fluidvolumedeficit)canoccur.(SeeFluidmovementinhyponatremia.)
FluidmovementinhyponatremiaThisillustrationshowsfluidmovementinhyponatremia.Whenserumosmolalitydecreasesbecauseofdecreasedsodiumconcentration,fluidmovesbyosmosisfromtheextracellularareatotheintracellulararea.
DepleteanddiluteHyponatremiaresultsfromsodiumloss,watergain(dilutionalhyponatremia),orinadequatesodiumintake(depletionalhyponatremia).Itmaybeclassifiedaccordingtowhetherextracellularfluidvolumeisabnormallydecreased(hypovolemichyponatremia),abnormallyincreased(hypervolemichyponatremia),orequaltointracellularfluidvolume(isovolemichyponatremia).
SodiumslipslowerInhypovolemichyponatremia,bothsodiumandwaterlevelsdecreaseintheextracellulararea,butsodiumlossisgreaterthanwaterloss.Causesmaybenonrenalorrenal.Nonrenalcausesincludevomiting,diarrhea,fistulas,gastricsuctioning,excessivesweating,cysticfibrosis,burns,andwounddrainage.Renalcausesincludeosmoticdiuresis,salt-losingnephritis,adrenalinsufficiency,anddiureticuse.Diureticspromotesodiumlossandvolumedepletionfromthebloodvessels,causingthe
individualtofeelthirstyandhiskidneystoretainwater.Drinkinglargequantitiesofwatercanworsenhyponatremia.Sodiumdeficitscanalsobecomemorepronouncedifthepatientisonasodium-restricteddiet.Diureticscancausepotassiumloss(hypokalemia),whichisalsolinkedtohyponatremia.(SeeDrugsassociatedwithhyponatremia.)
WaterriseshigherInhypervolemichyponatremia,bothwaterandsodiumlevelsincreaseintheextracellulararea,butthewatergainismoreimpressive.Serumsodiumlevelsaredilutedandedemaalsooccurs.Causesincludeheartfailure,liverfailure,nephroticsyndrome,excessiveadministrationofhypotonicI.V.fluids,andhyperaldosteronism.
WaterrisesaloneInisovolemichyponatremia,alsocalleddilutionalhyponatremia,sodiumlevelsmayappearlowbecausetoomuchfluidisinthebody.However,thesepatientshavenophysicalsignsoffluidvolumeexcess,andtotalbodysodiumremainsstable.Causesincludeglucocorticoiddeficiency(causinginadequatefluidfiltrationbythekidneys),hypothyroidism(causinglimitedwaterexcretion),andrenalfailure(Smeltzeretal.,2010).
Disturbingthebalance
Anothercauseofisovolemichyponatremiaissyndromeofinappropriateantidiuretichormone(SIADH)secretion.SIADHcausesexcessivereleaseofADH,whichcausesinappropriateandexcessivewaterretention,therebydisturbingfluidandelectrolytebalance.Thissyndromeisamajorcauseoflowsodiumlevels.ADHisreleasedwhenthebodydoesn’tneedit,whichresultsinwaterretentionandsodiumexcretion.(SeeWhathappensinSIADH.)
WhathappensinSIADHThisflowchartshowstheeventsthatoccurinSIADHsecretion.
SIADHoccurswith:•cancers,especiallycanceroftheduodenumandpancreasandoatcellcarcinomaofthelung•centralnervoussystem(CNS)disorders,suchastrauma,tumors,andstroke•pulmonarydisorders,suchastumors,asthma,andchronicobstructivepulmonarydisease•medications,suchascertainoralantidiabetics,chemotherapeuticdrugs,psychoactivedrugs,
diuretics,synthetichormones,andbarbiturates.
WhatliesbeneathThepatientistreatedfortheunderlyingcauseofSIADHandforhyponatremia.Forinstance,ifatumorcausedthesyndrome,thepatientwouldreceivecancertreatment;ifamedicationcausedit,thedrugwouldbestopped.Thelowsodiumlevelsaretreatedwithfluidrestriction(about1qt[1L]/day)anddiuretics,suchasfurosemide.Formanypatients,initialtreatmentmaybesimple.Thepatientisplacedonfluidrestrictionto
lowerwaterintaketomatchthelowvolumeofurinecausedbytheincreasedADH.Serumosmolalitythenincreases,causingtheADHleveltobalanceit.Ifthistreatmentisinadequate,thenthepatientmayreceiveoralureaorbeinstructedtofollowahigh-sodiumdiettoincreasethekidneys’excretionofsolutes(waterfollows).Thepatientmayalsoreceivemedications,suchasdemeclocyclineorlithium,toblockADHintherenaltubule.Iffluidrestrictiondoesn’traisethepatient’ssodiumlevels,hemayneedahypertonicsalinesolution.
WhattolookforAsyoulookforsignsofhyponatremia,rememberthattheyvaryfrompatienttopatient.Theyalsovarydependingonhowquicklythepatient’ssodiumleveldrops.Iftheleveldropsquickly,thepatientwillbemoresymptomaticthaniftheleveldropsslowly.Patientswithsodiumlevelsabove125mEq/Lmaynotshowsignsofhyponatremia—but,again,thisdependsonhowquicklysodiumlevelsdrop.Usually,acuteinitialsignsandsymptomsofnausea,vomiting,andanorexiabeginwhentheserumsodiumlevelsfallbetween115and120mEq/L(Smeltzeretal.,2010).Whensignsandsymptomsstart,they’reprimarilyneurologic.Thepatientmaycomplainofa
headacheorirritabilityorhemaybecomedisoriented.Hemayexperiencemuscletwitching,tremors,orweakness.Changesinlevelofconsciousness(LOC)maystartasashortenedattentionspanandprogresstolethargyorconfusion.Whensodiumlevelsdropto110mEq/L,thepatient’sneurologicstatusdeterioratesfurther(usuallyduetobrainedema),leadingtostupor,delirium,psychosis,ataxia,andpossiblyevencoma.Hemayalsodevelopseizures.
LowshowPatientswithhypovolemiamayhaveinelasticskinturgoranddry,crackedmucousmembranes.Assessmentofvitalsignsshowsaweak,rapidpulseandlowbloodpressureororthostatichypotension.Centralvenouspressure(CVP),pulmonaryarterypressure(PAP),andpulmonary
arterywedgepressure(PAWP)maybedecreased.
HighsignsPatientswithhypervolemia(fluidvolumeexcess)mayexperienceedema,hypertension,weightgain,andrapid,boundingpulse.TheymayalsohaveelevatedCVP,PAP,andPAWP(Georgeetal.,2013;Lindner&Funk,2013;Smeltzeretal.,2010).
WhattestsshowCommondiagnostictestresultsinpatientswithhyponatremiainclude:•serumosmolalitylessthan280mOsm/kg(diluteblood)•serumsodiumlevellessthan135mEq/L(lowsodiumlevelinblood)•urinespecificgravitylessthan1.010•increasedurinespecificgravityandelevatedurinesodiumlevels(above20mEq/L)inpatients
withSIADH•elevatedhematocritandplasmaproteinlevels.
Howit’streatedGenerally,treatmentvarieswiththecauseandseverityofhyponatremia.Forexample,thepatientwithanunderlyingendocrinedisordermayrequirehormonetherapy.
MildermeasuresTherapyformildhyponatremiaassociatedwithhypervolemiaorisovolemiausuallyconsistsofrestrictedfluidintakeandpossiblyoralsodiumsupplements.Ifhyponatremiaisrelatedtohypovolemia,thepatientmayreceiveisotonicI.V.fluidssuchasnormalsalinesolutiontorestorevolume.High-sodiumfoodsmayalsobeoffered.
CriticalstepsWhenserumsodiumlevelsfallbelow120mEq/L,treatmentintheintensivecareunitmayincludeinfusionofahypertonicsalinesolution(suchas3%or5%saline)ifthepatientissymptomatic(seizures,coma).Monitorthepatientcarefullyduringtheinfusionforsignsofcirculatoryoverloadorworseningneurologicstatus.Ahypertonicsalinesolutioncauseswatertoshiftoutofcells,whichmayleadtointravascularvolumeoverloadandseriousbraindamage(osmoticdemyelination),especiallyinthepons.Fluidvolumeoverloadcanbefatalifuntreated.Topreventfluidoverload,ahypertonicsodium
chloridesolutionisinfusedslowlyandinsmallvolumes.Furosemideisusuallyadministeredatthesametime.Infusionsofhypertonicsolution(3%to5%)areonlydoneintheintensivecareunitwithcardiacmonitoringavailable.Sodiumlevelsshouldnotberaisedmorethan25mEq/Linthe
first48hourswiththeratenotexceeding1to2mEq/L/hour(Smeltzeretal.,2010).Hypervolemicpatientsshouldn’treceivehypertonicsodiumchloridesolutions,exceptinrare
instancesofseveresymptomatichyponatremia.Duringtreatment,monitorserumsodiumlevelsandrelateddiagnosticteststofollowthepatient’sprogress(Georgeetal.,2013;Lindner&Funk,2013;Smeltzeretal.,2010).
HowyouinterveneWatchpatientsatriskforhyponatremia,includingthosewithheartfailure,cancer,orGIdisorderswithfluidlosses.Reviewyourpatient’smedications,notingthosethatareassociatedwithhyponatremia.Forpatientswhodevelophyponatremia,you’llwanttotakethefollowingactions:•Monitorandrecordvitalsigns,especiallybloodpressureandpulse,andwatchfororthostatic
hypotensionandtachycardia.•Monitorneurologicstatusfrequently.ReportanydeteriorationinLOC.Assessthepatientfor
lethargy,muscletwitching,seizures,andcoma.•Accuratelymeasureandrecordintakeandoutput.•Weighthepatientdailytomonitorthesuccessoffluidrestriction.•Assessskinturgoratleastevery8hoursforsignsofdehydration.•Watchforandreportextremechangesinserumsodiumlevelsandaccompanyingserum
chloridelevels.Alsomonitorothertestresults,suchasurinespecificgravityandserumosmolality.
•Restrictfluidintakeasordered.(Fluidrestrictionistheprimarytreatmentfordilutionalhyponatremia.)Postasignaboutfluidrestrictioninthepatient’sroomandmakesurethestaff,thepatient,andhisfamilyareawareoftherestrictions.(SeeTeachingabouthyponatremiaandhypernatremia,page99.)
Teachingpoints
Teachingpoints
TeachingabouthyponatremiaandhypernatremiaWhenteachingapatientwithhyponatremiaorhypernatremia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
explanationofhyponatremiaorhypernatremia,includingcausesandtreatment•
importanceofincreasingorrestrictingsodiumintake,includingbothdietarysourcesandover-the-countermedicationsthatcontainsodium•
drugtherapyandpossibleadverseeffects•
signsandsymptomsandwhentoreportthem.
•Administeroralsodiumsupplements,ifprescribed,totreatmildhyponatremia.Ifthepractitionerhasinstructedthepatienttoincreasehisintakeofdietarysodium,teachhimaboutfoodshighinsodium.
•Forseverehyponatremia,makesureapatentI.V.lineisinplace,thenadministerprescribedI.V.isotonicorhypertonicsalinesolutions.Dosocautiouslytoavoidinducinghypernatremia,braininjury,orfluidvolumeoverloadfromanexcessiveortoorapidinfusion.Watchcloselyforsignsofhypervolemia(dyspnea,crackles,engorgedneckorhandveins),andreportthemimmediately.Useaninfusionpumptoensurethatthepatientreceivesonlytheprescribedvolumeoffluid.
•Keepthepatientsafewhileheundergoestreatment.Provideasafeenvironmentforapatientwhohasalteredthoughtprocessesandreorienthimasneeded.Ifseizuresarelikely,padthebed’ssiderailsandkeepsuctionequipmentandanartificialairwayhandy.(SeeDocumentinghyponatremiaorhypernatremia,page99.)
Chartsmart
DocumentinghyponatremiaorhypernatremiaIfyourpatienthashyponatremiaorhypernatremia,makesureyoudocumentthefollowinginformation:•
assessmentfindings(includingneurologicstatus)•
vitalsigns•
typesofseizures,ifany•
dailyweight•
serumsodiumlevelandotherpertinentlaboratorytestresults•
intakeandoutput•
medicationsgivenandI.V.therapyimplemented•
notificationofthepractitionerwhenthepatient’sconditionchanges•
nursinginterventionsandpatientresponse•
patientcompliancewithfluidrestrictionsanddietarychanges•
patientteachingprovidedandpatientresponsetotheteaching•
safetymeasurestakentoprotectthepatient(seizureprecautions).
Hypernatremia
Hypernatremia,alesscommonproblemthanhyponatremia,referstoanelevatedsodiumlevelintheplasma(blood).Severehypernatremiacanleadtoseizures,coma,andpermanent
neurologicdamage.
HowithappensThirstisthebody’smaindefenseagainsthypernatremia.Thehypothalamus(withitsosmoreceptors)isthebrain’sthirstcenter.Highserumosmolality(increasedsoluteconcentrationsintheblood)stimulatesthehypothalamusandinitiatesthesensationofthirst.Thedrivetorespondtothirstissostrongthatsevere,persistenthypernatremiausuallyoccurs
onlyinpeoplewhocan’tdrinkvoluntarily,suchasinfants,confusedelderlypatients,andimmobileorunconsciouspatients.Hypothalamicdisorders,suchasalesiononthehypothalamus,maycauseadisturbanceofthethirstmechanism,butthisconditionisrare.Whenhypernatremiaoccurs,itusuallyhasahighmortalityrate(>50%).
StrivingforbalanceThebodystrivestomaintainanormalsodiumlevelbysecretingADHfromtheposteriorpituitarygland.Thishormonecauseswatertoberetained,whichhelpstolowerserumsodiumlevels.Thecellsalsoplayaroleinmaintainingsodiumbalance.Whenserumosmolalityincreases
becauseofhypernatremia,fluidmovesbyosmosisfrominsidethecelltooutsidethecell,tobalancetheconcentrationsinthetwocompartments.(Formoreinformation,seechapter1,Balancingfluids.)Asfluidleavesthecells,theybecomedehydratedandshrink—especiallythoseoftheCNS.
Whenthisoccurs,patientsmayshowsignsofneurologicimpairment.Theymayalsoshowsignsofhypervolemia(fluidoverload)fromincreasedextracellularfluidvolumeinthebloodvessels.(SeeFluidmovementinhypernatremia.)Iftheoverloadissevereenough,subarachnoid
hemorrhagemayoccur.
FluidmovementinhypernatremiaWithhypernatremia,thebodytriestomaintainbalancebyshiftingfluidfromtheinsideofcellstotheoutside.Thisillustrationshowsfluidmovementinhypernatremia.
IncreasedconcentrationAwaterdeficitcancausehypernatremia—thatis,moresodiumrelativetowaterinthebody.Excessiveintakeofsodiumcanalsocauseit.Regardlessofthecause,bodyfluidsbecomehypertonic(moreconcentrated).
WaterdeficitAwaterdeficitcanoccuraloneorwithasodiumloss(butmorewaterislostthansodium).Ineithercase,serumsodiumlevelsareelevated.Thiselevationismoredangerousindebilitatedpatientsandthosewithdeficientwaterintake.Insensiblewaterlossesofseverallitersperdaycanresultfromfeverandheatstroke,with
olderadultsandathletesbeingequallysusceptible.Significantwaterlossesalsooccurinpatientswithpulmonaryinfections,wholosewatervaporfromthelungsthroughhyperventilation,andinpatientswithextensiveburns.Vomitingandsevere,waterydiarrheaareothercausesofwaterlossandsubsequenthypernatremia;eithercanbeespeciallydangerousinchildren.(SeeInfants,children,elderlypatients,andcriticallyillatrisk.)
Agesandstages
Agesandstages
Infants,children,elderlypatients,andcriticallyillatriskHypernatremiaismorecommonininfantsandchildrenfortwokeyreasons:Theytendtolosemorewaterasaresultofdiarrhea,vomiting,inadequatefluidintake,andfever.Theirintakeofwaterisgenerallyinadequatebecausetheylackaccesstofluidsandcan’treadily
communicatetheirneeds.Elderlypatientsarealsoatincreasedriskforhypernatremia.Theymayhaveanimpairedthirst
response,ortheymayhavelimitedaccesstowaterbecauseofconfusion,immobility,oradebilitatingillness.Criticallyillpatientswhoareunconscious,intubated,orsedatedareatriskbecausetheycannot
expressthirstorcommunicatetheyarethirsty(Lindner&Funk,2013).
Patientswithhyperosmolarhyperglycemicnonketoticsyndromecanalsodevelophypernatremiaduetoseverewaterlossesfromosmoticdiuresis.Ureadiuresis,anothercauseofhypernatremia,occurswithadministrationofhigh-proteinfeedingsorhigh-proteindietswithoutadequatewatersupplementation(Georgeetal.,2013;Lindner&Funk,2013;Smeltzeretal.,2010).
ThirsttoanextremePatientswithdiabetesinsipidushaveextremethirstandenormousurinarylosses,inmanycases,morethan4gal(15L)/day.Usually,theycandrinkenoughfluidstomatchtheurinarylosses;otherwise,severedehydrationandhypernatremiaoccur.DiabetesinsipidusmayresultfromalackofADHfromthebrain(centraldiabetesinsipidus)oralackofresponsefromthekidneystoADH(nephrogenicdiabetesinsipidus)(Georgeetal.,2013;Lindner&Funk,2013;Smeltzeretal.,2010).Centraldiabetesinsipidusmaybecausedbyatumororheadtrauma(injuryorsurgery),orit
maybeidiopathic(noknowncause).Itrespondswelltovasopressin(anothernameforADH).Ontheotherhand,nephrogenicdiabetesinsipidusdoesn’trespondwelltovasopressinandismorelikelytooccurwithanelectrolyteimbalancesuchashypokalemiaorwithcertainmedicationssuchaslithium.
ExcessivesodiumintakeLikewaterlossesfromthebody,sodiumgainscancausehypernatremia.Severalfactorscancontributetoahighsodiumlevel,includingsalttablets,high-sodiumfoods,andmedicationssuchassodiumpolystyrenesulfonate(Kayexalate).Excessiveparenteraladministrationofsodiumsolutions,suchashypertonicsalinesolutionsorsodiumbicarbonatepreparations,andgastricor
enteraltubefeedingscanalsocausehypernatremia.(SeeDrugsassociatedwithhypernatremia.)
DrugsassociatedwithhypernatremiaThedrugslistedbelowcancausehighsodiumlevels.Askyourpatientifanyofthesemedicationsarepartofhisdrugtherapy:•
antacidswithsodiumbicarbonate•
antibioticssuchasticarcillindisodium-clavulanatepotassium(Timentin)•
salttablets•
sodiumbicarbonateinjections(suchasthosegivenduringcardiacarrest)•
I.V.sodiumchloridepreparations•
sodiumpolystyrenesulfonate(Kayexalate)•
corticosteroids(Deglinetal.,2013;InstituteforSafeMedicinePractices,2012)
Othercausesofincreasedsodiumlevelsincludeinadvertentintroductionofhypertonicsalinesolutionintomaternalcirculationduringtherapeuticabortionandneardrowninginsaltwater.Excessiveamountsofadrenocorticalhormones(asinCushing’ssyndromeandhyperaldosteronism)alsoaffectwaterandsodiumbalance.
WhattolookforThemostimportantsignsofhypernatremiaareneurologicbecausefluidshiftshaveasignificanteffectonbraincells.Thehyperosmolaritycausesashiftoffreewaterfromtheintracellulartotheextracellularspace,leadingtobraincellshrinkage.Vascularrupturecanoccurwithpermanentneurologicdeficitsifsevere.Remember,thebodycantolerateahighsodiumlevelthatdevelopsovertimebetterthanonethatoccursrapidly.Earlysignsandsymptomsofhypernatremiamayincluderestlessnessoragitation,anorexia,nausea,andvomiting.Thesemaybefollowedbyweakness,lethargy,confusion,stupor,seizures,andcoma.Neuromuscularsignsalsocommonlyoccur,includingtwitching,hyperreflexia,ataxia,andtremors.
Thatflushed,feveredfeeling
Youmayalsoobservealow-gradefeverandflushedskin.Thepatientmaycomplainofintensethirstfromstimulationofthehypothalamusfromincreasedosmolality.Othersignsandsymptomsvarydependingonthecauseofthehighsodiumlevels.Ifasodium
gainhasoccurred,fluidmaybedrawnintothebloodvesselsandthepatientwillappearhypervolemic,withanelevatedbloodpressure,boundingpulse,anddyspnea.Ifwaterlossoccurs,fluidleavesthebloodvesselsandyou’llnoticesignsofhypovolemia,
suchasdrymucousmembranes,oliguria,andorthostatichypotension(bloodpressuredropandheartrateincreasewithpositionchanges).
WhattestsshowNowthatyouknowhowhypernatremiaprogresses,youcanbetterunderstandhowitcausesthesecommondiagnosticfindings:•serumsodiumlevelgreaterthan145mEq/L•urinespecificgravitygreaterthan1.030(exceptindiabetesinsipidus,whereurinespecific
gravityisdecreased)•serumosmolalitygreaterthan300mOsm/kg.
Memoryjogger
Toremembersomecommonsignsandsymptomsofhypernatremia,thinkofthewordSALT:
Skinflushed
Agitation
Low-gradefever
Thirst.
Howit’streatedTreatmentforhypernatremiavarieswiththecause.Theunderlyingdisordermustbecorrected,andserumsodiumlevelsandrelateddiagnostictestsmustbemonitored.Iftoolittlewaterinthebodyiscausingthehypernatremia,treatmentmayincludeoralfluidreplacement.Notethatthefluidsshouldbegivengraduallyover48hourstoavoidshiftingwaterintobraincells.
BraindrainRemember,assodiumlevelsinthebloodvesselsrise,fluidshiftsoutofthecells—includingthe
braincells—todilutethebloodandequalizeconcentrations.Iftoomuchwaterisintroducedintothebodytooquickly,watermovesintobraincellsandtheygetbigger,causingcerebraledema.Ifthepatientcan’tdrinkenoughfluids,itwillbenecessarytoprovideI.V.fluidreplacement.A
patientmayreceivesalt-freesolutions(suchasdextrose5%inwater)toreturnserumsodiumlevelstonormal,followedbyinfusionofhalf-normalsalinesolutiontopreventhyponatremiaandcerebraledema.OthertreatmentsincluderestrictingsodiumintakeandadministeringdiureticsalongwithoralorI.V.fluidreplacementtoincreasesodiumloss.
Treatmentfordiabetesinsipidusmayincludevasopressin,hypotonicI.V.fluids,andthiazidediureticstodecreasefreewaterlossfromthekidneys.Theunderlyingcauseshouldalsobetreated.
HowyouinterveneTrytopreventhypernatremiainhigh-riskpatients(suchasthoserecoveringfromsurgerynearthepituitarygland)byobservingthemclosely.Also,findoutifthepatientistakingmedicationsthatmaycausehypernatremia.Ifyourpatientdoesdevelophypernatremia,takethefollowingmeasures:•Monitorandrecordvitalsigns,especiallybloodpressureandpulse.•IfthepatientneedsI.V.fluidreplacement,monitorfluiddeliveryandhisresponsetothe
therapy.Watchforsignsofcerebraledemaandcheckhisneurologicstatusfrequently.ReportanydeteriorationinLOC.
•Carefullymeasureandrecordintakeandoutput.Weighthepatientdailytocheckforbodyfluidloss.(SeeDocumentinghyponatremiaorhypernatremia.)
•Assessskinandmucousmembranesforsignsofbreakdownandinfectionaswellaswaterlossfromperspiration.
•Monitorthepatient’sserumsodiumlevelandreportanyincrease.Monitorurinespecificgravityandotherlaboratorytestresults.
•Ifthepatientcan’ttakeoralfluids,recommendtheI.V.routetothepractitioner.Ifthepatientcandrinkandisalertandresponsible,involvehiminhistreatment.Givehimatargetamountoffluidtodrinkeachshift,markcupswiththevolumetheyhold,leavefluidswithineasyreach,andprovidepaperandpentorecordamounts.Iffamilymemberswanttohelpthepatientdrink,givethemspecificinstructionsaswell.(SeeTeachingabouthyponatremiaandhypernatremia.)
•InsertandmaintainapatentI.V.asordered.UseaninfusionpumptocontroldeliveryofI.V.fluidstopreventcerebraledema.
•Assistwithoralhygiene.Lubricatethepatient’slipsfrequentlywithawater-basedlubricantandprovidemouthwashorgargleifhe’salert.Goodmouthcarehelpskeepmucousmembranesmoistanddecreasesmouthodor.
•Provideasafeenvironmentforconfusedoragitatedpatients.Ifseizuresarelikely,padthebed’ssiderailsandkeepanartificialairwayandsuctionequipmenthandy.Reorientthepatientasneeded,andreduceenvironmentalstimuli(Smeltzeretal.,2010).
That’sawrap!
Sodiumimbalancesreview
Sodiumbasics•
Majorcationinextracellularfluid(90%)•
Attractsfluids•
Helpstransmitimpulsesinnerveandmusclefibers•
Combineswithchlorideandbicarbonatetoregulateacid-basebalance•
Normalserumlevel:135to145mEq/L
Sodiumbalance•
BalanceismaintainedbyADH,whichissecretedfromtheposteriorpituitarygland.•
Thebalancedependsonwhat’seatenandhowsodiumisabsorbedintheintestines.•
Increasedsodiumintakeresultsinincreasedextracellularfluidvolume.•
Decreasedsodiumintakeresultsindecreasedextracellularfluidvolume.•
Increasedsodiumlevelsresultinincreasedthirst,releaseofADH,retentionofwaterbythekidneys,anddilutionofblood.•
Decreasedsodiumlevelsresultsinsuppressedthirst,suppressedADHsecretion,excretionofwaterbythekidneys,andsecretionofaldosteronetoconservesodium.•
Balanceismaintainedbydiffusion,whichmovessodiumionsintocellsandpotassiumout.•
Sodium-potassiumpumpusesenergytomovesodiumionsbackoutofcellsandreturnpotassiumtocells;italsocreatesanelectricalchargewithinthecellfromthemovementofions,allowingtransmissionofnerveimpulses.
Hyponatremia•
Commonelectrolyteimbalance•
Causedbyaninadequatesodiumintake,excessivewaterloss,orwatergain•
Serumsodiumlevellessthan135mEq/L•
Variedsignsandsymptoms,dependingontheindividual•
Resultsfromdecreasedserumosmolality•
Fluidshiftsintointracellularareas:neurologicsymptomsarerelatedtocerebraledema•
Maycausestuporandcomaifserumsodiumleveldropsto110mEq/L
Types•
Hypovolemic—bothsodiumandwateraredecreasedinextracellulararea,butsodiumlossisgreaterthanwaterloss•
Hypervolemic—bothsodiumandwaterareincreasedinextracellulararea,butwatergainismorethansodiumgain•
Isovolemic—waterincreases,buttotalsodiumlevelsremainstable;mayalsobecausedbySIADH
Signsandsymptoms•
Abdominalcramps•
Lethargyandconfusion(alteredLOC)•
Headache•
Muscletwitching•
Nauseaandvomiting•
Anorexia
Signsandsymptomswithdepletionalhyponatremia•
Drymucousmembranes•
Orthostatichypotension•
Poorskinturgor•
Tachycardia
Signsandsymptomswithdilutionalhyponatremia•
Hypertension•
Rapid,boundingpulse•
Weightgain
Hypernatremia•
Causedbywaterloss,inadequatewaterintake(rarelyfromfailureofthethirstmechanism),excessivesodiumintake,ordiabetesinsipidus•
Patientsatincreasedrisk:infants,elderly,immobileandcomatosepatients•
Alwaysresultsinincreasedserumosmolality•
Fluidshiftsoutofthecells,causingcellstoshrink•
Mustbecorrectedslowlytopreventarapidshiftofwaterbackintothecells,whichcouldcause
cerebraledema
Signsandsymptoms•
Agitation•
Confusion•
Flushedskin•
Lethargy•
Low-gradefever•
Thirst•
Restlessness•
Muscletwitching•
Weakness
Signsandsymptomsofhypervolemiawithsodiumgain•
Boundingpulse•
Dyspnea•
Hypertension
Signsandsymptomsofhypervolemiawithwaterloss•
Drymucousmembranes•
Oliguria•
Orthostatichypotension
Quickquiz
1.Inadditiontoitsresponsibilityforfluidbalance,sodiumisalsoresponsiblefor:A.goodeyesightandvitaminbalance.B.bonestructure.C.impulsetransmission.D.musclemass.
Answer:C.Besidesitsroleasthemainextracellularcationresponsibleforregulatingfluidbalanceinthebody,sodiumisalsoinvolvedinimpulsetransmissioninnerveandmusclefibers.
2.Signsandsymptomsofhyponatremiainclude:A.changeinLOC,abdominalcramps,andmuscletwitching.B.headache,rapidbreathing,andhighenergylevel.C.chestpain,fever,andpericardialrub.D.weightloss,slowpulse,andvisionchanges.
Answer:A.ThesignsandsymptomsofhyponatremiaincludechangeinLOC,abdominalcramps,andmuscletwitching.Apatientwithhyponatremiamayalsoexhibitheadache,nausea,coma,bloodpressurechanges,andtachycardia.
3.Theminimumdailyrequirementofsodiumforanaverageadultis:A.2g.B.4g.C.5g.D.8g.
Answer:A.Althoughtheminimumdailyrequirementis2g,mostpeopleconsumemorethan6g/day.
4.Increasedserumsodiumlevelscausethirstandthereleaseof:A.potassiumintothecells.B.fluidintotheinterstitium.C.ADHintothebloodstream.D.aldosteroneintothekidneys.
Answer:C.HigherbloodsodiumlevelspromptthereleaseofADHfromtheposteriorpituitarygland.
5.Thesodium-potassiumpumptransportssodiumions:A.intocells.B.outofcells.
C.intoandoutofcellsinequalamounts.D.intoskeletalmuscles.
Answer:B.Normallymostabundantoutsideofcells,sodiumtendstodiffuseinward.Thesodium-potassiumpumpreturnssodiumtotheextracellulararea.Potassiumionstendtodiffuseoutofthecellsandrequiretransportbackintocells.
6.You’reteachingapatientwithhypernatremiathatheneedstorestrictdailyintakeofsodium.Whichfoodshighinsodiumshouldyoutellhimtoavoid?
A.Bananas,peaches,andbroccoliB.Redmeat,chicken,andporkC.Milk,nuts,andliverD.Cannedsoups,ketchup,andcheese
Answer:D.Majordietarysourcesofsodiumincludecannedsoupsandvegetables,cheese,ketchup,processedmeats,tablesalt,saltysnackfoods,andseafood.
7.Whichofthefollowingdisorderscausesisovolemichyponatremia?A.HyperthyroidismB.SIADHC.HeartfailureD.Dementia
Answer:B.Causesofisovolemichyponatremiaincludeglucocorticoiddeficiency,hypothyroidism,renalfailure,andSIADH.
8.Drugsthatmaycausehighsodiumlevelsinclude:A.antacids.B.diuretics.C.antipsychotics.D.antidepressants.
Answer:A.Iftakenonaregularbasis,antacidswithsodiumbicarbonatemaycausehighsodiumlevels.
ScoringIfyouansweredalleightquestionscorrectly,congratulations!You’reaSodiumSomebody!Ifyouansweredsixorsevencorrectly,goodjob.You’reapillarofstrengthandintelligence(andnotsalt)!Ifyouansweredfewerthansixcorrectly,don’tfret.You’llstriketheproperbalanceinthefollowingchapters!
ReferencesDeglin,J.H.,Vallerand,A.H.,&Sanoski,C.A.(2013).Davis’sdrugguidefornurses(13thed.).
Philadelphia,PA:F.A.Davis.George,J.,Majeed,W.,Mackenzie,I.S.,MacDonald,T.M.,&Wei,L.(2013).Associationbetween
cardiovasculareventsandsodium-containingeffervescent,dispersible,andsolubledrugs:Nestedcase-controlstudy.BritishMedicalJournal,347.doi:10.1136/bmj.f6954
InstituteforSafeMedicinePractices.(2012).ISMP’slistofhighalertmedications.InstituteforSafeMedicinePracticesTools.Retrievedfromhttps://www.ismp.org/tools/highalertmedicationLists.asp
Lindner,G.,&Funk,G.C.(2013).Hypernatremiaincriticallyillpatients.JournalofCriticalCare,28,216.e11–216.e20.
Smeltzer,S.,Bare,B.,Hinkle,J.,&Cheever,K.(2010).Textbookofmedical-surgicalnursing(12thed.).Philadelphia,PA:LippincottWilliams&Wilkins.
U.S.DepartmentofAgriculture.(2013).Dietaryguidelines.Retrievedfromhttp://www.cnpp.usda.gov/DietaryGuidelines.htm
Chapter6
Whenpotassiumtipsthebalance
JustthefactsInthischapter,you’lllearn:
♦waysthatpotassiumcontributestofluidandelectrolytebalance
♦thebody’smechanismsforregulatingserumpotassiumlevels
♦treatmentsforpotassiumimbalances
♦careforpatientswithpotassiumimbalances
♦documentationtipsforpatientswithpotassiumimbalances.
AlookatpotassiumAmajorcation(ionwithapositivecharge)inintracellularfluid,potassiumplaysacriticalroleinmanymetaboliccellfunctions.Only2%ofthebody’spotassiumisfoundinextracellularfluid;98%isinintracellularfluid.Thatsignificantdifferenceinlocationaffectsnerveimpulsetransmission.
Diseases,injuries,medications,andtherapiescanalldisturbpotassiumlevels.Small,untreatedalterationsinserumpotassiumlevelscanseriouslyaffectneuromuscularandcardiacfunctioning.
Whyit’simportantPotassiumdirectlyaffectshowwellthebody’scells,nerves,andmusclesfunctionby:•maintainingcells’electricalneutralityandosmolality•aidingneuromusculartransmissionofnerveimpulses•assistingskeletalandcardiacmusclecontractionandelectricalconductivity•affectingacid-basebalanceinrelationshiptothehydrogen(H)ion(anothercation).(SeePotassium’sroleinacid-basebalance,page106.)
Potassium’sroleinacid-basebalanceTheillustrationsbelowshowthemovementofpotassiumionsinresponsetochangesinextracellularhydrogenionconcentration.Hydrogenionconcentrationchangeswithacidosisandalkalosis.
NormalbalanceUndernormalconditions,thepotassiumion(K)contentinintracellularfluidismuchgreaterthanthecontentinextracellularfluid.Hydrogenion(H)concentrationislowinbothcompartments.
AcidosisInacidosis,hydrogenioncontentinextracellularfluidincreasesandtheionsmoveintotheintracellularfluid.Tokeeptheintracellularfluidelectricallyneutral,anequalnumberofpotassiumionsleavethecell,whichcauseshyperkalemia(excessivepotassiuminthebloodstream).
AlkalosisInalkalosis,morehydrogenionsarepresentinintracellularfluidthaninextracellularfluid.Therefore,hydrogenionsmovefromtheintracellularfluidintotheextracellularfluid.Tokeeptheintracellularfluidelectricallyneutral,potassiumionsmovefromtheextracellularfluidintotheintracellularfluid,whichcauseshypokalemia(toolittlepotassiuminthebloodstream).
Howthebodyregulatespotassium
Normalserumpotassiumlevelsrangefrom3.5to5mEq/L.Inthecell,thepotassiumlevel(usuallynotmeasured)ismuchhigherat140mEq/L.Potassiummustbeingesteddailybecausethebodycan’tconserveit.Therecommendeddailyrequirementforadultsisabout40mEq;theaveragedailyintakeintheUnitedStatesis60to100mEq.(SeeDietarysourcesofpotassium.)
DietarysourcesofpotassiumHerearesomemaindietarysourcesofpotassium:•
chocolate•
driedfruit,nuts,andseeds•
fruits,suchasoranges,bananas,avocados,apricots,andcantaloupe•
meats•
vegetables,especiallybeans,potatoes,mushrooms,tomatoes,andcelery•
yogurt(TuftsUniversity,2012).
Extracellularfluidalsogainspotassiumwhencellsaredestroyed(thus,releasingintracellularpotassium)andwhenpotassiumshiftsoutoftheintracellularfluidintotheextracellularfluid.
JustpassingthroughAbout80%ofthepotassiumtakeninisexcretedinurine,witheachliterofurinecontaining20to40mEqoftheelectrolyte.Anyremainingpotassiumisexcretedinfecesandsweat.Extracellularpotassiumlossalsooccurswhenpotassiummovesfromtheextracellularfluidto
theintracellularfluidandwhencellsundergoanabolism.Threemorefactorsthataffectpotassiumlevelsincludethesodium-potassiumpump,renalregulation,andpHlevel.
PumpingactionThesodium-potassiumpumpisanactivetransportmechanismthatmovesionsacrossthecellmembraneagainstaconcentrationgradient.Specifically,thepumpmovessodiumfromthecellintotheextracellularfluidandmaintainshighintracellularpotassiumlevelsbypumpingpotassiumintothecell.Thebodyalsoridsitselfofexcesspotassiumthroughthekidneys.Asserumpotassiumlevels
rise,therenaltubulesexcretemorepotassium,leadingtoincreasedpotassiumlossintheurine.Sodiumandpotassiumhaveareciprocalrelationship.Thekidneysreabsorbsodiumandexcrete
potassiumwhenthehormonealdosteroneissecreted.Thekidneys,however,havenoeffectivemechanismtocombatlossofpotassiumandmayexcreteitevenwhentheserumpotassiumlevelislow.Evenwhenpotassiumintakeiszero,thekidneyswillexcrete10to15mEq/day.
FreetradeAchangeinpHmayaffectserumpotassiumlevelsbecausehydrogenionsandpotassiumionsfreelyexchangeacrossplasmacellmembranes.Forexample,inacidosis,excesshydrogenionsmoveintocellsandpushpotassiumintotheextracellularfluid.Thus,acidosiscancausehyperkalemiaaspotassiummovesoutofthecelltomaintainbalance.Likewise,alkalosiscancausehypokalemiabyincreasingpotassiummovementintothecelltomaintainbalance.
Hypokalemia
Inhypokalemia,theserumpotassiumleveldropsbelow3.5mEq/L.Inmoderatehypokalemia,theserumpotassiumlevelrangesfrom2.5to3mEq/L.Inseverehypokalemia,it’slessthan2.5mEq/L.Becausethenormalrangeforserumpotassiumisnarrow(3.5to5mEq/L),aslightdecreasehasprofoundeffects.
HowithappensRemember,thebodycan’tconservepotassium.Inadequateintakeandexcessiveoutputofpotassiumcancauseamoderatedropinitslevel,upsettingthebalanceandcausingapotassiumdeficiency.Conditionssuchasprolongedintestinalsuction,recentileostomy,andvillousadenomacan
causeadecreaseinthebody’soverallpotassiumlevel.Incertainsituations,potassiumshiftsfromtheextracellularspacetotheintracellularspaceandhidesinthecells.Becausethecellscontainmorepotassiumthanusual,lesscanbemeasuredintheblood.
Notenoughin...Inadequatepotassiumintakecausesadropinthebody’soverallpotassiumlevel.Thatcouldmeanapersonisn’teatingenoughpotassium-richfoods,isreceivingpotassium-deficientI.V.fluids,orisgettingtotalparenteralnutritionthatlackspotassiumsupplementation.Also,largeintakeofnaturalblacklicoriceproducesanaldosteroneeffect,whichcanleadtosodiumretentionandpotassiumloss.
...ToomuchoutIntestinalfluidscontainlargeamountsofpotassium.Severegastrointestinal(GI)fluidlossesfromsuction,lavage,orprolongedvomitingcandepletethebody’spotassiumsupply.Asaresult,
potassiumlevelsdrop.Diarrhea,fistulas,laxativeabuse,andseverediaphoresisalsocontributetopotassiumloss.(SeeCommoncausesofhypokalemiaintheoldandyoung.)
Agesandstages
CommoncausesofhypokalemiaintheoldandyoungInelderlypatients,themostcommoncausesofhypokalemiaarediuretictherapy,diarrhea,andchroniclaxativeabuse.Individualswhocan’tcookforthemselvesorhavedifficultlychewingandswallowingmayhavepoorpotassiumintake.Inpediatricpatients,gastroenteritisthatproducesvomitinganddiarrheaismorelikelytoleadto
dehydrationandhypokalemia.
Potassiumcanalsobedepletedthroughthekidneys.Diuresisthatoccurswithanewlyfunctioningtransplantedkidneycanleadtohypokalemia.Highurineglucoselevelscauseosmoticdiuresis,andpotassiumislostthroughtheurine.Otherpotassiumlossesareseeninrenaltubularacidosis,magnesiumdepletion,Cushing’ssyndrome,andperiodsofhighstress.
DepletingdrugsDrugs,suchasdiuretics(especiallythiazidesandfurosemide),corticosteroids,insulin,cisplatin,andcertainantibiotics(gentamicin,carbenicillin,andamphotericinB,forinstance),alsocausepotassiumloss.(SeeDrugsassociatedwithhypokalemia.)
DrugsassociatedwithhypokalemiaThesedrugscandepletepotassiumandcausehypokalemia:•
adrenergics,suchasalbuterolandepinephrine•
antibiotics,suchasamphotericinB,carbenicillin,andgentamicin•
cisplatin•
corticosteroids•
diuretics,suchasfurosemideandthiazides•
insulin•
laxatives(whenusedexcessively).
Excessivesecretionofinsulin,whetherendogenousorexogenous,mayshiftpotassiumintothecells.Insulincanbereleasedfromthebodyandcausehypokalemiainpatientsreceivinglargeamountsofdextrosesolutions.Potassiumlevelsalsodropwhenadrenergics,suchasepinephrineoralbuterol,areusedtotreatasthmaastheycausepotassiumtomoveintothecell(Lehnhardt&Kemper,2011).
DamagingdiseasesConditions(suchasvomitingordiarrhea)thatleadtothelossofGIfluidscancausealkalosisandhypokalemia.Alkalosismovespotassiumionsintothecellsashydrogenionsmoveout.Otherdisordersassociatedwithhypokalemiaarehepaticdisease,hyperaldosteronism,acute
alcoholism,heartfailure,malabsorptionsyndrome,nephritis,Bartter’ssyndrome,andacute
leukemias.
WhattolookforThesignsandsymptomsofalowpotassiumlevelreflecthowimportanttheelectrolyteistonormalbodyfunctions.
FeelingweakinthekneesSkeletalmuscleweakness,especiallyinthelegs,isasignofamoderatelossofpotassium.Weaknessprogressesandparesthesiadevelops.Legcrampsoccur.Deeptendonreflexesmaybedecreasedorabsent.Rarely,paralysisoccursandmayinvolvetherespiratorymuscles.Ifrespiratorymusclesbecomeweak,thepatientmayalsobecometachycardicandtachypneic.Becausepotassiumaffectscellfunction,severehypokalemiacanleadtorhabdomyolysis,a
breakdownofmusclefibersleadingtomyoglobinintheurine.Ashypokalemiaaffectssmoothmuscle,thepatientmaydevelopanorexia,nausea,andvomiting.
GItroubleThepatientmayexperienceintestinalproblems,suchasdecreasedbowelsounds,constipation,andparalyticileus.Thepatientmayalsohavedifficultyconcentratingurine(whenhypokalemiaisprolonged)andthereforepasslargevolumesofdiluteurine.
ThetelltaleheartCardiacproblemscanalsoresultfromalowpotassiumlevel.Thepulsemaybeweakandirregular.Thepatientmayhaveorthostatichypotensionorexperiencepalpitations.Theelectrocardiogram(ECG)mayshowaflattenedorinvertedTwave,adepressedSTsegment,andacharacteristicUwave.Inmoderatetoseverehypokalemia,ventriculardysrhythmias,ectopicbeats,bradycardia,tachycardia,andfullcardiacarrestmayoccur.Apatienttakingdigoxin,especiallyifhe’salsotakingadiuretic,shouldbewatchedcloselyfor
hypokalemia,whichcanpotentiatetheactionofthedigoxinandcauseatoxicreaction.(SeeDangersignsofhypokalemia.)
CAUTION!
Dangersignsofhypokalemia•
Dysrhythmias•
Cardiacarrest•
Digoxintoxicity•
Muscleparalysis•
Paralyticileus•
Respiratoryarrest
WhattestsshowThefollowingtestresultsmayhelpconfirmthediagnosisofhypokalemia:•serumpotassiumlevellessthan3.5mEq/L•increased24-hoururinelevel•elevatedpHandbicarbonatelevels•slightlyelevatedserumglucoselevel•decreasedserummagnesiumlevel•characteristicECGchanges•increaseddigoxinlevel(ifthepatientistakingthisdrug).
Howit’streatedTreatmentforhypokalemiafocusesonrestoringanormalpotassiumbalance,preventingseriouscomplications,andremovingortreatingtheunderlyingcauses.Treatmentvariesdependingontheseverityoftheimbalanceandtheunderlyingcause.Thepatientshouldbeplacedonahigh-potassium,low-sodiumdiet.However,increasingthe
intakeofdietarypotassiummaybeinsufficienttotreatmoreacutehypokalemia.Thepatientmayneedoralpotassiumsupplementsusingpotassiumsalts,inwhichcasepotassiumchlorideispreferred.Patientswhohaveseverehypokalemiaorwhocan’ttakeoralsupplementsmayneedI.V.
potassiumreplacementtherapy.Oralandparenteralpotassiumcanbesafelygivenatthesametime.Whetherthroughaperipheralorcentralcatheter,I.V.potassiummustbeadministeredwithcaretopreventseriouscomplications.
BouncingbacktobalancedAftertheserumpotassiumlevelisbacktonormal,thepatientmayreceiveasustained-releaseoralpotassiumsupplementandmayneedtoincreasethedietaryintakeofpotassium.Also,aftertheunderlyingcauseofthehypokalemiahasbeendeterminedandtreated,makesurethetreatmentplanisadequateandimplemented.Apatienttakingadiureticmaybeswitchedtoapotassium-sparingdiuretictopreventexcessivelossofpotassiumintheurine.Thepatientmayneedhisserumpotassiumlevelsmonitoredtodetermineifthereisaneedtoadjustthepotassiumsupplement.
CarefulmonitoringandskilledinterventionsCarefulmonitoringandskilledinterventionscanhelppreventhypokalemiaandspareyourpatientfromitsassociatedcomplications.Forpatientswhoareatriskfordevelopinghypokalemiaorwhoalreadyhavehypokalemia,you’llwanttoperformtheseactions:
•Monitorvitalsigns,especiallypulseandbloodpressure.Hypokalemiaiscommonlyassociatedwithhypovolemia,whichcancauseorthostatichypotension.
•CheckheartrateandrhythmandECGtracingsinpatientswithserumpotassiumlevelslessthan3mEq/L(severehypokalemia)becausehypokalemiaiscommonlyassociatedwithhypovolemia,andhypovolemiacancausetachyarrhythmias.
•Assessthepatient’srespiratoryrate,depth,andpattern.Hypokalemiamayweakenorparalyzerespiratorymuscles.Notifythepractitionerimmediatelyifrespirationsbecomeshallowandrapidorifoxygensaturationvaluesfall.Keepamanualresuscitationbagatthebedsideofapatientwithseverehypokalemia.(SeeWhentreatmentdoesn’twork,page112.)
It’snotworking
Whentreatmentdoesn’tworkIfyou’rehavingtroubleraisingapatient’spotassiumlevel,stepbackandtakealookattheentirefluidandelectrolytepicture.Askyourselfthesequestionstoguideyourassessmentoftheproblem:•
IsthepatientstillexperiencingdiuresisorsufferinglossesfromtheGItractortheskin?(Ifso,he’slosingfluidandpotassium.)•
Isthepatient’smagnesiumlevelnormal,ordoesheneedsupplementation?(Keepinmindthatlowmagnesiumlevelsmakeithardforthekidneystoconservepotassium.)
•Monitorserumpotassiumlevels.Changesinserumpotassiumlevelscanleadtoseriouscardiaccomplications.
•Assessthepatientforclinicalevidenceofhypokalemia,especiallyifhe’sreceivingadiureticordigoxin.Apatientwhohashypokalemiaandtakesdigoxinisatincreasedriskfordigoxintoxicitybecausethebodyhaslesspotassiumwithwhichtowork.(Potassiumisneededtobalancethelevelofthedigoxinintheblood.)
•Monitoranddocumentfluidintakeandoutput.About40mEqofpotassiumislostineachliterofurine.Diuresiscanputthepatientatriskforpotassiumloss.
•Checkforsignsofhypokalemia-relatedmetabolicalkalosis,includingirritabilityandparesthesia.
•InsertandmaintainpatentI.V.accessasordered.Whenchoosingavein,rememberthatI.V.potassiumpreparationscanirritateperipheralveinsandcausediscomfort.
•AdministerI.V.potassiumreplacementsolutionsasprescribed.(SeeGuidelinesforI.V.potassiumadministration.)
GuidelinesforI.V.potassiumadministrationBelowaresomeguidelinesforadministeringI.V.potassiumandformonitoringpatientsreceivingit.Remember,potassiumonlyneedstobereplacedintravenouslyifhypokalemiaissevereorifthepatientcan’ttakeoralpotassiumsupplements.
Administration•
Topreventorreducetoxiceffects,I.V.infusionconcentrationsshouldn’texceed40mEq/L.Ratesareusually10mEq/hour.Morerapidinfusionsmaybeusedinseverecases;however,rapidinfusionrequiresclosermonitoringofcardiacstatus.Arapidriseinserumpotassiumlevelscanleadtohyperkalemia,resultingincardiaccomplications.Themaximumadultdosegenerallyshouldn’texceed200mEq/24hoursunlessprescribed.•
Useinfusiondeviceswhenadministeringpotassiumsolutionstocontrolflowrate.•
NeveradministerpotassiumbyI.V.pushorbolus;doingsocancausecardiacarrhythmiasandcardiacarrest,whichcouldbefatal.
Patientmonitoring•
Monitorthepatient’scardiacrhythmduringrapidI.V.potassiumadministrationtopreventtoxiceffectsfromhyperkalemia.Immediatelyreportanyirregularities.•
Evaluatetheresultsoftreatmentbycheckingserumpotassiumlevelsandassessingthepatientforsignsoftoxicreaction,suchasmuscleweaknessandparalysis.
•WatchtheI.V.siteforsignsofinfiltration,phlebitis,ortissuenecrosis.•
Monitorthepatient’surineoutputandnotifythepractitionerifvolumeisinadequate.Urineoutputshouldexceed30ml/hourtoavoidhyperkalemia.•
Repeatpotassiumlevelmeasurementsevery1to3hours.
Whentreatingapatientwithdiabeticketoacidosis(DKA),thefollowingguidelinesarerecommended:•
TypicaldeficitsofpotassiuminDKAarebetween3and5mEq/kg.–
Ifpotassiumlevelsarelowerthan3.5mmol/L,replacementshouldstartimmediatelybeforeinsulintherapyisinitiated.–
Ifpotassiumlevelsarebetween3.5and5.5mmol/L,replacementisindicated.–
Ifpotassiumlevelsaregreaterthan5.5mmol/L,replacementshouldnotcommence(Garcia-Pascual&Kidby,2012).
•MonitorheartrateandrhythmandECGtracingsofpatientsreceivingpotassiuminfusionsofmorethan5mEq/houroraconcentrationofmorethan40mEq/Loffluid.
•AdministerI.V.potassiuminfusionscautiously.Makesureinfusionsaredilutedandmixedthoroughlyinadequateamountsoffluid.Usepremixedpotassiumsolutionswhenpossible.
•WatchtheI.V.infusionsiteforinfiltration.•NevergivepotassiumbyI.V.pushorasabolus.Itcouldbefatal.
•Topreventgastricirritationfromoralpotassiumsupplements,administerthesupplementsinatleast4oz(118ml)offluidorwithfood.
•Topreventaquickloadofpotassiumfromenteringthebody,don’tcrushslow-releasetablets.•UsethesamecarewhengivinganoralsupplementasyouwouldwhenadministeringanI.V.
supplement.•Provideasafeenvironmentforthepatientwhoisweakfromhypokalemia.Explainany
imposedactivityrestrictions.(SeeTeachingabouthypokalemiaandhyperkalemia,page120.)
Teachingpoints
TeachingabouthypokalemiaandhyperkalemiaWhenteachingapatientwithhypokalemiaorhyperkalemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
explanationofhypokalemiaorhyperkalemia,includingitssignsandsymptomsanditscomplications•
medication,includingdosageandpotentialforhypokalemiaorhypokalemia•
needforapotassium-restricteddietandimportanceofavoidingsaltsubstitutes•
preventionoffutureepisodesofhypokalemiaorhyperkalemia•
warningsignsandsymptomstoreporttothepractitioner.
•Checkforsignsofconstipation,suchasabdominaldistentionanddecreasedbowelsounds.Althoughmedicationmaybeprescribedtocombatconstipation,don’tuselaxativesthatpromotepotassiumloss.(SeeDocumentinghypokalemiaorhyperkalemia,page120.)
Chartsmart
DocumentinghypokalemiaorhyperkalemiaIfyourpatienthashypokalemiaorhyperkalemia,makesureyoudocumentthefollowinginformation:•
assessmentfindings•
vitalsigns(includingarrhythmias)•
serumpotassiumlevelandotherpertinentlaboratorytestresults•
intakeandoutput•
practitionernotification•
medicationsadministered•
nursinginterventionsandpatient’sresponse•
safetymeasuresimplemented•
patientteachingprovidedandpatientresponsetotheteaching.
•Emphasizetheimportanceoftakingpotassiumsupplementsasprescribed,especiallywhenthepatientisalsotakingdigoxinoradiuretic.Ifappropriate,teachthepatienttorecognizeandreportsignsandsymptomsofdigoxintoxicity,suchaspulseirregularities,anorexia,nausea,andvomiting.
•Makesurethepatientcanidentifythesignsandsymptomsofhypokalemia.
Memoryjogger
Toremembersomeofthesignsandsymptomsofhypokalemia,thinkofthewordSUCTION(keepinmindthathypokalemiacanbecausedbyalossofstomachcontentsfromnasogastricsuctioning):
Skeletalmuscleweakness
Uwave(ECGchanges)
Constipation
Toxiceffectsofdigoxin(fromhypokalemia)
Irregular,weakpulse
Orthostatichypotension
Numbness(paresthesia).
Hyperkalemia
Hyperkalemiaoccurswhentheserumpotassiumlevelrisesabove5mEq/L.Moderatehyperkalemiaischaracterizedbypotassiumlevelsof6.1to7.0mEq/L.Severehyperkalemiaischaracterizedbylevelsgreaterthan7.0mEq/L.Becausethenormalserumpotassiumrangeissonarrow(3.5to5mEq/L),aslightincreasecanhaveprofoundeffects.Althoughitoccurslesscommonlythanhypokalemia,hyperkalemiaismoreserious.Treatmentsandunderlyingconditionsarecommoncausesofhyperkalemia.(SeeHyperkalemiainprematureinfantsandelderlypatients.)
Agesandstages
Agesandstages
HyperkalemiainprematureinfantsandelderlypatientsPrematureinfantsandelderlypatientsareatgreatestriskforhyperkalemia.Prematureinfantsareathighriskbecauseoftheirimmaturerenalfunction.Theycommonlyexperiencehyperkalemiawithinthefirst48hoursoflife,dependingongestationalage.Individualsage60yearsandolderarealsoathighriskbecauserenalfunctiondeteriorateswith
age,renalbloodflowdecreases,andoralfluidintakedecreases(therebydecreasingurineflowrates).Theirplasmareninactivityandaldosteronelevelsalsodecreasewithage,thusdecreasingtheabilitytosecretepotassium.Elderlypeoplearemorelikelytotakemedicationsthatinterferewithpotassiumexcretion,suchasnonsteroidalanti-inflammatorydrugs,angiotensin-convertingenzymeinhibitors,andpotassium-sparingdiuretics.Patientswhoarebedriddenmaybeplacedonsubcutaneousheparin,whichalsodecreasesaldosteroneproduction,therebydecreasingpotassiumexcretion.
HowithappensRemember,potassiumisgainedthroughintakeandlostbyexcretion.Ifeitherisaltered,hyperkalemiacanresult.Thekidneys,whichexcretepotassium,arevitalinpreventingatoxicbuildupofthiselectrolyte.
Acid-baseimbalancescanalterpotassiumbalanceaswell.Acidosismovespotassiumoutsidethecellsashydrogenionsshiftintothecellsandinhibitpotassiummovementintothecells.Cellinjuryresultsinrelease,orspilling,ofpotassiumintotheserum,whichisreflectedinthepatient’slaboratorytestresults.
ToomuchintakeIncreaseddietaryintakeofpotassium(especiallywithdecreasedurineoutput)cancausepotassiumleveltorise.Excessiveuseofsaltsubstitutes(mostofwhichusepotassiumasasubstituteforsodium)furthercompoundsthesituation.Potassiumsupplements,whetheroralorI.V.,alsoraisethepotassiumlevel.Excessivedosescanleadtohyperkalemia.
DangerousdonationsTheserumpotassiumlevelofdonatedbloodincreasesthelongerthebloodisstored.Therefore,apatient’spotassiumlevelmayriseifhe’sgivenalargevolumeofdonatedbloodthat’snearingitsexpirationdate.Certainmedicationsareassociatedwithhighpotassiumlevels,suchasbeta-adrenergic
blockers(whichinhibitpotassiumshiftsintocells),potassium-sparingdiureticssuchasspironolactone,andsomeantibioticssuchaspenicillinGpotassium.Chemotherapy,whichcausescelldeath(andsometimesrenalinjury),canalsoleadtohyperkalemia.Angiotensin-convertingenzymeinhibitorsandangiotensinreceptorblockers,nonsteroidalanti-
inflammatorydrugs,andheparinarethoughttocausehyperkalemiabysuppressingaldosteronesecretion,whichdecreasespotassiumexcretioninthekidneys.Whenadministeringanymedicationthatcancauserenalinjury(suchasanaminoglycoside),monitorthepatientforhyperkalemia.(SeeDrugsassociatedwithhyperkalemia).
DrugsassociatedwithhyperkalemiaThesedrugsareassociatedwithincreasedpotassiumlevels:•
ACEs(angiotensin-convertingenzymeinhibitors)andARBs(angiotensinreceptorblockers)(Lehnhardt&Kemper,2011)•
antibiotics•
beta-adrenergicblockers•
chemotherapeuticdrugs•
digoxin•
heparin•
nonsteroidalanti-inflammatorydrugs•
potassium(inexcessiveamounts)•
potassium-sparingdiuretics(suchasspironolactone).
ToolittleoutputPotassiumexcretionisdiminishedinpatientswithacuteorchronicrenalfailure,especiallypatientswhoareondialysis.Anydiseasethatcancausekidneydamage(forexample,diabetes,sicklecelldisease,orsystemiclupuserythematosus)canleadtohyperkalemia.Addison’sdiseaseandhypoaldosteronismcanalsodecreasepotassiumexcretionfromthebody.
AninsultfrominjuryWhenaburn,severeinfection,trauma,crushinjury(rhabdomyolysis),orintravascularhemolysishasinjuredacell,potassiummayleavethecell.Thisisalsocalledrelativehyperkalemia.Chemotherapycausescelllysisandthereleaseofpotassium.Metabolicacidosisandinsulin
deficiencydecreasethemovementofpotassiumintocells.(SeeMakesuretheresultsaretrue.)
MakesuretheresultsaretrueWhenalaboratorytestresultindicatesthatyourpatienthasahighserumpotassiumlevelandtheresultjustdoesn’tseemtomakesense,makesureit’satrueresult.Ifthesamplewasdrawnusingpoortechnique,theresultsmaybefalselyhigh.Somecausesofhighpotassiumlevelsthatdon’ttrulyreflectthepatient’sserumpotassiumlevelinclude:•
drawingthesampleaboveanI.V.infusioncontainingpotassium•
usingarecentlyexercisedextremityforthevenipuncturesite•
causinghemolysis(celldamage)byroughhandlingofthespecimenasit’sobtainedortransported.
WhattolookforSignsandsymptomsofhyperkalemiareflectitseffectsonneuromuscularandcardiacfunctioninginthebody.Paresthesia,anearlysymptom,andirritabilitysignalhyperkalemia.
MusclemessagesHyperkalemiamaycauseskeletalmuscleweaknessthat,inturn,mayleadtoflaccidparalysis.Deeptendonreflexesmaybedecreased.Muscleweaknesstendstospreadfromthelegstothetrunkandinvolvesrespiratorymuscles.Hyperkalemiaalsocausessmoothmusclehyperactivity,particularlyintheGItract,whichcanresultinnausea,abdominalcramping,anddiarrhea(anearlysign).
HeartsignsOtherpossiblecomplicationsofhyperkalemiaincludeadecreasedheartrate,irregularpulse,decreasedcardiacoutput,hypotensionand,possibly,cardiacarrest.Atall,tentedTwaveisaprominentECGcharacteristicofapatientwithhyperkalemia.Other
ECGchangesincludeaflattenedPwave,aprolongedPRinterval,bundle-branchblockscausingawidenedQRScomplex,andadepressedSTsegment.Inthelatephase,seeninprolongedhyperkalemicstates,theQRScomplexandTwavemaycombinetoformabiphasicor“sine”wave,whichprecedesventricularstandstill.Theconditioncanalsoleadtoheartblock,ventriculararrhythmias,andasystole.Themoreseriousarrhythmiasbecomeespeciallydangerouswhenserumpotassiumlevelsreach7mEq/Lormore.
WhattestsshowThefollowingtestresultshelpconfirmthediagnosisanddeterminetheseverityofhyperkalemia:•serumpotassiumlevelgreaterthan5mEq/L•decreasedarterialpH,indicatingacidosis•ECGabnormalities.
Howit’streated
Treatmentforhyperkalemiaaimstolowerthepotassiumlevel,treatitscause,stabilizethemyocardium,andpromoterenalandGIexcretionofpotassium.Theseverityofhyperkalemiadictateshowitshouldbetreated.
MildmeasuresThepatientwithmildhyperkalemiamayreceivealoopdiuretictoincreasepotassiumlossfromthebodyortoresolveanyacidosispresent.Patientswillbeputonapotassium-restricteddietandhaveanymedicationsassociatedwithhighpotassiumlevelreadjustedorstopped.Underlyingdisordersleadingtothehighpotassiumlevelshouldalsobetreated.
StrongerstepsApatientwithmoderatetoseverehyperkalemiamayrequirefurthermeasuresortreatment.Ifthepatienthasrenalfailure,adiureticmaynotbeeffective.Ifthepatienthasacutesymptomatichyperkalemia,hemayneedhemodialysis.Sodiumpolystyrenesulfonate(Kayexalate),acation-exchangeresin,isacommontreatmentfor
hyperkalemia.Sorbitoloranotherosmoticsubstanceshouldbegivenwiththismedicationtopromoteitsexcretion.Kayexalatecanbegivenorally,throughanasogastrictube,orasaretentionenema(mayrequirerepeatedtreatments).Theonsetofactionmaytakeseveralhours;thedurationofactionis4to6hours.Asthemedicationsitsintheintestines,sodiummovesacrossthebowelwallintothebloodandpotassiummovesoutofthebloodintotheintestines.Loosestoolsremovepotassiumfromthebody.
TheperilsofpotassiumMoreseverehyperkalemiaistreatedasanemergency.Closelymonitorthepatient’scardiacstatus.ECGsareobtainedtofollowprogress.Tocounteractthemyocardialeffectsofhyperkalemia,administer10%calciumgluconate
(usually10ml)or10%calciumchloride(usually5ml)I.V.over2minutesasordered.Thepatientmustbeconnectedtoacardiacmonitor.However,calciumgluconateisn’tatreatmentforhyperkalemiaitself,andthehyperkalemiamuststillbetreatedbecausetheeffectsofcalciumlastonlyashorttime.(SeeCalciumalert!)
CAUTION!
Calciumalert!Eithercalciumchlorideorcalciumgluconatemaybeordered.Butthereisadifferencebetweenthetwo:Oneampuleofcalciumchloridehasthreetimesmorecalciumthancalciumgluconate.Therefore,whenpreparingadoseforadministration,checktheorderandreadthelabelcarefully.Ifbradycardiadevelopsduringadministration,stopeithertypeofinfusion.
ApatientwithacidosismayreceiveI.V.sodiumbicarbonate(usually50mEq),whichhelpsdecreaseserumpotassiumbytemporarilyshiftingpotassiumintothecells.ItalsoraisesbloodpH.Thedrugbecomeseffectivewithin15to30minutesandlasts1to3hours.Thisalkalinizingagentmaybegivenwithinsulintoenhanceitseffects.Anotherwaytomovepotassiumintothecellsandlowertheserumlevelistoadminister10
unitsofregularinsulinI.V.Thedrugbecomesactivewithin15to60minutesandlasts4to6hours.It’sgivenwithI.V.hypertonicdextrose(10%to50%dextrosesolution).Closelywatchthecardiacstatusofapatientwithseverehyperkalemia.Andlastly,anaerosolizedbeta-2agonist,suchasalbuterol,willdrivepotassiumintothecells.
Memoryjogger
Tohelpyourememberhowtotreathyperkalemia,think“seebigkid”(CBIGKD):
Calciumgluconate
Bicarbonate
Insulin
Glucose
Kayexalate
Dialysis.
HowyouintervenePatientsatriskforhyperkalemiarequirefrequentmonitoringofserumpotassiumandotherelectrolytelevels.Thoseatriskincludepatientswithacidosisorrenalfailureandthosereceivingapotassium-sparingdiuretic,anoralpotassiumsupplement,oranI.V.potassiumpreparation.Ifapatientdevelopshyperkalemia,taketheseactions:•Assessvitalsigns.Anticipatecardiacmonitoringifthepatient’sserumpotassiumlevelexceeds
6mEq/L.ApatientwithECGchangesmayneedaggressivetreatmenttopreventcardiacarrest.•Monitorthepatient’sintakeandoutput.Reportanoutputoflessthan30ml/hour.Aninabilityto
excretepotassiumadequatelymayleadtodangerouslyhighpotassiumlevels.(SeeThenextstep.)
It’snotworking
ThenextstepIfyoucan’tloweryourpatient’spotassiumlevelasexpected,considerthefollowingquestions:•
Isthepatienttakinganantacid?(Antacidscontainingmagnesiumorcalciumcaninterferewithionexchangeresins.)•
Isthepatient’srenalstatusworsening?•
Isthepatienttakingamedicationthatcouldraisethepotassiumlevel?•
Isthepatientreceivingolddonatedbloodduringtransfusions?
•PreparetoadministeraslowcalciumchlorideorgluconateI.V.infusioninacutecasestocounteractthemyocardialdepressanteffectsofhyperkalemia.
•Forapatientreceivingrepeatedinsulinandglucosetreatment,checkforclinicalsignsandsymptomsofhypoglycemia,includingmuscleweakness,syncope,hunger,anddiaphoresis.
•KeepinmindwhengivingKayexalatethatserumsodiumlevelsmayrise.Watchforsignsofheartfailure.
•Monitorbowelsoundsandthenumberandcharacterofbowelmovements.Hyperactivebowelsoundsresultfromthebody’sattempttomaintainhomeostasisbycausingsignificantpotassiumexcretionthroughthebowels.
•Monitorthepatient’sserumpotassiumlevelandrelatedlaboratorytestresults.Keepinmindthatpatientswithserumpotassiumlevelsexceeding6mEq/Lrequirecardiacmonitoringbecauseasystolemayoccurashyperkalemiamakesdepolarizationofcardiacmuscleeasierandshortensrepolarizationtimes.
•Monitorthepatient’sdigoxinlevelifheistakingthismedication.Hemaybeatriskfordigoxintoxicity.
•Administerprescribedmedicationsandmonitorthepatientfortheireffectivenessandforadverseeffects.
•EncouragethepatienttoretainKayexalateenemasfor30to60minutes.Monitorthepatientforhypokalemiawhenadministeringthisdrugon2ormoreconsecutivedays.
•Ifthepatienthasacutehyperkalemiathatdoesn’trespondtoothertreatments,preparehimfordialysis.
•Ifthepatienthasmuscleweakness,implementsafetymeasures.Advisehimtoaskforhelpbeforeattemptingtogetoutofbedandwalk.Continuetoevaluatemusclestrength.
•Administerprescribedantidiarrhealsandmonitorthepatient’sresponse.
Dietdetails•Helpthepatientselectfoodslowinpotassium(suchasapples,pears,berries,carrots,corn,
asparagus,rice,noodles,andbread).(SeeTeachingabouthypokalemiaandhyperkalemia.)•Ifthepatientwithhyperkalemianeedsatransfusion,obtainfreshblood.•Watchforsignsofhypokalemiaaftertreatment.•Documentallcaregivenandthepatient’sresponse.(SeeDocumentinghypokalemiaorhyperkalemia.)
•Explainthesignsandsymptomsofhyperkalemia,includingmuscleweakness,diarrhea,andpulseirregularities.Urgethepatienttoreportsuchsignsandsymptomstothepractitioner.
•Describethesignsandsymptomsofhypokalemiatopatientstakingmedicationstolowerserumpotassiumlevels.
That’sawrap!
Potassiumimbalancesreview
Potassiumbasics•
Majorcationinintracellularfluid(98%)•
Affectsnerveimpulsetransmission•
Canbedisturbedbydiseases,injuries,medications,andtherapies•
Normalrangeinblood:3.5to5mEq/L
Potassiumbalance•
Potassiummustbeingesteddaily(40mEq);thebodycan’tconserveit.•
Thesodium-potassiumpump,renalregulation,andpHlevelhelptomaintainbalance.
Hypokalemia•
Serumpotassiumlevelslessthan3.5mEq/L(moderatehypokalemia:2.5to3mEq/L;severehypokalemia:<2.5mEq/L)•
Underlyingmechanisms:medicationsorinadequateintakeorexcessiveoutputofpotassium•
Causedbyprolongedintestinalsuction,prolongedvomitingordiarrhea,laxativeabuse,severediaphoresis,recentileostomy,andvillousadenoma
Signsandsymptoms•
Skeletalmuscleweakness,Uwave(ECGchanges),Constipation,Toxicity(digoxin),Irregularandweakpulse,Orthostatichypotension,Numbness(SUCTIONistheacronymtoremember.)•
Othersignsandsymptoms–
Anorexia–
Cramps–
Decreasedbowelsounds–
ECGchanges–
Hyporeflexia–
Nausea–
Paresthesia–
Polyuria–
Vomiting–
Legcramps–
Decreasedorabsentdeeptendonreflexes–
Paralysis
Treatment•
High-potassiumdiet•
Oralpotassiumsupplements•
I.V.potassiumtherapy•
Potassium-sparingdiuretic,ifneeded
Hyperkalemia•
Mostdangerouselectrolytedisorder•
Commonlyaccompaniesmetabolicacidosis•
Underlyingmechanisms:increasedintakeofpotassium,decreasedurineexcretionofpotassium,shiftofpotassiumoutofthecellstoextracellularfluid,medications•
Bestclinicalindicators:serumpotassiumlevelsandECGtracings•
Serumpotassiumlevelsexceeding7mEq/L:possibleseriouscardiacarrhythmiasleadingtocardiacarrest(couldbefatal)
Signsandsymptoms•
Abdominalcramping•
Diarrhea•
ECGchanges(classicsign:tall,tentedTwavewithearlystagesandsinewavewithlatestages)•
Hypotension•
Irregularpulserate•
Irritability•
Muscleweakness,especiallyinthelowerextremities,whichmayleadtoflaccidparalysis•
Nausea•
Paresthesia•
Bradycardia
TreatmentFormildtomoderatecases•
LoopdiureticsForseverecases•
Calciumchlorideorgluconate•
Bicarbonate•
Insulin•
Glucose•
Kayexalate•
Dialysis(CBIGKD[“seebigkid”]istheacronymtoremember.)
Quickquiz
1.Potassiumisresponsiblefor:A.buildingmusclemass.B.buildingbonestructureandstrength.C.maintainingtheheartbeat.D.maintainingweight.
Answer:C.Potassiumisvitalforpropercardiacfunctionbecauseitplaysakeyroleincardiacmusclecontractionandelectricalconductivity.Changesinserumpotassiumlevelcallforearlyrecognitionandtreatment.
2.Whenthehormonealdosteroneissecreted,thekidneysreabsorb:A.sodium.B.potassium.
C.magnesium.D.calcium.
Answer:A.Thekidneysreabsorbsodiumandexcretepotassiumwhenaldosteroneissecreted.
3.Neuromuscularsignsandsymptomsofhypokalemiainclude:A.Tourette’ssyndrome.B.confusionandirritability.C.diminisheddeeptendonreflexes.D.Parkinsonian-typetremors.
Answer:C.Deeptendonreflexesmaybedecreasedorabsentinhypokalemia.Also,legcrampsmayoccurandrespiratorymusclesmaybeparalyzed.
4.Medicationstohelptreatseverehyperkalemiainclude:A.methylprednisoloneandmannitol.B.mannitolandregularinsulin.C.digoxinanddiuretics.D.10%calciumgluconateandregularinsulin.
Answer:D.Calciumgluconatehelpstostabilizecardiaccellmembranes,althoughitdoesn’tlowerahighpotassiumlevelitself.Regularinsulin,givenwithhypertonicdextrose,causespotassiumtomoveintothecells,thusloweringtheserumpotassiumlevel.
5.AhallmarkECGcharacteristicofhyperkalemiaisthepresenceof:A.irregularPRintervals.B.narrowedQRScomplexes.C.tall,tentedTwaves.D.peakedPwaves.
Answer:C.Tall,tentedTwavesareahallmarkofhyperkalemia,aconditionthatcanalsoleadtoheartblock,ventriculararrhythmias,andasystole.
6.An83-year-oldpatientwithheartfailuredevelopshypokalemiaasaresultofherdiuretictherapy.Yousuggestthatsheincreaseherdietaryintakeofpotassium.Whichfoodsshouldsheconsume?
A.Chocolate,orangejuice,andbananasB.Cannedsoups,peas,andmilkC.Apples,wholewheatbread,andoatmealD.Dairyproductsandwholegrains
Answer:A.Majordietarysourcesofpotassiumincludechocolate,driedfruit,nutsandseeds,oranges,bananas,apricots,cantaloupes,potatoes,mushrooms,tomatoes,andcelery.
7.WhenadministeringI.V.potassiumforseverehypokalemia,youshould:A.avoidinfusingthepotassiumwithallotherI.V.solutions.
B.infusethroughasmallI.V.catheter.C.verifythattheconcentrationofthesolutiondoesn’texceed40mEq/L.D.usethedripmethodtoinfusethepotassium.
Answer:C.Topreventorreducetoxiceffects,theI.V.infusionconcentrationshouldn’texceed40mEq/L.
ScoringIfyouansweredallsevenquestionscorrectly,wow!You’reTopBanana!Ifyouansweredfiveorsixcorrectly,super!You’vegreatpotassiumpower!Ifyouansweredfewerthanfivecorrectly,hanginthere.Rereadingthechaptermayhelpyouraiseyourpotassiumunderstandinglevel.
ReferencesGarcia-Pascual,M.,&Kidby,J.(2012).Proceduresandmedicationstohelppatientscontroltheir
diabetes.EmergencyNurse,20(8),30–35.Lehnhardt,A.,&Kemper,M.J.(2011).Pathogenesis,diagnosis,andmanagementofhyperkalemia.
PediatricNephrology,26,377–384.TuftsUniversity.(2012).Potassiumpower:Increasedpotassiumassociatedwithdecreasedhypertension.
TuftsUniversityHealthandNutritionLetter,30(1),4–5.
Chapter7
Whenmagnesiumtipsthebalance
JustthefactsInthischapter,you’lllearn:
♦theimportanceofmagnesium
♦thechallengesofinterpretingyourpatient’sserummagnesiumlevel
♦causesandstepstotakewhenyourpatient’sserummagnesiumlevelisaboveorbelownormal.
AlookatmagnesiumAfterpotassium,magnesiumisthemostabundantcation(positivelychargedion)inintracellularfluid.Thebonescontainabout60%ofthebody’smagnesium;extracellularfluidcontainslessthan1%.Intracellularfluidholdstherest.
Whyit’simportantMagnesiumperformsmanyimportantfunctionsinthebody.Forexample,it:•promotesenzymereactionswithinthecellduringcarbohydratemetabolism•helpsthebodyproduceanduseadenosinetriphosphate(ATP)forenergy•takespartinDNAandproteinsynthesis•influencesvasodilationandirritabilityandcontractilityofthecardiacmuscles,therebyhelping
thecardiovascularsystemfunctionnormally•aidsinneurotransmissionandhormone-receptorbinding•makestheproductionofparathyroidhormone(PTH)possible•helpssodiumandpotassiumionscrossthecellmembrane(thisexplainswhymagnesiumaffects
sodium,calcium,andpotassiumionlevelsbothinsideandoutsidethecell).
ManagingthosemusclesMagnesiumalsoregulatesmusclecontractions,makingitespeciallyvitaltotheneuromuscularsystem.Byactingonthemyoneuraljunctions—thesiteswherenerveandmusclefibersmeet—magnesiumaffectstheirritabilityandcontractilityofcardiacandskeletalmuscle.Magnesiumisimportantinmaintainingcardiacrhythm(DelGoboetal.,2013).Onestudyconcludedthatpatientswithvasculardiseaseandlowmagnesiumlevelswereatgreaterriskforneuromuscularevents(mostnotably,strokes).
What’scalciumgottodowithit?Magnesiumhasanotherfunctionthat’sworthremembering:Itinfluencesthebody’scalciumlevelthroughitseffectonPTH.YoumightrecallthatPTHmaintainsaconstantcalciumlevelinextracellularfluid.
InterpretingmagnesiumlevelsYou’llneedtokeepthemagnesium-calciumconnectioninmindwhenassessingapatient’slaboratoryvalues.However,thatisn’ttheonlythingyou’llneedtorememberforadults.Yourpatient’sserummagnesiumlevelitselfmaybemisleading.Normally,thebody’stotal
serummagnesiumlevelis1.5to2.5mEq/L.(SeeAtdifferentlevels.)Butthelevelmaynotaccuratelyreflectyourpatient’sactualmagnesiumstores.That’sbecausemostmagnesiumisfoundwithincells,whereitmeasuresabout40mEq/L.Inserum,magnesiumlevelsarerelativelylow.
Agesandstages
Agesandstages
AtdifferentlevelsDon’tforgetthatnormalmagnesiumlevelsinneonatesandchildrenaredifferentfromadultlevels.Inneonates,magnesiumlevelsrangefrom1.4to2.9mEq/L;inchildren,1.6to2.6mEq/L.
TiesthatbindHere’sanotherreasonwhyinterpretingapatient’sserummagnesiumlevelcanposeachallenge.Morethanhalfofcirculatingmagnesiummovesinafree,ionizedform.Another30%bindswithaprotein—mostlyalbumin—andtheremainderbindswithothersubstances.Ionizedmagnesiumisphysiologicallyactiveandmustberegulatedtomaintainhomeostasis.
However,thisformalonecan’tbemeasured,soapatient’smeasuredlevelsreflectthetotalamountofcirculatingmagnesium.Tocomplicatematters,magnesiumlevelsarelinkedtoalbuminlevels.Apatientwithalow
serumalbuminlevelalsohasalowtotalserummagnesiumlevel—evenifthelevelofionizedmagnesiumremainsunchanged.That’swhyserumalbuminlevelsneedtobemeasuredwithserummagnesiumlevels.Serumcalciumandcertainotherlaboratoryvaluesalsocomeintoplaywhenassessingand
treatingmagnesiumimbalances.Becausemagnesiumismainlyanintracellularelectrolyte,changesinthelevelsofotherintracellularelectrolytes,suchaspotassiumandphosphorus,canaffectserummagnesiumlevels,too.
HowthebodyregulatesmagnesiumThegastrointestinal(GI)andurinarysystemsregulatemagnesiumthroughabsorption,excretion,andretention—thatis,throughdietaryintakeandoutputinurineandfeces.Awell-balanceddietshouldprovideroughly25mEq(or300to350mg)ofmagnesiumdaily.(SeeDietarysourcesofmagnesium.)TheDietaryReferenceIntakes(DRIs)varywithaperson’sageandsex.Ofthisamount,about40%isabsorbedinthesmallintestine(U.S.DepartmentofAgriculture,2014).
DietarysourcesofmagnesiumMosthealthypeoplecangetallthemagnesiumtheyneedbyeatingawell-balanceddietthatincludesfoodsrichinmagnesium.Herearethe“lucky7”foodshighinmagnesium:•
chocolate(especiallydarkchocolate)•
drybeansandpeas•
green,leafyvegetables•
meats•
nuts•
seafood•
wholegrains.
AbalancingactThebodytriestoadjusttoanychangeinthemagnesiumlevel.Forinstance,iftheserummagnesiumleveldrops,theGItractmayabsorbmoremagnesiumand,ifthemagnesiumlevelrises,theGItractexcretesmoreinthefeces.
Thekidneys,fortheirpart,balancemagnesiumbyalteringitsreabsorptionattheproximaltubuleandloopofHenle.So,ifserummagnesiumlevelsclimb,thekidneysexcretetheexcessintheurine.Diureticsheightenthiseffect.Thereverseoccurs,too:Ifserummagnesiumlevelsfall,thekidneysconservemagnesium.Thatconservationissoefficientthatthedailylossofcirculatingionizedmagnesiumcanberestrictedtojust1mEq.
Hypomagnesemia
Hypomagnesemiaoccurswhenthebody’sserummagnesiumlevelfallsbelow1.5mEq/L.Thisimbalanceisrelativelycommon,affectingabout10%ofallhospitalizedpatients.Theconditionismostcommonamongcriticallyillpatients.(SeeDangersignsoflowmagnesiumlevels.)Patientswithahistoryofalcoholism,diabetesmellitus,GIdisorders,andrenaldiseasealongwiththeelderlyareathigherriskfordevelopinghypomagnesemia.
CAUTION!
DangersignsoflowmagnesiumlevelsSuspectthatyourpatientwithhypomagnesemiaisreallyintroubleifhehasanyoftheselate-developingdangersignsorsymptoms:•
cardiacarrhythmias•
digoxintoxicity•
laryngealstridor•
respiratorymuscleweakness•
seizures.
Mostsymptomsofhypomagnesemiaoccurwhenthemagnesiumleveldropsbelow1mEq/L.Signsandsymptomsofhypomagnesemiatendtobenonspecificbutmayincludehyperactivedeeptendonreflexes(DTRs),weakness,musclecramping,restlesslegsyndrome,rapidheartbeat,tremor,vertigo,insomnia,ataxia,anxiety,agitation,anddepression.Atitsworst,hypomagnesemiacanleadto:•respiratorymuscleparalysis•completeheartblock•alteredmentalstatusorcoma.
HowithappensAnyconditionthatimpairseitherofthebody’smagnesiumregulators—theGIsystemortheurinarysystem—canleadtoamagnesiumshortage.Theseconditionsfallintofourmaincategories:•poordietaryintakeofmagnesium•poormagnesiumabsorptionbytheGItract•excessivemagnesiumlossfromtheGItract•excessivemagnesiumlossfromtheurinarytract.
ThepriceofalcoholChronicalcoholicsareatriskforhypomagnesemiabecausetheytendtoeatapoordiet.What’sworse,alcoholoverusecausestheurinarysystemtoexcretemoremagnesiumthannormal.Alcoholicscanalsolosemagnesiumthroughpoorintestinalabsorptionorfromfrequentorprolongedvomiting.
Atrisk!Patientswhocan’ttakemagnesiumorallyareathighriskfordevelopingamagnesiumdeficiencyunlesstheygetadequatesupplementation.TheseincludepatientsreceivingprolongedI.V.fluidtherapy,totalparenteralnutrition(TPN),orenteralfeedingformulasthatcontaininsufficientmagnesium.Patientswhohavediabetesmellitusarealsoatriskformagnesiumlossduetoosmoticdiuresis.
AbsorptionproblemsIfapatient’sdietaryintakeseemsadequatebuthisserummagnesiumlevelremainslow,poorGIabsorptionmaybetheculprit.Forinstance,malabsorptionsyndromes,steatorrhea,ulcerativecolitis,celiacdisease,andCrohn’sdiseasecandiminishmagnesiumabsorption.Surgerytotreatthesedisorderscanalsoreduceabsorption.Bowelresectionorbypass,forexample,reducespotentialabsorptionsitesbydecreasingthesurfaceareawithintheGItract.OtherconditionsthatcancausehypomagnesemiafrompoorGIabsorptionincludecancer,
pancreaticinsufficiency,andexcessivecalciumorphosphorusintheGItract.
GIproblemsFluidsintheGItract(especiallythelowerpart)containmagnesium.That’swhyapersonwholosesagreatdealofthesefluids—fromprolongeddiarrheaorfistuladrainage,forexample—canhaveamagnesiumdeficiency.Apatientwhoabuseslaxativesorwhohasanasogastrictubeconnectedtosuctionisalsoatrisk.Inthelattercase,themagnesiumislostfromtheupper,notthelower,GItract.Inacutepancreatitis,magnesiumformssoapswithfattyacids(steatorrhea).Thisprocesstakes
someofthemagnesiumoutofcirculation,causingserumlevelstodrop.
UrinaryproblemsGreaterexcretionofmagnesiuminurinecanalsoleadtoalowserummagnesiumlevel.Conditionsthatboostsuchexcretionincludethefollowing:•primaryaldosteronism(overproductionofaldosterone,anadrenalhormone)•hyperparathyroidism(hyperfunctionoftheparathyroidglands)orhypoparathyroidism
(hypofunctionoftheparathyroidglands)•diabeticketoacidosis(DKA)•useofamphotericinB,cisplatin,cyclosporine,pentamidineisethionate,oraminoglycoside
antibiotics,suchastobramycinorgentamicin•prolongedadministrationoflooporthiazidediuretics(SeeDrugsassociatedwithhypomagnesemia.)
•impairedrenalabsorptionofmagnesiumresultingfromdiseasessuchasglomerulonephritis,pyelonephritis,andrenaltubularacidosis.
DrugsassociatedwithhypomagnesemiaBecausecertaindrugscancauseorcontributetohypomagnesemia,youshouldmonitoryourpatient’sserummagnesiumlevelsifhe’sreceiving:•
anaminoglycosideantibiotic,suchasamikacin,gentamicin,streptomycin,ortobramycin•
amphotericinB•
cisplatin•
cyclosporine•
insulin•
alaxative•
loop(suchasbumetanide,furosemide,ortorsemide)orthiazidediuretics(suchaschlorothiazideorhydrochlorothiazide)•
pentamidineisethionate.
OthercausesMagnesiumlevelsmayalsodropdramaticallyinpatientsundergoinghemodialysis;pregnantpatients(secondandthirdtrimester);andpatientsreceivingmagnesium-free,sodium-richI.V.fluidstoinduceextracellularfluidexpansion.Othersatriskincludethosewhohave:•excessivelossofbodyfluids(forexample,fromsweating,breast-feeding,diureticabuse,or
chronicdiarrhea)•hypercalcemiaorexcessiveintakeofcalcium•hypothermia•syndromeofinappropriateantidiuretichormonesecretion•sepsis•seriousburns•woundsrequiringdebridement•anyconditionthatpredisposesthemtoexcessivecalciumorsodiumintheurine.
WhattolookforSignsandsymptomsofhypomagnesemiacanrangefrommildtolife-threateningandcaninvolvethe:•centralnervoussystem(CNS)•neuromuscularsystem•cardiovascularsystem•GIsystem.Generallyspeaking,yourpatient’ssignsandsymptomsmayresemblethoseyouwouldseewith
apotassiumorcalciumimbalance.However,youcan’talwayscountondetectinghypomagnesemiafromclinicalfindingsalone.Occasionally,apatientremainssymptom-freeeventhoughhisserummagnesiumlevelmeasureslessthan1.8mEq/L.(SeeIdentifyinghypomagnesemia.)
IdentifyinghypomagnesemiaConsultthelistofsignsandsymptomsbelowwheneveryouneedtoassessyourpatientforhypomagnesemia.•
CNS:alteredLOC,confusion,hallucinations,nystagmus•
Neuromuscular:muscleweakness,legandfootcramps,hyperactiveDTRs,tetany,Chvostek’sandTrousseau’ssigns(Garrison,Allan,Sekhon,Musini,&Khan,2012)•
Cardiovascular:tachycardia,hypertension,characteristicelectrocardiogramchanges(DelGoboetal.,2013)•
GI:dysphagia,anorexia,nausea,vomiting
Soirritating!AlowserummagnesiumlevelirritatestheCNS.Suchirritationcanleadto:•alteredlevelofconsciousness(LOC)•ataxia•confusion•delusions•depression•emotionallability•hallucinations
•insomnia•psychosis•seizures•vertigo.
WhenmagnesiummovesoutThebodycompensatesforalowserummagnesiumlevelbymovingmagnesiumoutofthecells.Suchmovementcantakeanespeciallyhightollontheneuromuscularsystem.Ascellsbecomemagnesiumstarved,skeletalmusclesgrowweakandnervesandmusclesbecomehyperirritable.
ThethreeTsandhyperactiveDTRsWatchyourpatientforneuromuscularsignsofhypomagnesemia,suchas:•tremors•twitching•tetany•hyperactiveDTRs.(SeeGradingDTRs,page132.)
GradingDTRsIfyoususpectyourpatienthashypomagnesemia,you’llwanttotesthisDTRstodeterminewhetherhisneuromuscularsystemisirritable—acluethathismagnesiumlevelistoolow.Whengradingyourpatient’sDTRs,usethefollowingscale:
0 Absent+ Presentbutdiminished0++ Normal+++ Increasedbutnotnecessarilyabnormal++++ Hyperactive,clonic
Torecordthepatient’sreflexactivity,drawastickfigureandmarkthestrengthoftheresponseattheproperlocations.ThisfigureindicatesnormalDTRactivity.
Respiratorymusclesmaybeaffected,too,resultinginbreathingdifficulties.Somepatientsalsoexperiencelaryngealstridor,footorlegcramps,andparesthesia.
SignlanguageIfyoususpecthypomagnesemia,you’llalsowanttotestyourpatientforhypocalcemiabycheckingforthesesigns:•Chvostek’ssign—facialtwitchingwhenthefacialnerveistapped•Trousseau’ssign—carpalspasmwhentheupperarmiscompressed.(Formoreinformation
aboutthesesigns,seechapter8,Whencalciumtipsthebalance.)
HardontheheartYou’llrecallthatmagnesiumpromotescardiovascularfunction.Soifyou’rethinkingthathypomagnesemiamustaffecttheheartandbloodvessels,you’reright.Adropinthemagnesium
levelcanirritatethemyocardium—withpotentiallydisastrousconsequences.
WrongfulrhythmsMyocardialirritabilitycanleadtocardiacarrhythmias,whichcancauseadropincardiacoutput.Arrhythmiasarelikelytodevelopinpatientswithcoexistingpotassiumandcalciumimbalances,especiallyafteramyocardialinfarction(MI)orcardiacsurgery.Arrhythmiastriggeredbyalowserummagnesiumlevelinclude:•atrialfibrillation•heartblock•paroxysmalatrialtachycardia•prematureventricularcontractions•supraventriculartachycardia•torsadesdepointes•ventricularfibrillation•ventriculartachycardia.
Becauseoftheriskofarrhythmia,patientswithseverehypomagnesemia(serumlevelsbelow1mEq/L)shouldundergocontinuouscardiacmonitoring.PatientswhohavehadanMIorcardiacsurgerymaybegivenoralmagnesiumsupplementstopreventarrhythmias.Generalelectrocardiogram(ECG)changesthatcanoccurwithalowserummagnesiumlevel
include:•prolongedPRinterval•widenedQRScomplex•prolongedQTinterval•depressedSTsegment•broad,flattenedTwave
•prominentUwave.
Memoryjogger
You’llrecallthatstarvationmaycauseabelow-normalserummagnesiumlevel.ThewordSTARVEDcanhelpyouremembersomesignsandsymptomsofhypomagnesemia.Eachofitslettersstandsforatypicalclinicalfinding:
Seizures
Tetany
Anorexiaandarrhythmias
Rapidheartrate
Vomiting
Emotionallability
DTRsincreased.
TheplotmayturntoxicIfyourpatientwithhypomagnesemiaisreceivingdigoxin,watchhimcloselyforsignsandsymptomsofdigoxintoxicity—anotherconditionthatcantriggerarrhythmias.Alowmagnesiumlevelmayincreasethebody’sretentionofdigoxin.Digoxinmayalsocausemoremagnesiumtobelostintheurine.Suspectdigoxintoxicityifyourpatienthas:•anorexia•arrhythmias•nausea•vomiting•yellow-tingedvision.
ToughtimesfortheGItractApatientwhodoesn’thaveasufficientamountofmagnesiuminthebloodstreammaysuffersuchGIproblemsas:•anorexia•dysphagia•nauseaandvomiting.Theseconditionscanleadtopoordietarymagnesiumintakeorlossofmagnesiumthroughthe
GItract,whichinturnworsenthepatient’scondition.
WhattestsshowDiagnostictestresultsthatpointtohypomagnesemiainclude:•aserummagnesiumlevelbelow1.5mEq/L(possiblywithabelow-normalserumalbumin
level)•otherelectrolyteabnormalities,suchasabelow-normalserumpotassiumorcalciumlevel•characteristicECGchanges•elevatedserumlevelsofdigoxininapatientreceivingthedrug.
Howit’streatedTreatmentforhypomagnesemiadependsontheunderlyingcauseoftheconditionandthepatient’sclinicalfindings.Forpatientswithmildmagnesiumshortages,achangeindietandteachingmaybeenoughtocorrecttheimbalance.Somedoctorsalsoprescribeanoralsupplement,suchasmagnesiumgluconate,magnesiumoxide,ormagnesiumhydroxide.Becauseitmaytakeafewdaystoreplenishmagnesiumstoresinsidethecell,magnesiumreplacementmaybenecessaryforseveraldaysaftertheserummagnesiumlevelreturnstonormal.PatientswithmoreseverehypomagnesemiamayneedI.V.ordeepI.M.injectionsofmagnesium
sulfate.Beforemagnesiumadministration,renalfunctionshouldbeassessed.Ifrenalfunctionisimpaired,magnesiumlevelsshouldbemonitoredclosely.(SeeCheckthelabel.)
CheckthelabelWhenyouprepareamagnesiumsulfateinjection,keepinmindthatthedrugcomesinvariousconcentrations,suchas10%,12.5%,and50%.Checkthelabel(suchastheoneshownhere)tomakesureyou’reusingthecorrectconcentration.Thelabelshowsotherdosageinformationaswell.
Howyouintervene
Thebesttreatmentforhypomagnesemiaisprevention,sokeepawatchfuleyeonpatientsatriskforthisimbalancesuchasthosewhocan’ttolerateoralintake.Forpatientswhohavealreadybeendiagnosedwithhypomagnesemia,takethefollowingactions:•Assessthepatient’smentalstatusandreportchanges.•Evaluatethepatient’sneuromuscularstatusregularlybycheckingforhyperactiveDTRs,
tremors,andtetany.CheckforChvostek’sandTrousseau’ssignsifhypocalcemiaisalsosuspected.
•Checkthepatientfordysphagiabeforehe’sgivenfood,oralfluids,ororalmedications.Hypomagnesemiamayimpairhisabilitytoswallow.
•Monitorandrecordyourpatient’svitalsigns.Reportfindingsthatindicatehemodynamicinstability.
•Monitorthepatient’srespiratorystatus.Amagnesiumdeficiencycancauselaryngealstridorandcompromisetheairway.
•Connectyourpatienttoacardiacmonitorifhismagnesiumlevelisbelow1mEq/L.Watchtherhythmstripcloselyforarrhythmias.Besuretofollowyourfacility’spolicyregardingmagnesiumlevelsandwhencardiacmonitoringisrequired.
•Monitorpatientswhohavelostanexcessiveamountoffluid(forexample,duetoprolongeddiarrheaorfistuladrainageornasogastricsuction).Patientswhohaveexperiencedexcessivefluidlossareatriskformagnesiumdeficiency.
•Monitorurineoutputatleastevery4hours.Magnesiumgenerallyisn’tadministeredifurineoutputislessthan100mlin4hours.
•Assessvitalsignsevery15minutes.Ifpatientisexperiencingrespiratorydistress,assesshimforasharpdecreaseinbloodpressure.
•Ifthepatientisreceivingdigoxin,monitorhimcloselyforsignsandsymptomsofdigoxintoxicity(suchasnausea,vomiting,andbradycardia).Magnesiumdeficiencyenhancesthepharmacologicactionofdigoxin.
•Ifthepatientisreceivingamedicationthatcanaffectmagnesiumlevels,suchasanaminoglycosideantibiotic,amphotericinB,cisplatin,cyclosporine,insulin,alaxative,alooporthiazidediuretic,orpentamidineisethionate,monitorhisserummagnesiumlevelsclosely.
•Monitorthepatient’sserumelectrolytelevels,andnotifythepractitioneriftheserumpotassiumlevelorcalciumlevelislow.Bothhypocalcemiaandhypokalemiacancausehypomagnesemia.
•MonitorpatientswhohavereceivednothingbymouthandwhohavebeenreceivingI.V.fluidswithoutmagnesiumsalts.Prolongedadministrationofmagnesium-freefluidscanresultinlowserummagnesiumlevels.
•Instituteseizureprecautions.•Ifaseizureoccurs,reportthetypeofseizure,itslength,andthepatient’sbehaviorduringthe
seizure.Reorienthimasneeded.•Keepemergencyequipmentnearbyforairwayprotection.•Ensureyourpatient’ssafetyatalltimes.•Toeaseyourpatient’sanxiety,tellhimwhattoexpectbeforeeachprocedure.(SeeTeachingabouthypomagnesemia,page136.
Teachingpoints
TeachingabouthypomagnesemiaWhenteachingapatientwithhypomagnesemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
explanationsabouthypomagnesemia,itsriskfactors,anditstreatment•
prescribedmedications•
avoidanceofdrugsthatdepletemagnesiuminthebody,suchasdiureticsandlaxatives•
consumptionofhigh-magnesiumdiet•
dangersignsandsymptomsandwhentoreportthem•
referraltoappropriatesupportgroupssuchasAlcoholicsAnonymous.
•EstablishI.V.accessandmaintainapatentI.V.lineincaseyourpatientneedsI.V.magnesiumreplacementorI.V.fluids.
•Whenpreparinganinfusionofmagnesiumsulfate,keepinmindthatI.V.magnesiumsulfatecomesinvariousconcentrations(suchas10%,12.5%,and50%).Clarifyapractitioner’sorderthatspecifiesonlythenumberofampulesorvialstogive.Aproperorderstateshowmanygramsormillilitersofaparticularconcentrationtoadminister,thevolumeofdesired
solutionfordilution,andthelengthoftimeforinfusion.(SeeInfusingmagnesiumsulfate.)
Infusingmagnesiumsulfate
Ifthepractitionerprescribesmagnesiumsulfatetoboostyourpatient’sserummagnesiumlevel,you’llneedtotakesomespecialprecautions.Readonfordetails.•
Usinganinfusionpump,administermagnesiumsulfateslowly—nofasterthan150mg/minute.Injectingabolusdosetoorapidlycantriggercardiacarrest.•
Monitoryourpatient’svitalsignsandDTRsduringmagnesiumsulfatetherapy.Every15minutes,checkforsignsandsymptomsofmagnesiumexcess,suchashypotensionandrespiratorydistress.•
Checkthepatient’sserummagnesiumlevelaftereachbolusdoseoratleastevery6hoursifhehasacontinuousI.V.drip.•
Stayespeciallyalertforanabove-normalserummagnesiumlevelifyourpatient’srenalfunctionisimpaired.•
Placethepatientoncontinuouscardiacmonitoring.Observehimclosely,especiallyifhe’salsoreceivingdigoxin.•
Monitorurineoutputbefore,during,andaftermagnesiumsulfateinfusion.Notifythedoctorifoutputmeasureslessthan100mlover4hours.•
Keepcalciumgluconateonhandtocounteractadversereactions.Haveresuscitationequipmentnearby,andbepreparedtouseitifthepatientgoesintocardiacorrespiratoryarrest.
•WhenadministeringI.M.magnesium,injectthedoseintothedeepglutealmuscle.I.M.injectionsofmagnesiumcanbepainful.Ifgivingmorethanoneinjection,alternateinjection
sites.•Administermagnesiumsupplementsasneededandordered.(SeePreventingmederrors.)
CAUTION!
PreventingmederrorsWhendocumentingmagnesiumsulfateadministration,alwayswriteoutmagnesiumsulfatetopreventseriousmedicationerrors.Theabbreviationformagnesiumsulfate,MgSO4,iseasilyconfusedwiththatformorphinesulfate,MSO4.
•Duringmagnesiumreplacement,checkthecardiacmonitorfrequentlyandassessthepatientcloselyforsignsofmagnesiumexcess,suchashypotensionandrespiratorydistress.Keepcalciumgluconateatthebedsideincasesuchsignsoccur.
•Maintainanaccuraterecordofyourpatient’sfluidintakeandoutput.Reportanydecreaseinurineoutput.(SeeDocumentinghypomagnesemia.)
Chartsmart
DocumentinghypomagnesemiaIfyourpatienthashypomagnesemia,makesureyoudocumentthefollowinginformation:•
vitalsigns•
heartrhythm•
neurologic,neuromuscular,andcardiacassessmentfindings•
magnesiumsulfateorotherdrugsadministeredandthepatient’sresponse•
fluidintakeandoutput•
seizuresandsafetymeasuresused•
yourinterventionsandpatient’sresponse•
pertinentlaboratoryvalues,includingserumelectrolyte,albuminand,ifappropriate,digoxinlevels•
practitionernotification•
patientteaching.
Hypermagnesemia
Havingtoomuchmagnesiumcanbejustasbadashavingtoolittle.Hypermagnesemiaoccurswhenthebody’sserummagnesiumlevelrisesabove2.5mEq/L.However,hypermagnesemiaisuncommon;typically,thekidneyscanrapidlyreducetheamountofexcessmagnesiuminthebody,especiallyiftheexcessisfromfoodsources.
HowithappensHypermagnesemiaresultsfromtheconditionsoppositethosethatbringonamagnesiumshortage.Itsmaincausesareimpairedmagnesiumexcretion(forexample,fromrenaldysfunction)andexcessivemagnesiumintake.
KeepingitinRenaldysfunctionisthemostcommoncauseofhypermagnesemia.Justassomerenalconditionsboostmagnesiumexcretiontocausehypomagnesemia,otherscanmakethebodyretaintoomuchmagnesium,causinghypermagnesemia.Causesofpoorrenalexcretionofmagnesiuminclude:•advancingage,whichtendstoreducerenalfunction•renalfailure•Addison’sdisease•adrenocorticalinsufficiency•untreatedDKA.
ToomuchintakeMagnesiumbuildupiscommoninpatientswithrenalfailurewhousemagnesium-containingantacidsorlaxatives.(SeeDrugsandsupplementsassociatedwithhypermagnesemia.)
DrugsandsupplementsassociatedwithhypermagnesemiaMonitoryourpatient’sserummagnesiumlevelcloselyifhe’sreceivingortakinganyofthesemedications:•
antacids(Di-Gel,Gaviscon,Maalox)•
laxatives(MilkofMagnesia,Haley’sM-O,magnesiumcitrate)•
magnesiumsupplements(magnesiumoxide,magnesiumsulfate)•
rectalenemas•
potassium-sparingdiuretics.
Othercausesofexcessivemagnesiumintakeincludethefollowing:•hemodialysiswithamagnesium-richdialysate•TPNsolutionsthatcontaintoomuchmagnesium
•continuousinfusionofmagnesiumsulfatetotreatsuchconditionsasseizures,pregnancy-inducedhypertension,andpretermlabor.(Thefetusofawomanreceivingmagnesiumsulfatemaydevelopahigherserummagnesiumlevel,too.)
WhattolookforJustasanabnormallylowserummagnesiumleveloverstimulatestheneuromuscularsystem,anabnormallyhighonedepressesit.Specifically,hypermagnesemiablocksneuromusculartransmission,soexpectneuromuscularsignsandsymptomsoppositethoseofhypomagnesemia,suchas:•decreasedmuscleandnerveactivity•hypotension,bradycardia,andrespiratoryparalysis•hypoactiveDTRs•facialparesthesia(usuallywithmoderatelyelevatedserumlevels)•generalizedweakness(forinstance,apatientwhohasaweakhandgraspordifficulty
repositioninghimselfinbed);inseverecases,weaknessprogressestoflaccidparalysis•occasionalnauseaandvomiting.(SeeSignsandsymptomsofhypermagnesemia.)
CAUTION!
SignsandsymptomsofhypermagnesemiaUsethischarttocomparetotalserummagnesiumlevelswiththetypicalsignsandsymptomsthatmayappear.
Totalserummagnesiumlevel Signsandsymptoms3mEq/L •
Feelingsofwarmth•
Flushedappearance•
Mildhypotension•
Nauseaandvomiting4mEq/L •
Facialparesthesia•
DiminishedDTRs•
Muscleweakness5mEq/L •
Drowsiness•
ECGchanges•
Bradycardia•
Worseninghypotension7mEq/L •
LossofDTRs8mEq/L •
Respiratorycompromise12mEq/L •
Heartblock•
Flaccidparalysis•
Coma15mEq/L •
Respiratoryarrest20mEq/L •
Cardiacarrest
You’refeelingverysleepy...BecauseexcessmagnesiumdepressestheCNS,thepatientmayappeardrowsyandlethargic.HisLOCmayevendiminishtothepointofcoma.Hypermagnesemiacanposeadangertotherespiratorysystem—andtolifeitself—ifitweakens
therespiratorymuscles.Typically,slow,shallow,depressedrespirationsareindicatorsofsuchmuscleweakness.Eventually,thepatientmaysufferrespiratoryarrestandrequiremechanicalventilation.Ahighserummagnesiumlevelalsomaytriggerseriousheartproblems—amongthemaweak
pulse,bradycardia,heartblock,andcardiacarrest.Arrhythmiasmayleadtodiminishedcardiacoutput.Ahighserummagnesiumlevelalsocausesvasodilation,whichlowersthebloodpressureand
maymakeyourpatientfeelflushedandwarmallover.
WhattestsshowTohelpconfirmthediagnosisofhypermagnesemia,lookforaserummagnesiumlevelabove2.5mEq/LandthesetelltaleECGchanges:prolongedPRintervals,widenedQRScomplexes,andtallTwaves.
Howit’streatedAfterhypermagnesemiaisconfirmed,thepractitionerworkstocorrectboththemagnesiumimbalanceanditsunderlyingcause.
Fluidup,magnesiumdown
Ifthepatienthasnormalrenalfunction,expectthepractitionertoorderoralorI.V.fluids.Increasedfluidintakeraisesthepatient’surineoutput,riddinghisbodyofexcessmagnesium.Ifthepatientdoesn’trespondtoincreasedfluidintake,thepractitionermayorderaloopdiuretictopromotemagnesiumexcretion.
Worst-casescenariosInanemergency,expecttogivecalciumgluconate,amagnesiumantagonist.(You’llprobablygive10to20mlofa10%solution.)Somepatientswithtoxiclevelsofmagnesiuminthebloodalsoneedmechanicalventilationtorelieverespiratorydepression.Patientswhohavesevererenaldysfunctionmayneedhemodialysiswithmagnesium-free
dialysatetolowertheserummagnesiumlevel.(SeeIftreatmentdoesn’twork.)
It’snotworking
Iftreatmentdoesn’tworkWhatshouldyoudoifyourpatient’slaboratorytestresultscontinuetoshowthathisserummagnesiumlevelisabovenormal,despitetreatment?Yourfirststepistonotifythepractitioner.Expecttopreparethepatientforperitonealdialysisor
hemodialysisusingmagnesium-freedialysate.Thepatientneedstogetridoftheexcessmagnesiumfast—especiallyifhisrenalfunctionisfailing.
HowyouinterveneWheneverpossible,takestepstopreventhypermagnesemiabyidentifyinghigh-riskpatients.Thoseatriskinclude:•elderlypeople•patientswithrenalinsufficiencyorfailure•pregnantwomeninpretermlabororwithgestationalhypertension•neonateswhosemothersreceivedmagnesiumsulfateduringlabor•patientsreceivingmagnesiumsulfatetocontrolseizures•thosewithahighintakeofmagnesiumormagnesium-containingproducts,suchasantacidsor
laxatives•thosewithadrenalinsufficiency
•thosewithsevereDKA•dehydratedpatients•thosewithhypothyroidism.Ifyourpatientalreadyhashypermagnesemia,youmayneedtotakethefollowingactions:
Memoryjogger
Torememberthesignsandsymptomsofhypermagnesemia,thinkRENALbecausepoorrenalexcretionisamajorcauseofthiselectrolyteimbalance.Here’saletter-by-letterrundown:
Reflexesdecreased(plusweaknessandparalysis)
ECGchanges(bradycardia)andhypotension
Nauseaandvomiting
Appearanceflushed
Lethargy(plusdrowsinessandcoma).
•Monitoryourpatient’svitalsignsfrequently.Stayespeciallyalertforhypotension,bradycardia,andrespiratorydepression—indicatorsofhypermagnesemia.Notifythepractitionerimmediatelyifthepatient’srespiratorystatusdeteriorates.(SeeTeachingabouthypermagnesemia.)
Teachingpoints
Teachingpoints
TeachingabouthypermagnesemiaWhenteachingapatientwithhypermagnesemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
explanationofhypermagnesemia•
riskfactors•
hydrationrequirements•
dietarymodifications,ifneeded•
prescribedmedications•
warningsignsandsymptoms•
needtoavoidmedicationsthatcontainmagnesium•
dialysis,ifneeded.
•Checkforflushedskinanddiaphoresis.•Assessthepatient’sneuromuscularsystem,includingDTRsandmusclestrength.(SeeTestingthepatellarreflex.)
TestingthepatellarreflexOnewaytogaugeyourpatient’smagnesiumstatusistotestthepatellarreflex,oneoftheDTRsthattheserummagnesiumlevelaffects.Totestthereflex,strikethepatellartendonjustbelowthepatellawiththepatientsittingorlyinginasupineposition,asshownbelow.Lookforlegextensionorcontractionofthequadricepsmuscleinthefrontofthethigh.Ifthepatellarreflexisabsent,notifythedoctorimmediately.Thisfindingmaymeanyour
patient’sserummagnesiumlevelis7mEq/Lorhigher.
Sitting SupinepositionHavethepatientsitonthesideofthebedwiththelegsdanglingfreely(asshownhere).Thentestthereflex.
Flexthepatient’skneeata45-degreeangle,andplaceyournondominanthandbehinditforsupport(asshownhere).Thentestthereflex.
•Monitorlaboratorytestsandreportabnormalresults.Monitorserumelectrolytelevelsandotherlaboratorytestresultsthatreflectrenalfunction,suchasbloodureanitrogenandcreatininelevels.Monitorthepatientforhypocalcemia,whichmayaccompanyhypermagnesemia,becausealowserumcalciumlevelsuppressesPTHsecretion.
•Monitorurineoutput.Thekidneysexcretemostofthebody’smagnesium.•Evaluatethepatientforchangesinmentalstatus.Ifthepatient’sLOCdecreases,institutesafety
measures.Reorientthepatientifhe’sconfused.•Preparethepatientforcontinuouscardiacmonitoring.AssessECGtracingsforpertinent
changes.•Bepreparedtoadministerresuscitationdrugs,maintainapatentairway,andprovidecalcium
gluconate,asordered,incaseofahypermagnesemiaemergency.•Ifthepatient’smagnesiumlevelbecomesdangerouslyhigh,preparehimfordialysisas
ordered.•Bepreparedtoprovidemechanicalventilationasorderedforthepatientwithcompromised
respiratoryfunction.•Bepreparedtoapplyatranscutaneousexternalpacemakerortoassistwiththeinsertionofa
transvenouspacemakerforpatientswithbradyarrhythmias.
•EstablishI.V.accessandmaintainapatentI.V.line.•Provideadequatefluids,bothI.V.andoralifprescribed,tohelpyourpatient’skidneysexcrete
excessmagnesium.Whengivinglargevolumesoffluids,remembertokeepaccurateintakeandoutputrecordsandtowatchcloselyforsignsoffluidoverloadandkidneyfailure.Bothconditionscanarisequickly.(SeeDocumentinghypermagnesemia.)
Chartsmart
DocumentinghypermagnesemiaIfyourpatienthashypermagnesemia,makesureyoudocumentthefollowinginformation:•
LOC•
vitalsigns•
ECGchanges•
signsandsymptomsofhemodynamicinstability•
DTRassessment•
I.V.fluidtherapy•
drugsadministered•
safetymeasures•
yourinterventionsandthepatient’sresponses•
pertinentlaboratoryvalues,includingserumelectrolyteandalbuminlevels•
intakeandoutput•
practitionernotification•
patientteaching.
•Avoidgivingyourpatientmedicationsthatcontainmagnesium.Tomakesurenootherstaffmembersgivethem,flagthepatient’schartandmedicationadministrationrecordwithanotethatsays,“Nomagnesiumproducts.”
•Restrictthepatient’sdietarymagnesiumintakeasneeded.
That’sawrap!
Magnesiumimbalancesreview
Magnesiumbasics•
Secondmostabundantcationinintracellularfluid•
Performsmanyfunctions–
Promotesenzymereactionswithinthecellsduringcarbohydratemetabolism–
HelpsthebodyproduceanduseATPforenergy–
TakespartinDNAandproteinsynthesis–
Influencesvasodilationandcardiacmusclecontractility–
Aidsinneurotransmission–
Playsanessentialroleintheproductionofparathyroidhormone–
Helpssodiumandpotassiumcrosscellmembranes•
Normalserumlevels:1.5to2.5mEq/L;rangesdifferforneonatesandchildren
Magnesiumbalance•
Morethanhalfofmagnesiumionsarefree,circulatingions;othersbindtoalbuminandothersubstances.•
Magnesiumlevelsrelatetoalbuminlevels;lowmagnesiumequalslowalbumin;highmagnesiumequalshighalbumin.•
GIandurinarysystemsregulatemagnesiumlevelstomaintainbalance.
Hypomagnesemia•
Occurswhenserummagnesiumlevelsarelessthan1.5mEq/L•
Resultsfrompoordietaryintakeofmagnesium,poorGIabsorption,andincreasedlossfromGItractorurinarytract•
Occursinpatientswhoarepregnant;thosewithchronicdiarrhea,hemodialysis,hypercalcemia,hypothermia,sepsis,burns,andwounddebridement;andpatientstakingcertainmedications
Signsandsymptoms•
AlteredLOC•
Ataxia•
Confusion•
Depression•
Hallucinationsand/ordelusions•
Seizures•
Vertigo•
Skeletalmuscleweakness•
HyperactiveDTRs•
Tetany•
Chvostek’sandTrousseau’ssigns•
Arrhythmias•
Rapidheartrate•
Vomiting•
Insomnia(Crawford&Harris,2011)
Treatment•
Changeindiet•
OralorI.V.magnesiumreplacement
Hypermagnesemia•
Occurswhenserummagnesiumlevelsaregreaterthan2.5mEq/L•
Isusuallyuncommonexceptinpatientswithrenalfailure(especiallypatientstakingantacidsorlaxativesortheelderlywithdecreasedrenalfunction)•
CausedbyAddison’sdisease,adrenocorticalinsufficiency,anduntreatedDKA•
Mayresultfromincreasedintakeofmagnesium,usuallyfromhemodialysisusingmagnesium-richdialysate,TPNwithexcessmagnesium,orcontinuousmagnesiumsulfateinfusiontotreatcertainconditions
Signsandsymptoms•
Decreasedmuscleandnerveactivity•
HypoactiveDTRs•
Generalizedweakness,drowsiness,andlethargy•
Facialparesthesias•
Nauseaandvomiting•
Slow,shallow,depressedrespirationsorrespiratoryparalysis•
Respiratoryarrest•
ECGchanges•
Vasodilationandhypotension•
Arrhythmiasandbradycardia
Treatment•
OralorI.V.fluids
•Avoidanceofmagnesiumproducts•
Calciumgluconate,inemergentsituations•
Hemodialysiswithmagnesium-freedialysate(fordialysispatients)•
Mechanicalventilation(forseverecasesinwhichrespirationdepressionispresent)
Quickquiz
1.Magnesiumisanimportantelectrolytebecauseit:A.helpscontrolurinevolume.B.promotestheproductionofgrowthhormone.C.promotesbonegrowthandstrength.D.assistsinneuromusculartransmission.
Answer:D.Magnesiumactsatthemyoneuraljunctionandisvitaltonerveandmuscleactivity.
2.YourpatientwithCrohn’sdiseasedevelopstremorswhilereceivingTPN.Suspectingshemighthavehypomagnesemia,youassessherneuromuscularsystem.Youshouldexpecttosee:
A.Homans’sign.B.elevatedserumpotassium.C.hyperactiveDTRs.D.slowedheartrate.
Answer:C.Inapatientwithhypomagnesemia,expecttoseehyperactiveDTRsbecausehypomagnesemiaincreasesneuromuscularexcitability.
3.Whenteachingyourpatientwithhypomagnesemiaaboutaproperdiet,youshouldrecommendthatheconsumeplentyof:
A.seafood.B.fruits.C.cornproducts.D.dairyproducts.
Answer:A.Magnesiumisfoundinseafoodaswellasinchocolate;drybeansandpeas;meats;nuts;wholegrains;andgreen,leafyvegetables.
4.ThedoctorprescribesI.V.magnesiumsulfateforyourpatientwithhypomagnesemia.Beforegivingthemagnesiumpreparation,youreviewthepractitioner’sordertomakesureitspecifiesthe:
A.numberofgramsormilliliterstogive.B.numberofampulestogive.C.numberofvialstogive.D.numberofusespervial.
Answer:A.Magnesiumsulfatecomesinseveraldifferentconcentrations.Thepractitioner’sordershouldspecifythenumberofgramsormillilitersofaparticularconcentration,pluseithertheamountofsolutiontousefordilutionorthedurationoftheinfusion.
5.Yourpatientisdiagnosedwithhypermagnesemia.Totreatthisimbalance,thepractitionerislikelytoorder:
A.magnesiumcitrate.B.magnesiumsulfatedilutedinfluids.C.potassium-sparingdiuretics.D.oralandI.V.fluids.
Answer:D.BothoralandI.V.fluidsmaybeusedtotreathypermagnesemia.Bycausingdiuresis,thefluidspromoteexcretionofexcessmagnesiumbythekidneys.
6.Yourhemodialysispatientneedsalaxative.Whenyouseethatthepractitionerhasorderedmagnesiumcitrate,youdecidetoquestiontheorderbecause:
A.thismagnesiumsaltwouldbetoostrongforthepatient.B.magnesiumadministrationcouldworsenthepatient’scondition.C.magnesiumcitratemustbegivenorally.D.magnesiumcitratecancausenauseaandvomiting.
Answer:B.Magnesiumcitrateisapoorlaxativechoiceforapatientwitharenalimpairmentwhosekidneyscan’texcretemagnesiumproperly.Thepatientcoulddevelophypermagnesemia.
ScoringIfyouansweredallsixquestionscorrectly,youshouldbetwitchingwithpride.You’reamagnesiummagician!Ifyouansweredfourorfivecorrectly,excellent!You’rereadytobecomeamagnesiummagician’sassistant!Ifyouansweredfewerthanfourcorrectly,trynottoworry.You’renowenrolledasafirst-yearlearnerintheMagicalMagnesiumCollegeofFineElectrolytes.
References
Crawford,A.,&Harris,H.(2011).Balancingact:Hypomagnesemia&hypermagnesemia.Nursing,41(10),52–55.doi:10.1097/01.NURSE.0000403378.71042.f0.
Davidson,K.,&Kaplan,B.J.(2011).Vitaminandmineralintakesinadultswithmooddisorders:Comparisonstonutritionstandardsandassociationswithsociodemographicandclinicalvariables.JournaloftheAmericanCollegeofNutrition,30(6),547–558.
DelGobo,L.,Imamura,F.,Wu,J.,deOliveiraOtto,M.,Chiuve,S.,&Mozaffarian,D.(2013).Circulatinganddietarymagnesiumandriskofcardiovasculardisease:Asystematicreviewandmeta-analysisofprospectivestudies.AmericanJournalofClinicalNutrition,98(1),160–173.doi:10.3945/ajcn.112.053132
Ellam,S.,&Williamson,G.(2013).Cocoaandhumanhealth.AnnualReviewofNutrition,33,105–128.doi:10.1146/annurev-nutr-071811-150642
Garrison,S.,Allan,G.M.,Sekhon,R.K.,Musini,V.M.,&Khan,K.M.(2012).Magnesiumforskeletalmusclecramps.CochraneDatabaseofSystemicReviews,9,CD009402.doi:10.1002/14651858.CD009402.pub2
Harris,R.,Chavarro,J.E.,Malspeis,S.,Willett,W.C.,&Missmer,S.A.(2013).Dairy-food,calcium,magnesium,andvitaminDintakeandendometriosis:Aprospectivecohortstudy.AmericanJournalofEpidemiology,177(5),420–430.doi:10.1093/aje/kws247
Islam,M.R.,Ahmed,M.U.,Mitu,S.A.,Islam,M.S.,Rahman,G.K.,Qusar,M.M.,&Hasnat,A.(2013).Comparativeanalysisofserumzinc,copper,manganese,iron,calcium,andmagnesiumlevelandcomplexityofinterelementrelationsingeneralizedanxietydisorderpatients.BiologicalTraceElementResearch,154(1),21–27.doi:10.1007/s12011-013-9723-7
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Kanbay,M.Yilmaz,M.I.,Apetrii,M.,Saglam,M.,Yaman,H.,Unal,H.U.,...Covic,A.(2012).Relationshipbetweenserummagnesiumlevelsandcardiovasculareventsinchronickidneydiseasepatients.AmericanJournalofNephrology,36(3),228–237.
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Chapter8
Whencalciumtipsthebalance
JustthefactsInthischapter,you’lllearn:
♦waysthatcalciumworksinthebody
♦therelationshipbetweencalciumandalbumin
♦parathyroidhormone’sroleincalciumregulation
♦waystoassessapatientforsignsofcalciumimbalance
♦propercareforapatientwithhypocalcemiaorhypercalcemia.
AlookatcalciumCalciumisapositivelychargedion,orcation,foundinbothextracellularfluidandintracellularfluid.About99%ofthebody’scalciumisfoundinthebonesandtheteeth.Only1%isfoundinserumandinsofttissue.However,that1%iswhatmatterswhenmeasuringcalciumlevelsintheblood.
Whyit’simportantCalciumisinvolvedinnumerousbodyfunctions.Togetherwithphosphorus,calciumisresponsiblefortheformationandstructureofbonesandteeth.Ithelpsmaintaincellstructureandfunctionandplaysaroleincellmembranepermeabilityandimpulsetransmission.Calciumaffectsthecontractionofcardiacmuscle,smoothmuscle,andskeletalmuscle.Italso
playsaroleinthebloodclottingprocessandinthereleaseofcertainhormones.
MeasuringupCalciumcanbemeasuredintwoways.Themostcommonlyorderedlaboratorytestisatotalserumcalciumlevel,whichmeasuresthetotalamountofcalciuminblood.Thenormalrangefortotalserumcalciumis8.9to10.1mg/dl.(SeeCalciumlevelsbyage,page148.)
Agesandstages
CalciumlevelsbyageChildrenhavehigherserumcalciumlevelsthanadultsdo.Infact,serumlevelscanriseashighas11mg/dlduringperiodsofincreasedbonegrowth.Thenormalrangeforionizedcalciumlevelsisnarrowerforelderlypeople.Forelderlymen,the
rangeis2.3to3.7mg/dl;forelderlywomen,therangeis2.8to4.1mg/dl.Thesevaluesmayvaryslightlyfromlaboratorytolaboratory.
Thesecondtestmeasuresthevariousformsofcalciuminextracellularfluid.About41%ofallextracellularcalciumisboundtoprotein;9%isboundtocitrateorotherorganicions.Theotherhalfisionized(orfree)calcium,theonlybiologicallyactiveformofcalcium.Ionizedcalciumcarriesoutmostoftheion’sphysiologicfunctions.Inadults,thenormalrangeforionizedcalciumis4.4to5.3mg/dl;inchildren,it’s4.4to6.0mg/dl.Normalvaluesmayvaryslightlyfromlaboratorytolaboratory.Becausenearlyhalfofallcalciumisboundtotheproteinalbuminorimmunoglobulins,serum
proteinabnormalitiescaninfluencetotalserumcalciumlevels.Forexample,inhypoalbuminemia,
thetotalserumcalciumleveldecreases.However,ionizedcalciumlevels—themoreimportantofthetwolevels—remainunchanged.Sowhenconsideringtotalserumcalciumlevels,youshouldalsoconsiderserumalbuminlevels.(SeeCalculatingcalciumandalbuminlevels.)
CalculatingcalciumandalbuminlevelsForevery1g/dlthatapatient’sserumalbuminleveldrops,histotalcalciumleveldecreasesby0.8mg/dl.Todeterminewhatyourpatient’scalciumlevelwouldbeifhisserumalbuminlevelwerenormal—andtohelpfindoutiftreatmentisnecessary—justdoalittlemath.
CorrectingalevelAnormalalbuminlevelis4g/dl.Theformulaforcorrectingcalciumlevelis:
Totalserumcalciumlevel+0.8(4−albuminlevel)=correctedcalciumlevel
SampleproblemForexample,ifapatient’sserumcalciumlevelis8.2mg/dlandhisalbuminlevelis3g/dl,whatwouldhiscorrectedcalciumbe?
8.2+0.8(4−3)=9mg/dl
Thecorrectedcalciumleveliswithinthenormalrange,andtherefore,thepatientprobablywouldn’trequiretreatment.
HowthebodyregulatescalciumBothintakeofdietarycalciumandexistingstoresofcalciumaffectcalciumlevelsinthebody.Foradults,therangefortherecommendeddailyrequirementofcalciumis800to1,200mg/day.Requirementsvaryforchildren,pregnantpatients,andpatientswithosteoporosis.Dairyproductsarethemostcommoncalcium-richfoods,butcalciumcanalsobefoundinlarge
quantitiesingreen,leafyvegetables.(SeeDietarysourcesofcalcium.)Calciumisabsorbedbythesmallintestineandisexcretedinurineandfeces.
DietarysourcesofcalciumHere’salistofthemostcommondietarysourcesofcalcium:•
cannedsardinesandsalmon•
dairyproducts,suchasmilk,buttermilk,cheese,andyogurt•
green,leafyvegetables•
legumes•
molasses•
nuts•
wholegrains.
PTHisonthesceneSeveralfactorsinfluencecalciumlevelsinthebody.Thefirstisparathyroidhormone(PTH).Whenserumcalciumlevelsarelow,theparathyroidglandsreleasePTH,whichdrawscalciumfromthebonesandpromotesthetransferofcalcium(alongwithphosphorus)intoplasma.Thattransferincreasesserumcalciumlevels.PTHalsopromoteskidneyreabsorptionofcalciumandstimulatestheintestinestoabsorbthe
mineral.Phosphorusisexcretedatthesametime.Inhypercalcemia,wheretoomuchcalciumexistsintheblood,thebodysuppressesthereleaseofPTH.
EntercalcitoninCalcitonin,ahormoneproducedinthethyroidglandthatactsasanantagonisttoPTH,alsohelpstoregulatecalciumlevels.Whencalciumlevelsaretoohigh,thethyroidglandreleasescalcitonin.Highlevelsofthishormoneinhibitboneresorption,whichcausesadecreaseintheamountofcalciumavailablefrombone.Thiscausesadecreaseinserumcalciumlevel.Calcitoninalsodecreasesabsorptionofcalciumandenhancesitsexcretionbythekidneys.
VitaminDdeliversAnotherfactorthatinfluencescalciumlevelsisvitaminD.VitaminDisingestedwithfoods,particularlydairyproducts.Also,whentheskinisexposedtoultravioletlight,itsynthesizesvitaminD.TheactiveformofvitaminDpromotescalciumabsorptionthroughtheintestines,calcium
resorptionfrombone,andkidneyreabsorptionofcalcium,allofwhichraisetheserumcalciumlevel.(SeeCalciuminbalance,page150.)
CalciuminbalanceExtracellularcalciumlevelsarenormallykeptconstantbyseveralinterrelatedprocessesthatmovecalciumionsintoandoutofextracellularfluid.Calciumenterstheextracellularspacethroughresorptionofcalciumionsfrombone,throughtheabsorptionofdietarycalciuminthegastrointestinal(GI)tract,andthroughreabsorptionofcalciumfromthekidneys.Calciumleavesextracellularfluidasit’sexcretedinfecesandurineanddepositedinbonetissues.Thisillustrationshowshowcalciummovesthroughoutthebody.
PhosphorusfollowsPhosphorusalsoaffectsserumcalciumlevels.Phosphorusinhibitscalciumabsorptionintheintestines,theoppositeeffectofvitaminD.Whencalciumlevelsarelowandthekidneysretaincalcium,phosphorusisexcreted.Aninverserelationshipbetweencalciumandphosphorusexistsinthebody.Whencalcium
levelsrise,phosphoruslevelsdrop.Theoppositeisalsotrue:Whencalciumlevelsdrop,phosphoruslevelsrise.
Memoryjogger
TorecalltherolesofcalcitoninandPTH,think“Parathyroidpulls,calcitoninkeeps.”PTHpullscalciumoutofthebone.Calcitoninkeepsitthere.
SerumpH’spartSerumpHalsohasaninverserelationshipwithionizedcalcium.IftheserumpHlevelrises(bloodbecomesalkaline),morecalciumbindswithproteinandtheionizedcalciumleveldrops.Thus,apatientwithalkalosistypicallyhashypocalcemiaaswell.Theoppositeistrueforacidosis.WhenthepHleveldrops,lesscalciumbindstoproteinand
theionizedcalciumlevelrises.Whenallthebody’sregulatoryeffortsfailtocontrolthelevelofcalcium,oneoftwoconditionsmayresult:hypocalcemiaorhypercalcemia.
Hypocalcemia
Hypocalcemiaoccurswhencalciumlevelsfallbelowthenormalrange—thatis,whentotalserumcalciumlevelsfallbelow8.9mg/dlorionizedcalciumlevelsfallbelow4.4mg/dl.
HowithappensHypocalcemiaoccurswhenapersondoesn’ttakeinenoughcalcium,whenthebodydoesn’tabsorbthemineralproperly,orwhenexcessiveamountsofcalciumarelostfromthebody.Adecreasedlevelofionizedcalciumcanalsocausehypocalcemia.(SeeHypocalcemiainelderlypatients.)
Agesandstages
HypocalcemiainelderlypatientsSeveralfactorscontributetohypocalcemiainelderlypatients.Suchfactorsinclude:•
inadequatedietaryintakeofcalcium•
poorcalciumabsorption(especiallyinpostmenopausalwomenlackingestrogen)•
reducedactivityorinactivity(inactivitycausesalossofcalciumfromthebonesandosteoporosis,inwhichserumlevelsmaybenormalbutbonestoresofthemineralaredepleted)•
medications.(SeeDrugsassociatedwithhypocalcemia,page152.)
DrugsassociatedwithhypocalcemiaDrugsthatcancausehypocalcemiainclude:•
antibioticssuchasrifampin•
aluminum-containingantacids•
aminoglycosides•
anticonvulsants,especiallyphenytoinandphenobarbital•
beta-adrenergicblockers•
caffeine•
calcitonin•
corticosteroids•
drugsthatlowerserummagnesiumlevels(suchascisplatinandgentamicin)•
edetatedisodium(disodiumEDTA)•
heparin•
loopdiuretics•
mithramycin•
phosphates(oral,I.V.,rectal).
IntakeissuesInadequateintakeofcalciumcanputapatientatriskforhypocalcemia.Alcoholics—whotypicallyhavepoornutritionalintake,poorcalciumabsorption,andlowmagnesiumlevels(magnesiumaffectsPTHsecretion)—areespeciallyprone.Abreast-fedinfantcanhavelowcalciumandvitaminDlevelsifhismother’sintakeofthose
nutrientsisinadequate.Also,anyonewhodoesn’treceivesufficientexposuretosunlightmaysufferfromvitaminDdeficiencyand,subsequently,lowercalciumlevels.
MalabsorptionmaladiesHypocalcemiacanresultwhencalciumisn’tabsorbedproperlyfromtheGItract,aconditioncommonlycausedbymalabsorption.Malabsorptioncanresultfromincreasedintestinalmotilityfromseverediarrhea,laxativeabuse,orchronicmalabsorptionsyndrome.AbsorptionisalsoaffectedbyalackofvitaminDinthediet.Anticonvulsants,suchas
phenobarbitalandphenytoin(Dilantin),caninterferewithvitaminDmetabolismandcalciumabsorption.Ahighphosphoruslevelintheintestinescanalsointerferewithabsorption,ascanareduction
ingastricacidity,whichdecreasesthesolubilityofcalciumsalts.
ToomuchinthelosscolumnPancreaticinsufficiencycancausemalabsorptionofcalciumandasubsequentlossofcalciuminthefeces.Acutepancreatitiscancausehypocalcemiaaswell,althoughthemechanismisn’twellunderstood.PTHorpossiblythecombiningoffreefattyacidsandcalciuminpancreatictissuemaybeinvolved.HypocalcemiacanalsooccurwhenPTHsecretionisreducedoreliminated.Thyroidsurgery,
surgicalremovaloftheparathyroidgland,removalofaparathyroidtumor,orinjuryordiseaseoftheparathyroidgland(suchashypoparathyroidism)canallreduceorpreventPTHsecretion.Hypocalcemiacanalsoresultfrommedicationssuchascalcitoninandmithramycinbecause
thesedrugsdecreasecalciumresorptionfrombone.Thekidneysmayalsoexcretetoomuchexcesscalciumandcausehypocalcemia.Diuretics,
especiallyloopdiureticssuchasfurosemide(Lasix)andethacrynicacid(Edecrin),increaserenalexcretionofcalciumaswellaswaterandotherelectrolytes.Renalfailuremayalsoharmthekidneys’abilitytoactivatevitaminD,whichaffectscalciumabsorption.Edetatedisodium(disodiumEDTA),whichisusedtotreatleadpoisoning,cancombinewith
calciumandcarryitoutofthebodywhenexcreted.
AclusterofcausesAlowmagnesiumlevel(hypomagnesemia)canaffectthefunctionoftheparathyroidglandandcauseadecreaseincalciumreabsorptionintheGItractandkidneys.Drugsthatlowerserummagnesiumlevels,suchascisplatinandgentamicin,maydecreasecalciumabsorptionfrombone.(SeeDrugsassociatedwithhypocalcemia.)Lowserumalbumin(hypoalbuminemia)isthemostcommoncauseofhypocalcemia.
Hypoalbuminemiamayresultfromcirrhosis,nephrosis,malnutrition,burns,chronicillness,andsepsis.Hyperphosphatemia(ahighlevelofphosphorusintheblood)cancausecalciumlevelstofall
asphosphoruslevelsrise.Excessphosphoruscombineswithcalciumtoformsalts,whicharethendepositedintissues.Whenphosphatesareadministeredorally,I.V.,orrectally,thephosphorusbindswithcalcium
andserumcalciumlevelsdrop.Infantsreceivingcow’smilkarepredisposedtohypocalcemictetanybecauseofthehighlevelsofphosphorusinthemilk.Alkalosiscancausecalciumtobindtoalbumin,therebydecreasingionizedcalciumlevels.
Citrate,addedtostoredbloodtopreventclotting,bindswithcalciumandrendersitunavailableforuse.Therefore,patientsreceivingmassivebloodtransfusionsareatriskforhypocalcemia.Thatriskcanalsoapplytopediatricpatients.Othercausesofhypocalcemiaincludeincreasedcaffeineintake,severeburns,andinfections.
Burnedordiseasedtissuestrapcalciumionsfromextracellularfluid,therebyreducingserumcalciumlevels.
WhattolookforSignsandsymptomsofhypocalcemiareflectcalcium’seffectsonnervetransmissionandmuscleandheartfunction.Becauseofthat,you’remostlikelytoobserveneuromuscularandcardiovascularfindings.Theneurologiceffectsofalowcalciumlevelincludeanxiety,confusion,andirritability.Thesesymptomscanprogresstoseizuresordementiainadultsandmentalretardationinchildren.
Neuromuscularsymptomsmayalsodevelop.Thepatientmayexperienceparesthesiaofthetoes,fingers,orface,especiallyaroundthemouth.Patientsmayalsoexperiencetwitching,musclecramps,ortremors.Laryngealandabdominalmusclesareparticularlypronetospasm,leadingtolaryngospasmandbronchospasm.Anincreaseinnerveexcitabilitycanleadtotheclassicmanifestationoftetany,whichmaybeevidencedbypositiveTrousseau’sorChvostek’ssigns.(SeeCheckingforTrousseau’sandChvostek’ssigns,page154.)
CheckingforTrousseau’sandChvostek’ssignsTestingforTrousseau’sandChvostek’ssignscanhelpdiagnosetetanyandhypocalcemia.Here’showtocheckfortheseimportantsigns.
Trousseau’ssign Chvostek’ssignTocheckforTrousseau’ssign,applyabloodpressurecufftothepatient’supperarmandinflateittoapressure20mmHgabovethesystolicpressure.Trousseau’ssignmayappearafter1to4minutes.Thepatientwillexperienceanadductedthumb,flexedwristandmetacarpophalangealjoints,andextendedinterphalangealjoints(withfingerstogether)—carpopedalspasm—indicatingtetany,amajorsignofhypocalcemia.Note:Trousseau’ssignusuallyindicateslatetetany.
YoucaninduceChvostek’ssignbytappingthepatient’sfacialnerveadjacenttotheear.Abriefcontractionoftheupperlip,nose,oripsilateralsideofthefaceindicatesChvostek’ssign.Note:Chvostek’ssignmaybepresentinhealthyinfantsand,therefore,maynotindicatetetany.
MoresignsFracturesmayoccurmoreeasilyinapatientwho’shypocalcemicforanextendedperiod.Apatientmayalsohavebrittlenailsanddryskinorhair.Othersignsofhypocalcemiainclude:
•diarrhea•hyperactivedeeptendonreflexes•hypotension•diminishedresponsetodigoxin,dopamine,andnorepinephrine•decreasedcardiacoutputandsubsequentarrhythmias•prolongedSTsegmentonelectrocardiogram(ECG)•lengthenedQTintervalonECG,whichputsthepatientatriskfortorsadesdepointes(aformof
ventriculartachycardia)•decreasedmyocardialcontractility,leadingtoangina,bradycardia,hypotension,andheart
failure.
WhattestsshowThesetestresultscanhelpdiagnosehypocalcemiaanddeterminetheseverityofthedeficiency:•totalserumcalciumlevellessthan8.9mg/dl•ionizedcalciumlevelbelow4.4mg/dl(ionizedcalciummeasurementisthedefinitivemethod
todiagnosehypocalcemia)•lowalbuminlevel•characteristicECGchanges.Notethatfalselydecreasedlevelsmaybeseenwithhyperbilirubinemiaoradministrationof
heparin,oxalate,orcitrateorexcessiveI.V.fluids.
Howit’streatedTreatmentforhypocalcemiafocusesoncorrectingtheimbalanceasquicklyandsafelyaspossible.Theunderlyingcauseshouldbeaddressedtopreventrecurrence.AcutehypocalcemiarequiresimmediatecorrectionbyadministeringeitherI.V.calcium
gluconateorI.V.calciumchloride.Althoughcalciumchloridecontainsthreetimesasmuchavailablecalciumascalciumgluconate,thelatterismorecommonlyused.Calciumchlorideisadvisedforpatientsincardiacarrest.Magnesiumreplacementmayalsobeneededbecausehypocalcemiadoesn’talwaysrespondtocalciumtherapyalone.(SeeAdministeringI.V.calciumsafely,page156.)
ChronichypocalcemiarequiresvitaminDsupplementstopromoteGIabsorptionofcalcium.Oralcalciumsupplementsalsohelpincreasecalciumlevels.
DietdifferencesThepatient’sdietshouldalsobeadjustedtoallowforadequateintakeofcalcium,vitaminD,andprotein.Incaseswherethepatientalsohasahighphosphoruslevel,aluminumhydroxideantacidsmaybegiventobindwithexcessphosphorus.(SeeWhentreatmentdoesn’twork.)
It’snotworking
Whentreatmentdoesn’tworkIftreatmentforhypocalcemiadoesn’tseemtobeworking,considertheseinterventions:•
Checkthemagnesiumlevel.AlowmagnesiumlevelmustbecorrectedbeforeI.V.calciumcanincreaseserumcalciumlevels.•
Checkthephosphatelevel.Ifthephosphatelevelistoohigh,calciumwon’tbeabsorbed.Reducethephosphatelevelfirst.•
MixI.V.calciumindextrosesolutionsonlybecausenormalsalinemaycausecalciumtobeexcreted.Wheneverpossible,usepremixedsolutions.
HowyouinterveneIfyourpatientisatincreasedriskforhypocalcemia,assesscarefully,especiallyifthepatienthashadparathyroidorthyroidsurgeryorhasreceivedmassivebloodtransfusions.Ifyourpatientisabreast-feedingmother,assessherforadequatevitaminDintakeandexposuretosunlight.Whenassessingapatientyoususpecthashypocalcemia,obtainacompletemedicalhistory.
Noteifthepatienthaseverhadnecksurgery.Hypoparathyroidismmaydevelopimmediatelyorseveralyearsafternecksurgery.Askapatientwhohaschronichypocalcemiaifhehasahistoryoffractures.Obtainalistofmedications,includingover-the-countersupplements,thepatientistaking;thelistmayhelpyoudeterminetheunderlyingcauseofhypocalcemia.Makesureyoualsoassessthepatient’sabilitytoperformactivitiesofdailyliving,whichmaybeaffectedbyhypocalcemia.Teachthepatientaboutthesignsandsymptomsofhypocalcemia.(SeeTeachingabouthypocalcemia,page157.)
Teachingpoints
Teachingpoints
TeachingabouthypocalcemiaWhenteachingapatientwithhypocalcemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
descriptionofhypocalcemia,itscauses,andtreatment•
importanceofahigh-calciumdiet•
dietarysourcesofcalcium•
avoidanceoflong-termlaxativeuse•
medications•
importanceofexercise•
warningsignsandsymptoms(suchasparesthesiaandmuscleweakness)andwhentoreportthem(promptcaremaypreventthedevelopmentofmoreseveresymptoms)•
needtoreportpainduringI.V.infusionofcalcium•
possibleuseoffemalehormonesinpatientswithosteoporosis.
WhenthebottomdropsoutIfyourpatientisrecoveringfromparathyroidorthyroidsurgery,keepcalciumgluconateonhand.Areadysupplyofthedrugensuresaquickresponsetosignsofasuddendropincalciumlevels.Ifthepatientdevelopshypocalcemia,here’swhatyoucando:
•Monitorvitalsignsandassessthepatientfrequently.Monitorrespiratorystatus,includingrate,depth,andrhythm.Watchforstridor,dyspnea,andcrowing.
•Ifthepatientshowsovertsignsofhypocalcemia,keepatracheotomytrayandahandheldresuscitationbagatthebedsideincaselaryngospasmoccurs.
•Placeyourpatientonacardiacmonitor,andevaluatehimforchangesinheartrateandrhythm.Notifythepractitionerifthepatientdevelopsarrhythmias,suchasventriculartachycardiaorheartblock.
•CheckthepatientforChvostek’sandTrousseau’ssigns.•InsertandmaintainapatentI.V.lineforcalciumtherapyasordered.•MonitorapatientreceivingI.V.calciumforarrhythmias,especiallyifhe’salsotakingdigoxin.
Calciumanddigoxinhavesimilareffectsontheheart.•AdministerI.V.calciumreplacementtherapycarefully.EnsurethepatencyoftheI.V.line
becauseinfiltrationcancausetissuenecrosisandsloughing.•Administeroralreplacementsasordered.Givecalciumsupplements1to1½hoursaftermeals.
IfGIupsetoccurs,givethesupplementwithmilk.•Monitorpertinentlaboratorytestresults,includingnotonlycalciumlevelsbutalsoalbumin
levelsandthoseofotherelectrolytes,suchasmagnesiumandphosphorus.Remembertochecktheionizedcalciumlevelafterevery4unitsofbloodtransfused.
•EncouragetheolderpatienttotakeacalciumsupplementwithvitaminDasorderedandtoexerciseasmuchashecantoleratetopreventcalciumlossfrombones.
•Takeprecautionsforseizuressuchaspaddingbedsiderails.•Reorientaconfusedpatient.Provideacalm,quietenvironment.•Teachthepatientaboutthesignsandsymptomsofhypocalcemia.•Documentallcaregiventothepatient,thepatient’sresponsetotreatment,andallobservations
andassessmentsmade.(SeeDocumentinghypocalcemia,page158.)
Chartsmart
DocumentinghypocalcemiaIfyourpatienthashypocalcemia,makesureyoudocumentthefollowinginformation:•
vitalsigns,includingcardiacrhythm•
intakeandoutput•
seizureactivity•
safetymeasures•
assessments,interventions,andthepatient’sresponse•
patencyandappearanceofI.V.sitebeforeandaftercalciuminfusion•
typeofcalciuminfusionadministered,thesiteofinfusion,andrateofinfusion•
pertinentlaboratoryresults,includingcalciumlevels•
timethatyounotifiedthepractitioner•
patientteachingandteach-back.
Hypercalcemia
Hypercalcemiaisacommonmetabolicemergencythatoccurswhenserumcalciumlevelrisesabove10.1mg/dl,ionizedserumcalciumlevelrisesabove5.3mg/dl,ortherateofcalciumentryintoextracellularfluidexceedstherateofcalciumexcretionbythekidneys.
Howithappens
Anysituationthatcausesanincreaseintotalserumorionizedcalciumlevelcanleadtohypercalcemia.Thisconditionisusuallycausedbyanincreaseintheresorptionofcalciumfrombone.Hyperparathyroidismandcancerarethetwomaincausesofhypercalcemia.
BlametheotherhyperWithprimaryhyperparathyroidism,themostcommoncauseofhypercalcemia,thebodyexcretesmorePTHthannormal,whichgreatlystrengthenstheeffectsofthehormone.Calciumresorptionfromboneandreabsorptionfromthekidneysarealsoincreased,asiscalciumabsorptionfromtheintestines.
MalignantinvasionCancer,thesecondmostcommoncauseofhypercalcemia,causesbonedestructionasmalignantcellsinvadethebonesandcausethereleaseofahormonesimilartoPTH.ThatPTH-likesubstancecausesanincreaseinserumcalciumlevels.Whenserumcalciumlevelsrise,thekidneyscanbecomeoverwhelmedandcan’texcreteall
thatexcesscalcium,whichinturnkeepscalciumlevelselevated.Patientswhohavesquamouscellcarcinomaofthelung,myeloma,Hodgkin’slymphoma,renalcellcarcinoma,orbreastcancerareespeciallypronetohypercalcemia.
StillmorecausesHypercalcemiacanalsobecausedbyanincreaseintheabsorptionofcalciumintheGItractorbyadecreaseintheexcretionofcalciumbythekidneys.Thesemechanismsmayoccuraloneorincombination.Afalsehighlevelcanresultfromprolongedblooddrawswithanexcessivelytighttourniquetorprolongeddehydration.
Hyperthyroidismcancauseanincreaseincalciumreleaseasmorecalciumisresorbedfrombone.Multiplefractures,lackofweightbearing,orprolongedimmobilizationcanalsocauseanincreaseincalciumreleasefrombone.Hypophosphatemiaandacidosis(whichincreasescalciumionization)aremetabolicconditions
thatarelinkedwithhypercalcemia.Certainmedicationsarealsoassociatedwiththecondition.Forinstance,abusingantacidsthatcontaincalcium,receivinganoverdoseofcalcium(fromcalciummedicationsgivenduringcardiopulmonaryresuscitation,forexample),oringestingexcessiveamountsofvitaminDorcalciumsupplementscanpromptanincreaseinserumcalciumlevels.(SeeDrugsassociatedwithhypercalcemia.)
DrugsassociatedwithhypercalcemiaMedicationsthatcancausehypercalcemiainclude:•
antacidsthatcontaincalcium•
calciumpreparations(oralorI.V.)•
lithium•
thiazidediuretics•
thyroxine•
vitaminA•
vitaminD.
VitaminAoverdosecanleadtoincreasedboneresorptionofcalcium,whichcanalsoresultinhypercalcemia.Useoflithiumorthiazidediureticscandecreasecalciumexcretionbythekidneys.Milk-alkalisyndrome,aconditioninwhichcalciumandalkaliarecombined,alsoraisescalciumlevels.
WhattolookforSignsandsymptomsofhypercalcemiaareintensifiediftheconditiondevelopsacutely.They’re
alsomoresevereifcalciumlevelsaregreaterthan14mg/dl.Elderlypatientsaremorelikelytohavesymptomsfromonlymoderateelevationsincalciumlevels.Manysignsandsymptomsstemfromtheeffectsofexcesscalciuminthecells,whichcausesa
decreaseincellmembraneexcitability,especiallyinthetissuesofskeletalmuscle,heartmuscle,andthenervoussystem.Apatientwithhypercalcemiamaycomplainoffatigueorexhibitconfusion,memoryloss,
alteredmentalstatus,depression,orpersonalitychanges.Lethargycanprogresstocomainseverecases.
TuningintomuscletoneAscalciumlevelsrise,muscleweakness,hyporeflexia,ataxia,anddecreasedmuscletoneoccur.Hypercalcemiamayleadtohypertension.Becauseheartmuscleandthecardiacconductionsystemareaffectedbyhypercalcemia,
arrhythmias(suchasbradycardia)canleadtocardiacarrest.ECGsmayrevealashortenedQTintervalandashortenedSTsegment.Alsolookfordigoxintoxicityifthepatientisreceivingdigoxin.
IntestinalissuesHypercalcemiacanalsoleadtoGIeffects,whicharecommonlythefirstindicationsthepatientnotices.Thepatientmayexperiencethirst,anorexia,nausea,andvomiting.Bowelsoundswilldecrease.Constipationcanoccurbecauseofcalcium’seffectonsmoothmuscleandthesubsequentdecreaseinGImotility.Abdominalorflankpainandparalyticileusmayresult.Asthekidneysworkovertimetoremoveexcesscalcium,renalproblemsmaydevelop.The
patientmayexperiencepolyuriaandsubsequentdehydration.Hypercalcemiacanalsocausekidneystonesandothercalcifications.Renalfailuremaybetheendresult.Also,thepatientmaydeveloppathologicfracturesandbonepain.(SeeDangersignsofhypercalcemia.)
CAUTION!
DangersignsofhypercalcemiaIfyoususpecthypercalcemiainapatient,thesesignsmayindicatethattheconditionhasbecomelife-threatening:•
arrhythmiassuchasbradycardia•
cardiacarrest•
coma•
paralyticileus•
renalfailure•
stupor.
WhattestsshowIfyoususpectthatyourpatienthashypercalcemia,lookfor:•serumcalciumlevelabove10.1mg/dl•ionizedcalciumlevelabove5.3mg/dl•digoxintoxicity(ifyourpatientistakingdigoxin)•X-raysrevealingpathologicfractures•characteristicECGchanges(shortenedQTinterval,prolongedPRinterval,flattenedTwaves,
andheartblock).
Howit’streatedIfhypercalcemiaproducesnosymptoms,treatmentmayconsistonlyofmanagingtheunderlyingcause.Dietaryintakeofcalciummaybereduced,andmedicationsorinfusionscontainingcalciummaybestopped.Treatmentforasymptomatichypercalcemiaalsoincludesmeasurestoincreasetheexcretionofcalciumandtodecreaseboneresorptionofit.
Hydrate!Youcanhelpincreaseexcretionofcalciumbyhydratingthepatient,whichencouragesdiuresis.Normalsalinesolutionistypicallyusedforhydrationinthesecases.Thesodiuminthesolutioninhibitsrenaltubularreabsorptionofcalcium.Loopdiureticssuchasfurosemide(Lasix)andethacrynicacid(Edecrin)alsopromotecalcium
excretion.Thiazidediureticsaren’tusedforhypercalcemiabecausetheyinhibitcalciumexcretion.Forpatientswithlife-threateninghypercalcemiaandthosewithrenalfailure,measuresto
increasecalciumexcretionmayincludehemodialysisorperitonealdialysiswithasolutionthatcontainslittleornocalcium.
BacktothebonesMeasurestoinhibitboneresorptionofcalciummayalsobeusedtohelpreducecalciumlevelsinextracellularfluids.CorticosteroidsadministeredI.V.andthenorallycanblockboneresorptionanddecreasecalciumabsorptionfromtheGItract.Bisphosphonatesareusedtotreathypercalcemiacausedbymalignancy.Zoledronateinhibits
boneresorptionbyactingonosteoclasts.
Etidronatedisodium,commonlyusedtotreathypercalcemia,alsoinhibitstheactionofosteoclasts.Thismedicationtakesfulleffectin2to3days.Pamidronatedisodium,whichissimilartoetidronatedisodium,canalsobeusedtoinhibitboneresorption.Plicamycin(mithramycin),achemotherapeutic(antineoplastic)drug,candecreasebone
resorptionofcalciumandisusedprimarilywhenhypercalcemiaiscausedbycancer.Calcitonin,anaturallyoccurringhormone,inhibitsboneresorptionaswell,butitseffectsareshortlived.(SeeWhentreatmentdoesn’twork.)
It’snotworking
Whentreatmentdoesn’tworkIfyourpatientdoesn’tseemtoberespondingtotreatmentforhypercalcemia,makesureheisn’tstilltakingvitaminDsupplements.Keepinmindthatcalcitoninmaybegiventodecreasecalciumlevelsrapidly,buttheeffectsare
onlytemporary.Ifhypercalcemiaissevere,youmaygiveoneortwodoseswithfluidsandfurosemidetoproviderapidreductionofcalciumlevels.
HowyouinterveneBesuretomonitorthecalciumlevelsofpatientswhoareatriskforhypercalcemia,suchasthosewhohavecancerorparathyroiddisorders,areimmobile,orarereceivingacalciumsupplement.Forapatientwhodevelopshypercalcemia,takethefollowingactions:•Monitorvitalsignsandassessthepatientfrequently.•Watchthepatientforarrhythmias.•Assessneurologicandneuromuscularfunctionandlevelofconsciousnessandreportchanges.•Monitorthepatient’sfluidintakeandoutput.•Monitorserumelectrolytelevels,especiallycalcium,todeterminetheeffectivenessof
treatmentandtodetectnewimbalancesthatmightresultfromtherapy.•InsertanI.V.catheterandmaintainI.V.access.Normalsalinesolutionisusuallyadministeredat
aninitialrateof200to300ml/hourintheabsenceofedema,andthentheflowrateisadjustedtomaintainaurineoutputofapproximately100ml/hour.Monitorthepatientforsignsoffluidoverloadsuchascracklesanddyspnea.
•Ifadministeringadiuretic,makesurethepatientisproperlyhydratedfirstsothathedoesn’texperiencevolumedepletion.
•Encouragethepatienttodrink3to4qt(3to4L)offluiddaily,unlesscontraindicated,tostimulatecalciumexcretionfromthekidneysandtodecreasetheriskofcalculiformation.(SeeTeachingabouthypercalcemia.)
Teachingpoints
Teachingpoints
TeachingabouthypercalcemiaWhenteachingapatientwithhypercalcemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
descriptionofhypercalcemia,itscauses,andtreatment•
riskfactors•
importanceofincreasedfluidintake•
dietaryguidelinesforalow-calciumdiet•
prescribedmedications,includingpossibleadverseeffects•
warningsignsandsymptoms•
avoidanceofsupplementsandantacidsthatcontaincalcium.
•Straintheurineforcalculi.Alsocheckforflankpain,whichcanindicatethepresenceofrenalcalculi.
•Ifthepatientisreceivingdigoxin,watchforsignsandsymptomsofatoxicreaction,suchasanorexia,nausea,vomiting,oranirregularheartrate.
•Getthepatientupandmovingassoonaspossibletopreventbonesfromreleasingcalcium.
Agentletouch•Handleapatientwhohaschronichypercalcemiagentlytopreventpathologicfractures.
Repositionbedriddenpatientsfrequently.Performactiveorpassiverange-of-motionexercisestopreventcomplicationsfromimmobility.
•Provideasafeenvironment.Keepthesiderailsraisedasneeded,maintainthebedinitslowestposition,andkeepthewheelslocked.Makesurethepatient’sbelongingsandcallbuttonarewithinreach.Ifthepatientisconfused,reorienthim.
•Offeremotionalsupporttothepatientandhisfamilythroughouttreatment.Overtsignsofhypercalcemiacanbeemotionallydistressingforallinvolved.
•Chartallcaregivenandthepatient’sresponse.(SeeDocumentinghypercalcemia.)
Chartsmart
DocumentinghypercalcemiaIfyourpatienthashypercalcemia,makesureyoudocumentthefollowinginformation:•
assessmentfindings,includingneurologicexaminationandlevelofconsciousness•
vitalsigns,includingcardiacrhythm•
intakeandoutput•
interventions,includingI.V.therapy,andthepatient’sresponsetothem•
signsandsymptoms•
safetymeasurestaken•
patientteachingdoneandthepatient’sresponse•
notificationofthepractitioner•
pertinentlaboratoryresults,includingcalciumlevels.
That’sawrap!
Balancingfluidsreview
Calciumbasics•
Positivelychargedion(cation)•
Ninety-ninepercentinbonesandteeth;1%inextracellularfluid
•Importantforboneandtoothformation,normalcellfunction,andneuraltransmission•
Affectscontractionofmuscles,bloodclotting,andhormonebalance•
Mostlyboundtoalbumin(alwayslookatalbuminlevelwithcalcium)•
Normaltotalserumcalciumlevels:8.9to10.1mg/dl•
Normalionizedcalciumlevels:adults,4.4to5.3mg/dl;children,4.4to6.0mg/dl;elderly,2.3to4.1mg/dl.
Calciumbalance•
Calciumlevelisaffectedbydietaryintakeandexistingstoresofcalciuminthebody.•
PTHisreleasedbytheparathyroidglandwhencalciumstoresarelow;itpullscalciumfrombonesandpromotestransferofcalciumintoplasma,kidneyreabsorptionofcalcium,andabsorptionfromintestines.•
Calcitonin,anotherhormonereleasedbythethyroid,antagonizesPTH;ifcalciumlevelsaretoohigh,calcitonininhibitsboneresorption,decreasesabsorptionofcalcium,andincreasesexcretionofcalciumbythekidneys.•
VitaminDpromotescalciumabsorptionfromintestines,resorptionfrombones,andreabsorptionbykidneystoincreasecalciumlevels.•
Phosphorusisinverselyrelatedtocalciumandinhibitscalciumabsorptionfromintestines;whencalciumlevelsarelow,kidneysretaincalciumandexcretephosphorus.•
SerumpHhasaninverserelationshipwithionizedcalcium.IfpHrises,morecalciumbindswithproteinandionizedcalciumleveldrops;ifpHdrops,lesscalciumbindstoproteinandionizedcalciumlevelrises.
Hypocalcemia•
Majorcause:hypoalbuminemia•
Alsocausedbypoordietaryintake,malabsorption,pancreatitis,parathyroidandthyroidglandsurgery,medications,kidneyfailure,hypomagnesemia,hyperphosphatemia,andalkalosis
Signsandsymptoms
•Predominantlyneuromuscularandcardiovascular•
Classicsign:tetanyevidencedbyTrousseau’sandChvostek’ssigns•
Alsoincludeanxiety;confusion;irritability;decreasedcardiacoutput;arrhythmias;prolongedSTsegmentandQTintervals;fractures;musclecramps;tremors;twitching;andparesthesiaoftheface,fingers,andtoes
Treatment•
I.V.calciumgluconateorcalciumchloride•
Possiblymagnesiumsupplements,vitaminDsupplements,andadequatedietaryintakeofcalcium(forchronichypocalcemia)
Hypercalcemia•
Commonelectrolytedisorder•
Consideredametabolicemergency•
Twomajorcauses:primaryhyperparathyroidism,whichreleasesexcessPTH,andcancer,whichreleasesasubstancesimilartoPTH•
Othercauses:hyperthyroidism,fractures,prolongedimmobilization,hypophosphatemia,acidosis,vitaminAoverdose,andcertainmedications
Signsandsymptoms•
Heart,skeletalmuscle,andnervoussystemaremostaffected.•
Includeconfusion,lethargy,depression,alteredmentalstatus,muscleweakness,hyporeflexia,characteristicECGchanges,hypertension,bonepain,abdominalpainandconstipation,nausea,vomiting,anorexia,polyuria,andextremethirst
Treatment•
Hydration•
Decreasedcalciumintake•
Diuretics,corticosteroids,bisphosphonates,andplicamycin•
Hemodialysisorperitonealdialysis(forlife-threateningcases)
Quickquiz
1.Albuminaffectscalciumlevelsby:A.blockingphosphorusabsorption,whichpreventscalciumexcretion.B.bindingwithcalcium,whichmakescalciumineffective.C.inhibitingmagnesiumuptake,whichpreventscalciumabsorption.D.affectingpHlevel.
Answer:B.Albuminbindswithcalciumandrendersitineffective.
2.Hypocalcemiainvolvesadysfunctionof:A.calcitonin.B.antidiuretichormone.C.growthhormone.D.PTH.
Answer:D.PTHpromotesreabsorptionofcalciumfromthebonetotheserum.WhensecretionofPTHisdecreased,hypocalcemiaresults.
3.Ifyourpatientishypercalcemic,youwouldexpectto:A.administerI.V.sodiumbicarbonate.B.administervitaminD.C.hydratethepatient.D.administerdigoxin.
Answer:C.HydratingapatientwithoralorI.V.fluidsincreasestheurineexcretionofcalciumandhelpslowerserumcalciumlevels.
4.Hypercalcemiawouldbemostlikelytodevelopin:A.a60-year-oldmanwhohassquamouscellcarcinomaofthelung.B.an80-year-oldwomanwhohasheartfailureandistakingfurosemide(Lasix).C.a25-year-oldtraumapatientwhohasreceivedmassivebloodtransfusions.D.a40-year-oldmanwithhypoalbuminemia.
Answer:A.Squamouscellcarcinomaofthelungcanleadtohypercalcemia.
5.You’retoldduringshiftreportthatyourpatienthasapositiveChvostek’ssign.Youwouldexpecthislaboratorytestresultstoreveal:
A.atotalserumcalciumlevelbelow8.9mg/dl.B.atotalserumcalciumlevelabove10.1mg/dl.C.anionizedcalciumlevelabove5.3mg/dl.D.anionizedcalciumlevelbetween4.4and5.3mg/dl.
Answer:A.Chvostek’sandTrousseau’ssignsareassociatedwithhypocalcemia.Atotalserumcalciumlevelbelow8.9mg/dlconfirmsthepresenceofthatcondition.
ScoringIfyouansweredallfivequestionscorrectly,we’reimpressed!Wewonder,haveyoubeenhangingoutinProfessorChvostek’slab?Ifyouansweredfourquestionscorrectly,ohmy!HaveyoubeenreadingProfessorTrousseau’sdiary,bychance?Ifyouansweredfewerthanfourquestionscorrectly,that’sfine.WehaveagreatseatforyouattheChvostek-Trousseaulectureseries.
ReferencesBansal,N.,Katz,R.,deBoer,I.H.,Kestenbaum,B.,Siscovick,D.S.,Hoofnagle,A.N.,...Ix,J.H.
(2013).Influenceofestrogentherapyoncalcium,phosphorus,andotherregulatoryhormonesinpostmenopausalwomen:TheMESAstudy.JournalofClinicalEndocrinologyandMetabolism,98(12),4890–4898.
Bech,A.,Reichert,L.,Telting,D.,&deBoer,H.(2013).Assessmentofcalciumbalanceinpatientsonhemodialysis,basedonionizedcalciumandparathyroidhormoneresponses.JournalofNephrology,26(5),925–930.
Bell,D.A.,Crooke,M.J.,Hay,N.,&Glendenning,P.(2013).ProlongedvitaminDintoxication:Presentation,pathogenesisandprogress.InternalMedicineJournal,43(10),1148–1150.
Bouillon,R.,VanSchoor,N.M.,Gielen,E.,Boonen,S.,Mathieu,C.,Vanderschueren,D.,&Lips,P.(2013).OptimalvitaminDstatus:Acriticalanalysisonthebasisofevidence-basedmedicine.JournalofClinicalEndocrinologyandMetabolism,98(8),E1283–E1304.
Carter,T.,&Ratnam,S.(2013).Calciphylaxis:Adevastatingcomplicationofderangementsofcalcium-phosphorusmetabolism—Acasereportandreviewoftheliterature.NephrologyNursingJournal,40(5),431–435.
Cauley,J.,Chlebowski,R.T.,Wactawski-Wende,J.,Robbins,J.A.,Rodabough,R.J.,Chen,Z.,...Manson,J.E.(2013).CalciumplusvitaminDsupplementationandhealthoutcomesfiveyearsactiveinterventionended:TheWomen’sHealthInitiative.JournalofWomen’sHealth,22(11),915–929.
Jamal,S.A.,Vandermeer,B.,Raggi,P.,Mendelssohn,D.C.,Chatterley,T.,Dorgan,M.,...Tsuyuki,R.T.(2013).Effectofcalcium-basedversusnon-calcium-basedphosphatebindersonmortalityinpatientswithchronickidneydisease:Anupdatedsystematicreviewandmeta-analysis.Lancet,382(9900),1268–1277.
Jungert,A.,&Neuhäuser-Berthold,M.(2013).DietaryvitaminDintakeisnotassociatedwith25-hydroxyvitaminD3orparathyroidhormoneinelderlysubjects,whereasthecalcium-to-phosphateratioaffectsparathyroidhormone.NutritionResearch,33(8),661–667.
McCarthy,M.S.,Loan,L.A.,Azuero,A.,&Hobbs,C.(2010).Theconsequencesofmodernmilitarydeploymentoncalciumstatusandbonehealth.NursingClinicsofNorthAmerica,45(2),109–122.
Mocanu,V.,&Vieth,R.(2013).Three-yearfollow-upofserum25-hydroxyvitaminD,parathyroidhormone,andbonemineraldensityinnursinghomeresidentswhohadreceived12monthsofdailybreadfortificationwith125mugofvitaminD3.NutritionJournal,12(1),137.
Pipili,C.,&Oreopoulos,D.G.(2012).VitaminDstatusinpatientswithrecurrentkidneystones.NephronClinicalPractice,122(3–4),134–138.
Shirazi,L.,Almquist,M.,Malm,J.,Wirfält,E.,&Manjer,J.(2013).DeterminantsofserumlevelsofvitaminD:Astudyoflifestyle,menopausalstatus,dietaryintake,serumcalcium,andPTH.BMCWomen’sHealth,13,33.
Chapter9
Whenphosphorustipsthebalance
JustthefactsInthischapter,you’lllearn:
♦therolethatphosphorusplaysinthebody
♦thebody’smechanismsforregulatingphosphorus
♦waystoassessapatientforaphosphorusimbalance
♦managementofhypophosphatemiaandhyperphosphatemia.
AlookatphosphorusPhosphorusistheprimaryanion,ornegativelychargedion,foundinintracellularfluid.It’scontainedinthebodyasphosphate.(Thetwowords—phosphorusandphosphate—arecommonlyusedinterchangeably.)About85%ofphosphorusexistsinboneandteeth,combinedina1:2ratiowithcalcium.About14%isinsofttissue,andlessthan1%isinextracellularfluid.
Whyit’simportantAnessentialelementofallbodytissues,phosphorusisvitaltovariousbodyfunctions.Itplaysacrucialroleincellmembraneintegrity(phospholipidsmakeupthecellmembranes);musclefunction;neurologicfunction;andthemetabolismofcarbohydrates,fat,andprotein.Phosphorusisaprimaryingredientin2,3-diphosphoglycerate(2,3-DPG),acompoundinredbloodcells(RBCs)thatpromotesoxygendeliveryfromRBCstothetissues.Phosphorusalsohelpsbufferacidsandbases.Itpromotesenergytransfertocellsthroughthe
formationofenergy-storingsubstancessuchasadenosinetriphosphate(ATP).It’salsoimportantforwhitebloodcell(WBC)phagocytosisandforplateletfunction.Finally,withcalcium,phosphorusisessentialforhealthybonesandteeth.
ThelowdownonlowphosphoruslevelsNormalserumphosphoruslevelsinadultsrangefrom2.5to4.5mg/dl(or1.8to2.6mEq/L).Incomparison,thenormalphosphoruslevelinthecellsis100mEq/L.Becausephosphorusislocatedprimarilywithinthecells,serumlevelsmaynotalwaysreflectthetotalamountofphosphorusinthebody.Forexample,it’simportanttodistinguishbetweenadecreaseinthelevelofserumphosphate(hypophosphatemia)andadecreaseintotalbodystorageofphosphate(phosphatedeficiency).
HowthebodyregulatesphosphorusThetotalamountofphosphorusinthebodyisrelatedtodietaryintake,hormonalregulation,kidneyexcretion,andtranscellularshifts.Foradults,therangefortherecommendeddailyrequirementofphosphorusis800to1,200mg.Phosphorusisreadilyabsorbedthroughthegastrointestinal(GI)tract,withtheamountabsorbedproportionaltotheamountingested.(SeeDietarysourcesofphosphorus.)
DietarysourcesofphosphorusMajordietarysourcesofphosphorusinclude:•
dairyproducts,suchasmilkandcheese•
driedbeans•
eggs•
fish•
nutsandseeds•
organmeats,suchasbrainandliver•
poultry•
wholegrains(Shutoetal.,2009)
Mostingestedphosphorusisabsorbedthroughthejejunum.Thekidneysexcreteabout90%ofphosphorusastheyregulateserumlevels.(TheGItractexcretestherest.)Ifdietaryintakeofphosphorusincreases,thekidneysincreaseexcretiontomaintainnormallevelsofphosphorus.Alow-phosphorusdietcausesthekidneystoconservephosphorusbyreabsorbingmoreofitintheproximaltubules.
BalancingitoutwithPTHTheparathyroidglandcontrolshormonalregulationofphosphoruslevelsbyaffectingtheactivityofparathyroidhormone(PTH).(SeePTHandphosphorus.)Changesincalciumlevels,ratherthanchangesinphosphoruslevels,affectthereleaseofPTH.Youmayrecallthatphosphorusbalanceiscloselyrelatedtocalciumbalance.
PTHandphosphorusThisillustrationshowshowPTHaffectsserumphosphorus(P)levelsbyincreasingphosphorusreleasefrombone,increasingphosphorusabsorptionfromtheintestines,anddecreasingphosphorusreabsorptionintherenaltubules.
Normally,calciumandphosphorushaveaninverserelationship.Forinstance,whentheserumcalciumlevelislow,thephosphoruslevelishigh.ThiscausestheparathyroidglandtoreleasePTH,whichcausesanincreaseincalciumandphosphorusresorptionfrombone,raisingbothcalciumandphosphoruslevels.Phosphorusabsorptionfromtheintestinesalsoincreases.(ActivatedvitaminD—calcitriol—alsoenhancesphosphorusabsorptionintheintestines.)
KidneysentertheequationPTHalsoactsonthekidneystoincreaseexcretionofphosphorus.TherenaleffectofPTHoutweighsitsothereffectsontheserumphosphoruslevel,particularlythatofreturningthephosphorusleveltonormal.ReducedPTHlevelsallowforphosphorusreabsorptionbythekidneys.Asaresult,serumlevelsrise(Connor,2009).
ShiftybusinessCertainconditionscausephosphorustomove,orshift,inandoutofcells.Insulinmovesnotonlyglucosebutalsophosphorusintothecell.Alkalosisresultsinthesamekindofphosphorusshift.Thoseshiftsaffectserumphosphoruslevels.(SeeElderlypatientsatrisk,page170.)
Agesandstages
Agesandstages
ElderlypatientsatriskElderlypatientsareparticularlyatriskforalteredelectrolytelevelsfortwomainreasons.First,theyhavealowerratioofleanbodyweighttototalbodyweight,whichplacesthematriskforwaterdeficit.Second,theirthirstresponseisdiminishedandtheirrenalfunctiondecreased,whichmakesmaintainingelectrolytebalancemoredifficult.Age-relatedrenalchangesincludechangesinrenalbloodflowandglomerularfiltrationrate.Medicationscanalsoalterelectrolytelevelsbyaffectingtheabsorptionofphosphate.Somakesure
youaskelderlypatientsifthey’reusingsuchover-the-countermedicationsasantacids,laxatives,herbs,andteas.
Hypophosphatemia
Hypophosphatemiaoccurswhentheserumphosphoruslevelfallsbelow2.5mg/dl(or1.8mEq/L).Althoughthisconditiongenerallyindicatesadeficiencyofphosphorus,itcanoccurundervariouscircumstanceswhentotalbodyphosphorusstoresarenormal.Severehypophosphatemiaoccurswhenserumphosphoruslevelsarelessthan1mg/dlandthebodycan’tsupportitsenergyneeds.Theconditionmayleadtoorganfailure.
HowithappensThreeunderlyingmechanismscanleadtohypophosphatemia:ashiftofphosphorusfromextracellularfluidtointracellularfluid,adecreaseinintestinalabsorptionofphosphorus,andanincreasedlossofphosphorusthroughthekidneys.Somecausesofhypophosphatemiamayinvolvemorethanonemechanism.Severalfactorsmaycausephosphorustoshiftfromextracellularfluidintothecell.Herearethe
mostcommoncauses.
WhenhyperventilationhappensRespiratoryalkalosis,oneofthemostcommoncausesofhypophosphatemia,canstemfromanumberofconditionsthatproducehyperventilation,includingsepsis,alcoholwithdrawal,heatstroke,pain,anxiety,diabeticketoacidosis,hepaticencephalopathy,andacutesalicylatepoisoning.Althoughthemechanismthatpromptsrespiratoryalkalosistoinducehypophosphatemiaisunknown,theresponseisashiftofphosphorusintothecellsandaresultingdecreaseinserum
phosphoruslevels.
SugarhighHyperglycemia,anelevatedserumglucoselevel,causesthereleaseofinsulin,whichtransportsglucoseandphosphorusintothecells.Thesameeffectmayoccurinapatientwithdiabeteswho’sreceivinginsulinorinasignificantlymalnourishedpatient;atparticularriskformalnourishmentareelderly,debilitated,oralcoholicpatientsandthosewithanorexianervosa.
FailuretoaddphosphorusAfterinitiationofenteralorparenteralfeedingwithoutsufficientphosphorussupplementation,phosphorusshiftsintothecells.Thisshift—calledrefeedingsyndrome—usuallyoccurs3ormoredaysafterfeedingsbegin.Patientsrecoveringfromhypothermiacanalsodevelophypophosphatemiaasphosphorusmovesintothecells.
AbnormalabsorptionMalabsorptionsyndromes,starvation,andprolongedorexcessiveuseofphosphorus-bindingantacidsorsucralfateareamongthemanycausesofimpairedintestinalabsorptionofphosphorus.BecausevitaminDcontributestointestinalabsorptionofphosphorus,inadequatevitaminDintakeorsynthesiscaninhibitphosphorusabsorption.ChronicdiarrheaorlaxativeabusecanalsoresultinincreasedGIlossofphosphorus.Decreaseddietaryintakerarelycauseshypophosphatemiabecausephosphateisfoundinmostfoods.
CallingthekidneystoaccountDiureticuseisthemostcommoncauseofphosphoruslossthroughthekidneys.Thiazides,loopdiuretics,andacetazolamidearethediureticsthatmostcommonlycausehypophosphatemia.(SeeDrugsassociatedwithhypophosphatemia.)
DrugsassociatedwithhypophosphatemiaThefollowingdrugsarecommonlyassociatedwithhypophosphatemia:•
acetazolamide,thiazidediuretics(chlorothiazideandhydrochlorothiazide),loopdiuretics(bumetanideandfurosemide),andotherdiuretics•
antacids,suchasaluminumcarbonate,aluminumhydroxide,calciumcarbonate,andmagnesiumoxide•
insulin•
laxatives.
Thesecondmostcommoncauseisdiabeticketoacidosis(DKA)indiabeticpatientswhohavepoorlycontrolledbloodglucoselevels.InDKA,highglucoselevelsinduceanosmoticdiuresis.Thisresultsinasignificantlossofphosphorusfromthekidneys.Ethanolaffectsphosphorusreabsorptioninthekidneyssothatmorephosphorusisexcretedinurine.AbuildupofPTH,whichoccurswithhyperparathyroidismandhypocalcemia,alsoleadsto
hypophosphatemiabecausePTHstimulatesthekidneystoexcretephosphate.Finally,hypophosphatemiaoccursinpatientswhohaveextensiveburns.Althoughthemechanismisunclear,theconditionseemstooccurinresponsetotheextensivediuresisofsaltandwaterthattypicallyoccursduringthefirst2to4daysafteraburninjury.Respiratoryalkalosisandcarbohydrateadministrationmayalsoplayarolehere.
WhattolookforMildtomoderatehypophosphatemiadoesn’tusuallycausesymptoms.Noticeableeffectsofhypophosphatemiatypicallyoccuronlyinseverecases.Thecharacteristicsofseverehypophosphatemiaareapparentinmanyorgansystems.Signsandsymptomsmaydevelopacutely
becauseofrapiddecreasesinphosphorusorgraduallyastheresultofslow,chronicdecreasesinphosphorus.Hypophosphatemiaaffectsthemusculoskeletal,centralnervous,cardiac,andhematologic
systems.Becausephosphorusisrequiredtomakehigh-energyATP,manyofthesignsandsymptomsofhypophosphatemiaarerelatedtolowenergystores.
WeakandwearyWithhypophosphatemia,muscleweaknessisthemostcommonsymptom.Othersymptomsmayincludediplopia(doublevision),malaise,andanorexia.Thepatientmayexperienceaweakenedhandgrasp,slurredspeech,ordysphagia.Healsomaydevelopmyalgia(tendernessorpaininthemuscles).Respiratoryfailuremayresultfromweakenedrespiratorymusclesandpoorcontractilityofthe
diaphragm.Respirationsmayappearshallowandineffective.Inlaterstages,thepatientmaybecyanotic.Keepinmindthatitmaybedifficulttoweanamechanicallyventilatedpatientwithhypophosphatemiafromtheventilator.Withseverehypophosphatemia,rhabdomyolysis(skeletalmuscledestruction)canoccurwith
alteredmusclecellactivity.Muscleenzymessuchascreatinekinasearereleasedfromthecellsintotheextracellularfluid.Lossofbonedensity,osteomalacia(softeningofthebones),andbonepainmayalsooccurwithprolongedhypophosphatemia.Fracturescanresult.
LogicalneurologiceffectsWithoutenoughphosphorus,thebodycan’tmakeenoughATP,acornerstoneofenergymetabolism.Asaresult,centralnervoussystemcellscanmalfunction,causingparesthesia,irritability,
apprehension,memoryloss,andconfusion.Theneurologiceffectsofhypophosphatemiamayprogresstoseizuresorcoma.
Whentheheartisn’thardyTheheart’scontractilitydecreasesbecauseoflowenergystoresofATP.Asaresult,thepatientmaydevelophypotensionandlowcardiacoutput.Severehypophosphatemiamayleadtocardiomyopathy,whichtreatmentcanreverse.
Oxygendeliverydrop-offAdropinproductionof2,3-DPGcausesadecreaseinoxygendeliverytotissues.Becausehemoglobinhasastrongeraffinityforoxygenthanforothergases,oxygenislesslikelytobegivenuptothetissuesasitcirculatesthroughthebody.Asaresult,lessoxygenisdeliveredtothemyocardium,whichcancausechestpain.Hypophosphatemiamayalsocausehemolyticanemiabecauseofchangesinthestructureand
functionofRBCs.PatientswithhypophosphatemiaaremoresusceptibletoinfectionbecauseoftheeffectoflowlevelsofATPinWBCs.LackofATPresultsinadecreasedfunctioningofleukocytes.Chronichypophosphatemiaalsoaffectsplateletfunction,resultinginbruisingandbleeding,particularlymildGIbleeding.
WhattestsshowThesediagnostictestresultsmayindicatehypophosphatemiaorarelatedcondition:•serumphosphorusleveloflessthan2.5mg/dl(or1.8mEq/L);severehypophosphatemia,less
than1mg/dl•elevatedcreatinekinaselevelifrhabdomyolysisispresent•X-raystudiesthatrevealtheskeletalchangestypicalofosteomalaciaorbonefractures•abnormalelectrolytes(decreasedmagnesiumlevelsandincreasedcalciumlevels).
Howit’streatedTreatmentvarieswiththeseverityandcauseofthecondition.Itincludestreatingtheunderlyingcauseandcorrectingtheimbalancewithphosphorusreplacementandahigh-phosphorusdiet.Therouteofreplacementtherapydependsontheseverityoftheimbalance.
MildermeasuresTreatmentformildtomoderatehypophosphatemiaincludesadiethighinphosphorus-richfoods,suchaseggs,nuts,wholegrains,organmeats,fish,poultry,andmilkproducts.However,ifcalciumiscontraindicatedorthepatientcan’ttoleratemilk,heshouldinsteadreceiveoralphosphorussupplements.OralsupplementsincludeNeutra-PhosandNeutra-Phos-Kandcanbe
usedformoderatehypophosphatemia.Dosagelimitationsarerelatedtotheadverseeffects,mostnotablynauseaanddiarrhea.(SeeWhendietarychangesaren’tworking.)
It’snotworking
Whendietarychangesaren’tworkingIfyourpatient’sphosphorus-richdiethasn’traisedserumphosphoruslevelsasyouhadhoped,it’stimetoaskthesequestions:•
IsaGIproblemmakingphosphorusdigestiondifficult?•
Isyourpatientusingaphosphate-bindingantacid?•
Isyourpatientabusingalcohol?•
Isyourpatientusingathiazidediuretic?•
Isyourpatientcomplyingwiththetreatmentregimenfordiabetes?
SternerstepsForpatientswithseverehypophosphatemiaoranonfunctioningGItract,I.V.phosphorusreplacementistherecommendedchoice.Twopreparationsareused:I.V.potassiumphosphateandI.V.sodiumphosphate.Dosageisguidedbythepatient’sresponsetotreatmentandserumphosphoruslevels.Potassiumphosphaterequiresslowadministration(nomorethan10mEq/hour).Adverse
effectsofI.V.replacementforhypophosphatemiaincludehyperphosphatemiaandhypocalcemia.
HowyouinterveneIfyourpatientbeginstotalparenteralnutritionorisotherwiseatriskfordevelopinghypophosphatemia,monitorhimforsignsandsymptomsofthisimbalance.Ifthepatienthasalreadydevelopedhypophosphatemia,yournursingcareshouldfocusoncarefulmonitoring,safetymeasures,andinterventionstorestorenormalserumphosphoruslevels.(SeeTeaching
abouthypophosphatemia.)Alertthepractitionertoanychangesinthepatient’sconditionandtaketheseotheractions:
Teachingpoints
TeachingabouthypophosphatemiaWhenteachingapatientwithhypophosphatemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
descriptionofhypophosphatemiaanditsriskfactors,prevention,andtreatment•
medicationsordered•
needtoconsultwithadietitian•
needforahigh-phosphorusdiet(1qtofcow’smilkperdayprovidestheaverageamountofphosphaterequired)•
avoidanceofphosphate-bindingantacids•
warningsignsandsymptomsandwhentoreportthem•
needtomaintainfollow-upappointments.
•Monitorvitalsigns.Remember,hypophosphatemiacanleadtorespiratoryfailure,lowcardiacoutput,confusion,seizures,orcoma.
•Assessthepatient’slevelofconsciousnessandneurologicstatuseachtimeyoucheckhisvitalsigns.Documentyourobservationsandthepatient’sneurologicstatusonaflowsheetsochangescanbenotedimmediately.(SeeDocumentinghypophosphatemia.)
Chartsmart
DocumentinghypophosphatemiaIfyourpatienthashypophosphatemia,makesureyoudocumentthefollowinginformation:•
vitalsigns•
neurologicstatus,includinglevelofconsciousness,restlessness,andapprehension•
musclestrength•
respiratoryassessment•
serumelectrolytelevelsandotherpertinentlaboratorydata•
notificationofthepractitioner•
I.V.therapy,includingconditionofI.V.site,medication,dose,andthepatient’sresponse•
seizures,ifany•
yourinterventionsandthepatient’sresponse•
safetymeasurestoprotectthepatient•
patientteaching.
•Monitortherateanddepthofrespirations,especiallyifthepatienthasseverehypophosphatemia.Reportsignsofhypoxia,suchasconfusion,restlessness,increasedrespiratoryrateand,inlaterstages,cyanosis.Ifpossible,takestepstopreventhyperventilationbecauseitworsensrespiratoryalkalosisandcanlowerphosphoruslevels.Followarterialbloodgasresultsandpulseoximetrylevelstomonitortheeffectivenessofventilation.Ifthepatientisonaventilator,weanhimoffslowly.
•Monitorthepatientforevidenceofheartfailurerelatedtoreducedmyocardialfunctioning.Signsandsymptomsincludecrackles,shortnessofbreath,decreasedbloodpressure,and
elevatedheartrate.•Monitorthepatient’stemperatureatleastevery4hours.CheckWBCcounts.Followstrict
steriletechniqueinchangingdressings.Reportsignsofinfection.•Assessthepatientfrequentlyforevidenceofdecreasingmusclestrength,suchasweakhand
graspsorslurredspeech,anddocumentyourfindingsregularly.•Administerprescribedphosphorussupplements.Keepinmindthatoralsupplementsmaycause
diarrhea.Toimprovetheirtaste,mixthemwithjuice.VitaminDmayalsobeorderedwiththeoralphosphatesupplementstoincreaseabsorption.
•InsertanI.V.lineasordered,andkeepitpatent.Infusephosphorussolutionsslowlyusinganinfusiondevicetocontroltherate.Duringinfusions,watchforsignsofhypocalcemia,hyperphosphatemia,andI.V.infiltration;potassiumphosphatecancausetissuesloughingandnecrosis.Monitorserumphosphatelevelsevery6hours.
•Administerananalgesic,ifordered.•Ifordered,makesurethepatientmaintainsbedrestforsafety.Keepthebedinitslowest
position,withthewheelslockedandthesiderailsraised.Ifthepatientisatriskforseizures,padthesiderailsandkeepanartificialairwayatthepatient’sbedside.
•Orientthepatientasneeded.Keepclocks,calendars,andfamiliarpersonalobjectswithinhissight.
•Informthepatientandhisfamilythatconfusioncausedbyalowphosphoruslevelisonlytemporaryandwilllikelydecreasewiththerapy.
•Recordthepatient’sfluidintakeandoutput.•Closelymonitorserumelectrolytelevels,especiallycalciumandphosphoruslevels,aswellas
otherpertinentlaboratorytestresults.Reportabnormalities.•Assistthepatientwithambulationandactivitiesofdailyliving,ifneeded,andkeepessential
objectsnearthepatienttopreventaccidents.
Hyperphosphatemia
Hyperphosphatemiaoccurswhenserumphosphoruslevelsexceed4.5mg/dl(or2.6mEq/L)andusuallyreflectsthekidneys’inabilitytoexcreteexcessphosphorus.Theconditioncommonlyoccursalongwithanincreasedreleaseofphosphorusfromdamagedcells.Severehyperphosphatemiaoccurswhentheserumphosphoruslevelsreach6mg/dlorhigher.
HowithappensHyperphosphatemiacanresultfromanumberofunderlyingmechanisms,includingimpairedrenalexcretionofphosphorus,ashiftofphosphorusfromtheintracellularfluidtotheextracellularfluid,andanincreaseindietaryintakeofphosphorus.
KidneyfilterfailureNormally,renalexcretionofphosphorusequalstheamounttheGItractabsorbsdaily.Hyperphosphatemiamostcommonlyresultsfromrenalfailureduetothekidneys’inabilitytoexcreteexcessphosphorus.Whenglomerularfiltrationratedropsbelow30ml/minute,thekidneyscan’tfilterexcess
phosphorusadequately.Becausethekidneysareresponsibleformostoftheexcretionofphosphorus,theirinabilitytofilterphosphorusleadstoanelevatedserumphosphoruslevel(Spaia,2011).
PTHproblemAriskafterthyroidorparathyroidsurgery,hypoparathyroidismimpairssynthesisofPTH.WhenlessPTHissynthesized,lessphosphorusisexcretedfromthekidneys.Theresult?Elevatedserumphosphoruslevels.
ShiftworkSeveralconditionscancausephosphorustoshiftfromtheintracellularfluidtotheextracellularfluid.Acid-baseimbalances,suchasrespiratoryacidosisandDKA,arecommonexamples.Anythingthatcausescellulardestructioncanalsoresultinatranscellularshiftofphosphorus.
Destructionofcellscantriggerthereleaseofintracellularphosphorusintoextracellularfluid,causingserumphosphoruslevelstorise.Chemotherapy,forexample,causessignificantcelldestruction,asdomusclenecrosisandrhabdomyolysis,conditionsthatcanstemfrominfection,heatstroke,andtrauma.
IncreasedintakeExcessiveintakeofphosphoruscanresultfromoveradministrationofphosphorussupplementsoroflaxativesorenemasthatcontainphosphorus(suchasFleetenemas).(SeeDrugsassociatedwithhyperphosphatemia.)
DrugsassociatedwithhyperphosphatemiaThefollowingdrugsmaycausehyperphosphatemia:•
enemassuchasFleetenemas•
laxativescontainingphosphorusorphosphate•
oralphosphorussupplements(Neutra-Phos)•
parenteralphosphorussupplements(sodiumphosphate,potassiumphosphate)•
vitaminDsupplements.
Ininfants,excessiveintakeofvitaminDcanresultinincreasedabsorptionofphosphorusandleadtoelevatedserumphosphoruslevels.(SeeCow’smilkandhyperphosphatemia.)
Agesandstages
Cow’smilkandhyperphosphatemiaInfantswhoarefedcow’smilkarepredisposedtohyperphosphatemiabecausecow’smilkcontainsmorephosphorusthanbreastmilk.Inaddition,infantshavenaturallyhighphosphoruslevels.
WhattolookforHyperphosphatemiacausesfewclinicalproblemsbyitself.However,phosphorusandcalciumlevelshaveaninverserelationship:Ifoneishigh,theotherislow.Becauseofthisseesawrelationship,hyperphosphatemiamayleadtohypocalcemia,whichcanbelife-threatening.Signsandsymptomsofacutehyperphosphatemiaareusuallycausedbytheeffectsofhypocalcemia.
Memoryjogger
Toremembersomeofthesignsandsymptomsofhyperphosphatemia,thinkofthewordCHEMO(keepinginmindthatchemotherapycanleadtohyperphosphatemia):
Cardiacirregularities
Hyperreflexia
Eatingpoorly
Muscleweakness
Oliguria.
Thepatientmaydevelopparesthesiainthefingertipsandaroundthemouth,whichmayincreaseinseverityandspreadproximallyalongthelimbsandtotheface.Severemusclespasm,cramps,pain,andweaknessmaypreventthepatientfromperformingnormalactivities.ThepatientmayexhibithyperreflexiaandpositiveChvostek’sandTrousseau’ssigns.Thesesignsareduetolowcalciumlevelsandmayprogresstotetanyandneurologicdisorders.Neurologicsignsandsymptomsincludedecreasedmentalstatus,delirium,andseizures.
Electrocardiogram(ECG)changesincludeaprolongedQTintervalandSTsegment.Thepatient
mayalsoexperiencehypotension,heartfailure,anorexia,nausea,andvomiting.Bonedevelopmentmayalsobeaffected.
CalcificationcuesWhenphosphoruslevelsrise,phosphorusbindswithcalcium,forminganinsolublecompoundcalledcalciumphosphate.Organdysfunctioncanresultwhencalciumphosphateprecipitates,orisdeposited,intheheart,lungs,kidneys,orothersofttissues.Thisprocess,calledcalcification,usuallyoccursasaresultofchronicallyelevatedphosphoruslevels.(SeeAlookatcalcification,page178.)
AlookatcalcificationWhenserumphosphoruslevelsarehigh,phosphorusbindswithcalciumtoformaninsolublecompoundcalledcalciumphosphate.Thecompoundisdepositedintheheart,lungs,kidneys,eyes,skin,andothersofttissueswhereitinterfereswithnormalorganandtissuefunction.Thisillustrationshowssomeoftheorgansaffectedandtheeffectcalcificationhasontheseorgans.
Withcalcification,thepatientmayexperiencearrhythmias,anirregularheartrate,anddecreasedurineoutput.Cornealhaziness,conjunctivitis,cataracts,andimpairedvisionmayoccur,andpapulareruptionsmaydevelopontheskin.
Whattestsshow
Thefollowingdiagnostictestsresultsmayindicatehyperphosphatemiaorarelatedconditionsuchashypocalcemia:•serumphosphoruslevelabove4.5mg/dl(or2.6mEq/L)•serumcalciumlevelbelow8.5mg/dl•X-raystudiesthatrevealskeletalchangesduetoosteodystrophy(defectivebonedevelopment)
inchronichyperphosphatemia•increasedbloodureanitrogen(BUN)andcreatininelevels,whichreflectworseningrenal
function•ECGchangescharacteristicofhypocalcemia(suchasaprolongedQTinterval).
Howit’streatedAnelevatedserumphosphoruslevelmaybetreatedwithdrugsandothertherapeuticmeasures.Treatmentaimstocorrecttheunderlyingdisorder,ifoneexists,andcorrecthypocalcemia.
GoinglowphosphoIfapatient’selevatedserumphosphoruslevelresultsfromexcessivephosphorusintake,theconditionmaybeeasilyremediedbyreducingphosphorusintake.Therapeuticmeasuresincludereducingdietaryintakeofphosphorusandeliminatingtheuseofphosphorus-basedlaxativesandenemas.(SeeWhendietarychangesaren’tenough.)
It’snotworking
Whendietarychangesaren’tenoughIfyourpatient’slow-phosphorusdiethasn’tchangedhisserumphosphoruslevel,it’stimetoaskthesequestions:•
Isthepatienttakingmedications(suchasphosphorus-bindingantacids)asdirected?•
Isthepatientcontinuingtouselaxativesorenemasthatcontainphosphate?•
Arethepatient’skidneysfunctioning?•
Hastheunderlyingcauseofhyperphosphatemiabeencorrected?
AlteringabsorptionDrugtherapymayhelpdecreaseabsorptionofphosphorusintheGIsystem.Suchtherapymayincludealuminum,magnesium,orcalciumgelorphosphate-bindingantacids.Althoughwidelyused,suchcalciumsaltsascalciumcarbonateandcalciumacetatemaycausehypercalcemia,sothepatientwillneedcarefuldosing.Polymericphosphatebinderssuchassevelamerhydrochloridemayalsobegiven.Apatientwithunderlyingrenalinsufficiencyorrenalfailureshouldnotreceivemagnesiumantacidsbecausetheymaycausehypermagnesemia.Apatientwithend-stagerenaldiseasemayreceivelanthanumcarbonate,anoncalcium,nonaluminumphosphatebinder.Keepinmindthatamildlyelevatedphosphoruslevelmaybenefitapatientwithrenalfailure.
Higherphosphoruslevels(onthehighersideofthenormalrange)allowmoreoxygentomovefromtheRBCstotissues,whichcanhelppreventhypoxemiaandlimittheeffectsofchronicanemiaonoxygendelivery.
Treatwhat’sunderneathTreatmentoftheunderlyingcauseofhyperphosphatemia,includingconditionssuchasrespiratoryacidosisorDKA,canlowerserumphosphoruslevels.Inapatientwithdiabetes,administeringinsulincausesphosphorustoshiftbackintothecells,whichcanresultindecreasedserumphosphoruslevels.
Situation:severePatientswithseverehyperphosphatemiamayreceiveI.V.salinesolutiontopromoterenalexcretionofphosphorus.However,thistreatmentrequiresthepatienttohavefunctionalkidneysandtheabilitytotoleratetheincreasedloadofsodiumandfluid.Patientsmayalsoreceiveproximaldiureticssuchasacetazolamidetoincreaserenalexcretionofphosphorus.Asafinaltherapeuticintervention,hemodialysisorperitonealdialysismaybeinitiatedifthe
patienthaschronicrenalfailureoranextremecaseofacutehyperphosphatemiawithsymptomatichypocalcemia.
HowyouinterveneKeepaneyeoutforpatientsatriskforhyperphosphatemia,andmonitorthemcarefully.Also,usecarewhenadministeringphosphorusinI.V.infusions,enemas,andlaxativesbecausetheextraphosphorusmaycausehyperphosphatemia.Ifyourpatienthasalreadydevelopedhyperphosphatemia,yourcareshouldfocusoncareful
monitoring,safetymeasures,andinterventionstorestorenormalserumphosphoruslevels.Followthesestepstoprovidecareforthepatient:•Monitorvitalsigns.•Watchforsignsandsymptomsofhypocalcemia,suchasparesthesiainthefingersoraroundthe
mouth,hyperactivereflexes,ormusclecramps.Ifanyoftheseoccur,immediatelynotifythedoctor.(SeeTeachingabouthyperphosphatemia.)Alsonotifythepractitionerifyoudetectsignsorsymptomsofcalcification,includingoliguria,visualimpairment,conjunctivitis,irregularheartrateorpalpitations,andpapulareruptions.
Teachingpoints
Teachingpoints
TeachingabouthyperphosphatemiaWhenteachingapatientwithhyperphosphatemia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
causesandtreatment•
prescribedmedications•
avoidanceofpreparationsthatcontainphosphorus,suchaslaxatives,enemas,andsupplements•
avoidanceofhigh-phosphorusfoods,suchasdairyproducts,organmeats,fish,poultry,eggs,andnutsandseeds•
warningsignsandsymptoms•
referralstoadietitianandsocialservices,ifindicated.
•Monitorfluidintakeandoutput.Ifurineoutputfallsbelow30ml/hour,immediatelynotifythepractitioner.Decreasedurineoutputcanseriouslyaffectrenalclearanceofexcessserumphosphorus.
•Closelymonitorserumelectrolytelevels,especiallycalciumandphosphorus.Reportchangesimmediately.Also,monitorBUNandserumcreatininelevelsbecausehyperphosphatemiacanimpairrenaltubuleswhencalcificationoccurs.
•Keepaflowsheetofdailylaboratorytestresultsforapatientatrisk.IncludeBUNandserumphosphorus,calcium,andcreatininelevelsaswellasfluidintakeandoutput.Keeptheflowsheetonaclipboardsochangescanbedetectedimmediately.(SeeDocumentinghyperphosphatemia.)
Chartsmart
DocumentinghyperphosphatemiaIfyourpatienthashyperphosphatemia,makesureyoudocumentthefollowinginformation:•
allassessmentfindings•
intakeandoutput•
I.V.therapyandmedicationsgiven•
musclespasms,cramps,pain,andmusclestrength•
paresthesiainthefingertipsandaroundthemouth•
visualdisturbances•
safetymeasurestoprotectpatient•
notificationofthepractitioner•
yourinterventions,includingpatientteaching,andthepatient’sresponse.
•Administerprescribedmedications,monitortheireffectiveness,andassessthepatientforpossibleadversereactions.Giveantacidswithmealstoincreasetheireffectivenessinbindingphosphorus.
•Preparethepatientwithseverehyperphosphatemiaforpossibledialysis.•Ifapatient’sconditionresultsfromchronicrenalfailureorifhistreatmentincludesalow-
phosphorusdiet,consultadietitiantohelpthepatientcomplywithdietaryrestrictions.Dietaryphosphorusshouldberestrictedto0.6to0.9g/day.
That’sawrap!
Phosphorusimbalancesreview
Phosphorusbasics•
Primaryanioninintracellularfluid•
About85%foundinbonesandteeth,combinedwithcalciumina1:2ratio•
Crucialtocellmembraneintegrity,muscleandneurologicfunction,andmetabolismofcarbohydrates,fats,andproteins•
PromotesoxygendeliveryfromRBCstotissues•
Buffersacidsandbases,promotesenergytransferbyformingATP,andisessentialforhealthybonesandteeth•
Normalrange:2.5to4.5mg/dl(1.8to2.6mEq/L)
Phosphorusbalance•
Dietaryintakeandrenalexcretionmaintainnormallevels;ifintakeincreases,renalexcretionalsoincreases.•
TheparathyroidglandcontrolshormonalregulationofphosphoruslevelsbyaffectingPTH.•
PTHreleaseisaffectedbycalciumlevel;PTHcausesthekidneystoincreaseexcretionofphosphorusifthecalciumlevelishighandtoreabsorbphosphorusifthecalciumlevelislow.•
Balanceisaffectedbycertainconditionsthatcausetranscellularshiftofphosphorus;forexample,insulinmovesglucoseandphosphorusintocells;alkalosiscausesthesamekindofshift.
Hypophosphatemia•
Severehypophosphatemia:serumphosphoruslevelslessthan1mg/dl;mayleadtoorganfailure•
Threeunderlyingmechanisms:–
Shiftofphosphorusintointracellularfluid–
Decreaseinintestinalabsorption–
Increasedexcretionfromkidneys•
Mostcommoncauses:respiratoryalkalosis,hyperglycemia,refeedingsyndrome,malabsorptionsyndrome,excessiveuseofphosphorus-bindingantacids,diarrhea,laxativeabuse,diuretics,DKAhyperparathyroidism,hypocalcemia,andextensiveburns
Signsandsymptoms•
Mostcommonlyoccurasaresultofseverehypophosphatemiathataffectsthemusculoskeletal,centralnervous,cardiac,andhematologicsystems•
Mostcommon:muscleweakness•
Slurredspeech,dysphagia,cardiomyopathy,hypotension,decreasedcardiacoutput,rhabdomyolysis,cyanosis,andrespiratoryfailure
TreatmentFormildtomoderateconditions•
Oralsupplements•
IncreaseddietaryintakeForsevereconditions•
I.V.phosphorus(potassiumphosphateorsodiumphosphate)
Hyperphosphatemia•
Severe:6mg/dlorhigher•
Usuallycausedbyimpairedrenalexcretionofphosphorus•
Othercauses:hypoparathyroidism(usuallyafterthyroidorparathyroidsurgery),resultinginreducedPTHlevelsandreducedphosphateexcretion•
Conditionscausingshiftofphosphorusintoextracellularfluid:respiratoryacidosis,DKA,celldestructioncausedbychemotherapy,necrosis,rhabdomyolysis,trauma,heatstroke,andinfection•
Alsocausedbyoveradministrationofphosphorussupplementsorphosphorus-containinglaxativesandenemasandexcessiveintakeofvitaminD
Signsandsymptoms•
Usuallycausedbyhypocalcemia•
Includeparesthesia,musclecramps,muscleweakness,tetany,positiveTrousseau’sandChvostek’ssigns,decreasedmentalstatus,hyperreflexia,anorexia,nauseaandvomiting,andcalcification(whichcausesarrhythmias,irregularheartrate,decreasedurineoutput,conjunctivitis,cataracts,impairedvision,andpapulareruptions)
Treatment•
Aimedatcorrectingunderlyingproblem•
Includeslow-phosphorusdietanddrugstodecreaseabsorptionofphosphorus(aluminum,calciumsalts,magnesium[exceptinthosewithrenalfailure],orphosphate-bindingantacids)Forseverehyperphosphatemia•
I.V.salinesolution•
Proximaldiureticstopromoteexcretion•
Dialysisifnecessary
Quickquiz
1.Ifyourpatienthashyperphosphatemia,heorshemayalsohavethesecondaryelectrolytedisturbance:
A.hypermagnesemia.B.hypocalcemia.C.hypernatremia.D.hyperkalemia.
Answer:B.Phosphorusandcalciumhaveaninverserelationship:Ifserumphosphoruslevelsareincreased,thenserumcalciumlevelsaredecreased.
2.Forapatientwithhyperphosphatemiaandrenalfailure,avoidgivingthephosphate-bindingantacid:
A.aluminumhydroxide.B.calciumcarbonate.C.calciumacetate.D.magnesiumoxide.
Answer:D.Administeringanantacidthatcontainsmagnesiumtoapatientwithrenalfailurecanresultinhypermagnesemia.
3.Manyofthesignsandsymptomsofhypophosphatemiaarerelatedto:A.lowenergystores.B.hypercalcemia.C.extensivediuresis.D.hypocalcemia.
Answer:A.ThebodyneedsphosphorustomakeATP,whichprovidesallthecells—especiallymuscles—withenergy.
4.Thebindingofphosphorusandcalciuminapatientwithhyperphosphatemiacanleadto:
A.increasedcalciumreleasebythekidneys.B.widespreadcalcificationoftissues.C.decreasedcalciumuptakebythepituitarygland.D.increasedproductionofPTH.
Answer:B.Hyperphosphatemiaresultsinhypocalcemia.Thecalciumandphosphorusbindtogetherandaredepositedinthetissues,resultingincalcification.
5.Itmightbedifficulttoweanyourpatientfrommechanicalventilationifhehasaserumphosphoruslevel:
A.higherthan8mg/dl.B.between4.5and6.0mg/dl.C.between2and4mg/dl.D.lowerthan1mg/dl.
Answer:D.Severehypophosphatemiacanleadtorespiratorymuscleweaknessandimpairedcontractilityofthediaphragm,whichcompromisesthepatient’sabilitytobreathespontaneously.
ScoringIfyouansweredallfivequestionscorrectly,you’rephosphabulous!Keepupthegoodwork.Ifyouansweredfourquestionscorrectly,waytogo!You’reanaturalwhenitcomestophosphorusbalance.Ifyouansweredfewerthanfourquestionscorrectly,that’sokay.Takeabreaktorenewyourmentalpowerandthenreviewthechapteragain.
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Spaia,S.(2011).Phosphatebinders:Sevelamerinthepreventionandtreatmentofhyperphosphataemiainchronicrenalfailure.Hippokratia,15(Suppl1),22–26.
Vemuri,N.,Michelis,M.F.,&Matalon,A.(2011).Conversiontolanthanumcarbonatemonotherapyeffectivelycontrolsserumphosphoruswithareducedtabletburden:Amulticenteropen-labelstudy.BMCNephrology,12,49.
Verdonck,J.,Geuens,G.,Delaere,P.,VanderPoorten,V.,Evenepoel,P.,&Debruyne,E.(2009).Surgicalfindingsandpost-operativeparathormonelevelsinpatientswithsecondaryhyperparathyroidism.B-ENT,5(3),143–148.
Chapter10
Whenchloridetipsthebalance
JustthefactsInthischapter,you’lllearn:
♦theimportanceofchlorideinthebody
♦therelationshipbetweenchlorideandsodium
♦thebody’smechanismsforregulatingchloride
♦waystorecognizeandtreathighandlowchloridelevels.
AlookatchlorideChlorideisthemostabundantanion(negativelychargedion)inextracellularfluid.Itmovesinandoutofthecellswithsodiumandpotassiumandcombineswithmajorcations(positivelychargedions)toformsodiumchloride,hydrochloricacid,potassiumchloride,calciumchloride,andotherimportantcompounds.Highlevelsofchlorideexistincerebrospinalfluid(CSF),buttheanioncanalsobefoundinbileandingastricandpancreaticjuices.
Whyit’simportantBecauseofitsnegativecharge,chloridetravelswithpositivelychargedsodiumandhelpsmaintainserumosmolalityandwaterbalance.ChlorideandsodiumalsoworktogethertoformCSF.Thechoroidplexus,atangledmassoftinybloodvesselsinsidetheventriclesofthebrain,dependsonthesetwoelectrolytestoattractwaterandformthefluidcomponentofCSF.Inthestomach,thegastricmucosasecreteschlorideashydrochloricacid,providingtheacid
mediumnecessaryfordigestionandenzymeactivation.Chloridealsohelpsmaintainacid-basebalanceandhelpstransportcarbondioxideintheredbloodcells.
OnthelevelSerumchloridelevelsnormallyrangebetween98and108mEq/L.Valuesmayvaryslightlydependingonthelaboratorydoingtheanalysis.Bycomparison,thechloridelevelinsideacellis4mEq/L.Chloridelevelsremainrelativelystablewithage.Becausechloridebalanceiscloselylinkedwithsodiumbalance,thelevelsofbothelectrolytesusuallychangeindirectproportiontooneanother.
HowthebodyregulateschlorideChlorideregulationdependsonintakeandexcretionofchlorideandreabsorptionofchlorideionsinthekidneys.Thedailychloriderequirementforadultsis1.8to2.3g/daypertheNationalInstitutesofHealth(NIH)guidelines.Mostdietsprovidesufficientchlorideintheformofsalt(usuallyassodiumchloride)orprocessedfoods.(SeeDietarysourcesofchloride.)
DietarysourcesofchlorideDietarysourcesofchlorideinclude:•
cannedvegetables•
eggs•
freshfruitsandvegetables,especiallyhighconcentrationintomatoes,celery,lettuce,andolives•
milk•
processedmeats•
saltyfoods•
tableorseasalt.
Mostchlorideisabsorbedintheintestines,withonlyasmallportionlostinfeces.Chlorideisproducedmainlyinthestomachintheformofhydrochloricacid,sochloridelevelscanbeinfluencedbygastrointestinal(GI)disorders.
BestbuddiesBecausechlorideandsodiumarecloselylinked,achangeinoneelectrolytelevelcausesacomparablechangeintheother.Chloridelevelscanalsobeindirectlyaffectedbyaldosteronesecretion,whichcausestherenaltubulestoreabsorbsodium.Aspositivelychargedsodiumionsarereabsorbed,negativelychargedchlorideionsarepassivelyreabsorbedbecauseoftheirelectricalattractiontosodium.
BattlingacidsandbasesRegulationofchloridelevelsalsoinvolvesacid-basebalance.Chlorideisreabsorbedandexcretedindirectoppositiontobicarbonate.Whenchloridelevelschange,thebodyattemptstokeepitspositive-negativebalancebymakingcorrespondingchangesinthelevelsofbicarbonate(anothernegativelychargedion)inthekidneys.(Remember,bicarbonateisalkaline.)
Whenchloridelevelsdecrease,thekidneysretainbicarbonateandbicarbonatelevelsincrease.Whenchloridelevelsincrease,thekidneysexcretebicarbonateandbicarbonatelevelsdecrease.Therefore,changesinchlorideandbicarbonatelevelscanleadtoacidosisoralkalosis.(SeeChlorideandbicarbonate,page188.)
ChlorideandbicarbonateChloride(Cl)andbicarbonate(HCO3
−)haveaninverserelationship.Whenthelevelofonegoesup,theleveloftheothergoesdown.
Hypochloremia
Hypochloremiaisadeficiencyofchlorideinextracellularfluid.Thisoccurswhenserumchloridelevelsfallbelow98mEq/L.Whenserumchloridelevelsdrop,levelsofsodium,potassium,calcium,andotherelectrolytesmayalsobeaffected.Ifmuchmorechloridethansodiumislost,hypochloremicalkalosismayoccur.
HowithappensSerumchloridelevelsdropwhenchlorideintakeorabsorptiondecreasesorwhenchloridelossesincrease.Lossesmayoccurthroughtheskin(chlorideisfoundinsweat),theGItract,orthekidneys.Changesinsodiumlevelsoracid-basebalancealsoalterchloridelevels.
Downwithintake
Reducedchlorideintakemayoccurininfantsbeingfedchloride-deficientformulaandinpeopleonsalt-restricteddiets.PatientsdependentonI.V.fluidsarealsoatriskifthefluidslackchloride(forexample,D5W).Excessivechloridelossescanoccurwithprolongedvomiting,diarrhea,severe
diaphoresis,burns,Addison’sdisease,gastricsurgery,nasogastric(NG)suctioning,andotherGItubedrainage.Severevomitingcancausealossofhydrochloricacidfromthestomach,anaciddeficitinthebody,andsubsequentmetabolicalkalosis.Patientswithcysticfibrosiscanalsolosemorechloridethannormal.Anyprolongedanduntreatedhypochloremicstatecanresultinastateofhypochloremicalkalosis.(SeeDangerousdevelopment.)
DangerousdevelopmentHere’showhypochloremiacanleadtohypochloremicmetabolicalkalosis.
Hypochloremicalkalosiscanaffectinfantsandchildrenaswellasadults.(SeeHypochloremicalkalosisininfants,page190.)Peopleatriskforhypochloremiaincludethosewithprolongedvomitingfrompyloricobstructionandthosewithdrainingfistulasandileostomies,whichcan
causealossofchloridefromtheGItract.
Agesandstages
HypochloremicalkalosisininfantsBefore1980,someinfantswerefedchloride-deficientformulas.Hypochloremicalkalosisdeveloped,causingthoseinfantstoexhibitcognitivedelays,languagedisorders,andimpairedvisualmotorskills.Asaresult,theU.S.Congresspassedalawrequiringinfantformulatocontainaminimumchloridecontentof55to65mg/100kcalandamaximumof150mg/100kcal.Breastmilkcontainsabout420mg/L,andundilutedcow’smilkcontains900to1,020mg/L.Infantformulacontains10.6to13.5mEq/L;formulaforolderinfants(follow-upformula),14to19.2mEq/L.Despitetheregulationofchlorideininfantformula,hypochloremicalkalosisisn’tuncommonin
childrenandiscommonlyseeninneonates.HypochloremicalkalosismaybecausedbydiuretictherapyinbronchopulmonarydysplasiaorbyNGsuctioning.Itmayalsobeseenininfantswithchloride-wastingsyndromesresultingfromrenalcauses(Bartter’ssyndrome),intestinalcauses(congenitalchloride-losingdiarrhea),orchloridelossfromcysticfibrosis.
DecreaserdrugsVariousdrugsmaydecreasechloride,includingbicarbonate,corticosteroids,laxatives,andtheophylline.Diuretics,suchasfurosemide(Lasix),ethacrynicacid(Edecrin),andhydrochlorothiazidecanalsocauseanexcessivelossofchloridefromthekidneys.(SeeDrugsassociatedwithhypochloremia.)
DrugsassociatedwithhypochloremiaDrugsthatcancausehypochloremiainclude:•
loopdiuretics(suchasfurosemide)•
osmoticdiuretics(suchasmannitol)•
thiazidediuretics(suchashydrochlorothiazide)•
bicarbonate•
corticosteroids•
laxatives•
theophylline.
Wait,there’smoreOthercausesofhypochloremiaincludesodiumandpotassiumdeficiencyormetabolicalkalosis;conditionsthataffectacid-baseorelectrolytebalance,suchasuntreateddiabeticketoacidosis,waterintoxication,andAddison’sdisease;andrapidremovalofasciticfluid(whichcontainssodium)duringparacentesis.Also,patientswhohaveheartfailuremaydevelophypochloremiabecauseserumchloridelevelsaredilutedbyexcessfluidinthebody.
WhattolookforPatientswhohavehypochloremiamayexhibitsignsandsymptomsofacid-baseandelectrolyteimbalances.Youmaynoticesignsofhyponatremia,hypokalemia,ormetabolicalkalosis.AlkalosisresultsinahighpHandtocompensate,respirationsbecomeslowandshallowasthebodytriestoretaincarbondioxideandrestoreanormalpHlevel.Thenervesalsobecomemoreexcitable,solookfortetany,hyperactivedeeptendonreflexes,
andmusclehypertonicity.(SeeDangersignsofhypochloremia.)Thepatientmayhavemusclecramps,twitching,fever,weaknessandbeagitatedorirritable.Ifhypochloremiagoesunrecognized,itcanbecomelife-threatening.Asthechlorideimbalanceworsens(alongwithotherimbalances),thepatientmaysufferarrhythmias,seizures,coma,orrespiratoryarrest.
CAUTION!
DangersignsofhypochloremiaSuspectthatyourpatientwithhypochloremiaisreallyintroubleifheexhibitsanyoftheselate-developingdangersigns:•
seizures•
coma•
arrhythmias•
respiratoryarrest.
WhattestsshowThesediagnostictestresultsareassociatedwithhypochloremia:•serumchloridelevelbelow98mEq/L•serumsodiumlevelbelow135mEq/L(indicateshyponatremia)•serumpHgreaterthan7.45andserumbicarbonatelevelgreaterthan26mEq/L(indicates
metabolicalkalosis).
Howit’streatedTreatmentforhypochloremiafocusesoncorrectingtheunderlyingcause.Chloridemaybereplacedthroughfluidadministrationordrugtherapy.Treatmentmaybenecessaryforassociatedmetabolicalkalosisorotherelectrolyteimbalances.Chloridemaybegivenorally—forexample,inasaltybroth.Ifthepatientcan’ttakeoral
supplements,hemayreceiveI.V.medicationsornormalsalinesolution.Toavoidhypernatremia(highsodiumlevel)ortotreathypokalemia,potassiumchloridemaybeadministeredI.V.
AddressingthealkalosisTreatmentforassociatedmetabolicalkalosisusuallyaddressestheunderlyingcauses,suchas
diaphoresis,vomitingorotherGIlosses,orrenallosses.Rarely,metabolicalkalosismaybetreatedbyadministeringammoniumchloride,anacidifyingagentthat’susedwhenalkalosisiscausedbychlorideloss.Drugdosagedependsontheseverityofthealkalosis.Theeffectsofammoniumchloridelastonly3days.Afterthat,thekidneysbegintoexcretetheextraacid.(SeeWhentreatmentdoesn’twork.)
It’snotworking
Whentreatmentdoesn’tworkIftreatmentforhypochloremiadoesn’tseemtobeworking,makesurethepatientisn’tdrinkinglargeamountsoftapwater,whichcancausehimtoexcretelargeamountsofchloride.Reviewthecausesofhypochloremiatoidentifyneworcoexistingconditionsthatmightbecausingchlorideloss.
HowyouinterveneMonitorpatientsatriskforhypochloremia,suchasthosereceivingdiuretictherapyorNGsuctioning.Whencaringforapatientwithhypochloremia,you’llalsowanttotaketheseactions:•Monitorlevelofconsciousness(LOC),musclestrength,andmovement.Notifythedoctorifthe
patient’sconditionworsens.•Monitorvitalsigns,especiallyrespiratoryrateandpattern,andobserveforworsening
respiratoryfunction.Also,monitorcardiacrhythmbecausehypokalemiamaybepresentwithhypochloremia.Haveemergencyequipmenthandyincasethepatient’sconditiondeteriorates.
•Monitorandrecordserumelectrolytelevels,especiallychloride,sodium,potassium,andbicarbonate.Alsoassessarterialbloodgas(ABG)resultsforacid-baseimbalance.
•Ifthepatientisalertandcanswallowwithoutdifficulty,offerfoodshighinchloride,suchastomatojuiceorsaltybroth.Don’tletthepatientfillupontapwater.(SeeTeachingabouthypochloremia.)
Teachingpoints
Teachingpoints
TeachingabouthypochloremiaWhenteachingapatientwithhypochloremia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
signsandsymptoms,complications,andriskfactors•
warningsignsandsymptomstoreporttothepractitioner•
dietarysupplements•
medicationsifprescribed•
importanceofreplenishinglostfluidsfromvomitingordiarrhea.
•InsertanI.V.lineasordered,andkeepitpatent.Administerchlorideandpotassiumreplacementsasordered.
•Ifadministeringammoniumchloride,assessthepatientforpainattheinfusionsiteandadjusttherateasneeded.Thisdrugismetabolizedbytheliver,sodon’tgiveittopatientswithseverehepaticdisease.
•Usenormalsalinesolution,nottapwater,toflushthepatient’sNGtube.•Accuratelymeasureandrecordintakeandoutput,includingthevolumeofvomitusandgastric
contentsfromsuctionandotherGIdrainagetubes.•Provideasafeenvironment.Helpthepatientambulate,andkeephispersonalitemsandcall
buttonwithinreach.Instituteseizureprecautionsasneeded.•Provideaquietenvironment,explaininterventions,andreorientthepatientasneeded.•Documentallcareandthepatient’sresponse.(SeeDocumentinghypochloremia.)
Chartsmart
DocumentinghypochloremiaIfyourpatienthashypochloremia,makesureyoudocumentthefollowinginformation:•
vitalsigns,includingcardiacandrespiratoryrhythm•
intakeandoutput•
serumelectrolytelevelsandABGresults•
yourassessment,includingLOC,seizureactivity,andrespiratorystatus•
timeofnotificationofthepractitioner•
I.V.therapy,alongwithotherinterventions,andthepatient’sresponse•
safetymeasuresimplemented•
patientteachingperformedandthepatient’sresponse.
Hyperchloremia
Hyperchloremia,anexcessofchlorideinextracellularfluid,occurswhenserumchloridelevelsexceed108mEq/L.Thisconditionisassociatedwithotheracid-baseimbalances,suchasmetabolicacidosis,andrarelyoccursalone.
HowithappensBecausechlorideregulationandsodiumregulationarecloselyrelated,hyperchloremiamayalsobeassociatedwithhypernatremia.Chlorideandbicarbonatehaveaninverserelationship,soanexcessofchlorideionsmaybelinkedtoadecreaseinbicarbonate.Excessserumchlorideresultsfromincreasedchlorideintakeorabsorption,fromacidosis,orfromchlorideretentionbythekidneys.
Upwithintakeandabsorption
Increasedintakeofchlorideintheformofsodiumchloridecancausehyperchloremia,especiallyifwaterlossfromthebodyoccursatthesametime.Thewaterlossraisesthechloridelevelevenmore.Increasedchlorideabsorptionbythebowelcanoccurinpatientswhohavehadanastomosesjoiningtheureterandintestines.Conditionsthatalterelectrolyteandacid-basebalanceandcausemetabolicacidosis
includedehydration,renaltubularacidosis,diabetesinsipidus,renalfailure,respiratoryalkalosis,salicylatetoxicity,hyperparathyroidism,hyperaldosteronism,andhypernatremia.
Drug-relatedretentionSeveralmedicationscanalsocontributetohyperchloremia.Forexample,directingestionofammoniumchlorideorotherdrugsthatcontainchlorideorcausechlorideretentioncanleadtohyperchloremia.Ionexchangeresinsthatcontainsodium,suchasKayexalate,cancausechloridetobeexchangedforpotassiuminthebowel.Whenchloridefollowssodiumintothebloodstream,
serumchloridelevelsrise.Carbonicanhydraseinhibitors,suchasacetazolamide,alsopromotechlorideretentioninthebodybyincreasingbicarbonateionloss.(SeeDrugsassociatedwithhyperchloremia.)
DrugsassociatedwithhyperchloremiaDrugsthatcancausehyperchloremiainclude:•
acetazolamide•
ammoniumchloride•
androgensandestrogens•
cortisone•
phenylbutazone•
salicylates(overdose)•
sodiumpolystyrenesulfonate(Kayexalate)•
diureticssuchastriamterene.
WhattolookforHyperchloremiararelyproducessignsandsymptomsonitsown.Instead,themajorindicationsareessentiallythoseofmetabolicacidosis,includingtachypnea,lethargy,thirst,weakness,dehydration,hypotensiondiminishedcognitiveability,anddeep,rapidrespirations(Kussmaul’srespirations).Leftuntreated,acidosiscanleadtoarrhythmias,decreasedcardiacoutput,afurtherdecreasein
LOC,andevencoma.Metabolicacidosisrelatedtoahighchlorideleveliscalledhyperchloremicmetabolicacidosis.(SeeAniongapandmetabolicacidosis.)
AniongapandmetabolicacidosisHyperchloremiaincreasesthelikelihoodthatapatientwilldevelophyperchloremicmetabolicacidosis.Theillustrationbelowshowstherelationshipbetweenchlorideandbicarbonateinthedevelopmentofthatformofacidosis.
HowithappensAnormalaniongapinapatientwithmetabolicacidosisindicatestheacidosisismostlikelycausedbyalossofbicarbonateionsbythekidneysorGItract.Insuchcases,acorrespondingincreaseinchlorideionsalsooccurs.Acidosiscanalsoresultfromanaccumulationofchlorideionsintheformofacidifyingsalts.A
correspondingdecreaseinbicarbonateionsoccursatthesametime.Inthisillustration,thechloridelevelishigh(>108mEq/L)andthebicarbonatelevelislow(<22mEq/L).
Ifapatienthasanincreasedserumchloridelevel,hisserumsodiumlevelisprobablyhighaswell,whichcanleadtofluidretention.Healsomaybeagitatedandhavedyspnea,tachycardia,hypertension,orpittingedema—signsofhypernatremiaandhypervolemia.
WhattestsshowThefollowingdiagnostictestresultstypicallyoccurinhyperchloremia:•serumchloridelevelgreaterthan108mEq/L•serumsodiumlevelgreaterthan145mEq/L.Inaddition,thepatientmayhaveaserumpHlevellessthan7.35,aserumbicarbonatelevel
lessthan22mEq/L,andanormalaniongap(8to14mEq/L).Thesefindingssuggestmetabolicacidosis.
Howit’streatedTreatmentforhyperchloremiaincludescorrectingtheunderlyingcauseaswellasrestoringfluid,electrolyte,andacid-basebalance.(SeeDiureticstotherescue.)Adehydratedpatientmayreceivefluidstodilutethechlorideandspeedrenalexcretionofchlorideions.Thepatient’ssodiumandchlorideintakemayalsoberestricted.
It’snotworking
DiureticstotherescueIfthepatientdoesn’trespondtotherapy,thedoctormayorderdiureticstoeliminatechloride.Althoughotherelectrolytesarealsolost,chloridelevelshoulddecreasewiththistreatment.
Ifthepatienthasnormalliverfunction,hemayreceiveaninfusionoflactatedRinger’ssolutiontoconvertlactatetobicarbonateintheliver,therebyincreasingthebasebicarbonatelevelandcorrectingacidosis.Inseverehyperchloremia,thepatientmayneedI.V.sodiumbicarbonatetoraiseserumbicarbonatelevels.Becausebicarbonateandchloridecompeteforsodium,I.V.sodiumbicarbonatetherapycanleadtorenalexcretionofchlorideionsandcorrectionofacidosis.
HowyouinterveneTrytopreventhyperchloremiabymonitoringhigh-riskpatients.Ifyourpatientdevelopsachlorideimbalance,followthesesteps:•Monitorvitalsigns,includingcardiacandrespiratoryrhythm.•Ifthepatientisconfused,reorienthimasneeded,andprovideasafe,quietenvironmentto
preventinjury.Teachthepatient’sfamilytodothesame.(SeeTeachingabouthyperchloremia.)
Teachingpoints
Teachingpoints
TeachingabouthyperchloremiaWhenteachingapatientwithhyperchloremia,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
signsandsymptoms,complications,andriskfactors•
warningsignsandsymptomstoreporttothepractitioner•
dietaryrestrictionsifordered•
medicationsifprescribed•
importanceofreplenishinglostfluidsduringhotweather.
•Continuallyassessthepatient,payingparticularattentiontotheneurologic,cardiac,andrespiratoryexaminations.Immediatelyreportchangestothepractitioner.
•Lookforchangesintherespiratorypatternthatmayindicateaworseningofacid-baseimbalance.
•InsertanI.V.andmaintainitspatency.AdministerI.V.fluidsandmedicationsasordered.Watchforsignsandsymptomsoffluidoverload.
•Evaluatemusclestrengthandadjustthepatient’sactivitylevelaccordingly.•Ifthepatientisreceivinghighdosesofsodiumbicarbonate,watchforsignsandsymptomsof
overcompensation,suchasmetabolicalkalosis,whichmaycausecentralandperipheralnervoussystemoverstimulation.Also,watchforsignsandsymptomsofhypokalemiaaspotassiumisforcedintothecells.
•Restrictfluids,sodium,andchloride,ifordered.•MonitorandrecordserumelectrolytelevelsandABGresults.•Monitorandrecordfluidintakeandoutput.(SeeDocumentinghyperchloremia.)
Chartsmart
DocumentinghyperchloremiaIfyourpatienthashyperchloremia,makesureyoudocumentthefollowinginformation:•
vitalsigns,includingcardiacrhythm•
LOC•
musclestrength•
activitylevel•
serumelectrolyteandABGlevels•
fluidintakeandoutput•
safetyprecautionstaken•
yourassessmentsandinterventionsandthepatient’sresponse•
patientteachingandresponse.
That’sawrap!
Chlorideimbalancesreview
Chloridebasics•
Mostabundantanioninextracellularfluid•
Moveswithsodiumandpotassium
•Helpsmaintainserumosmolalityandwaterbalance•
Cancombinewithsodium,helpingthechoroidplexustoattractwaterandformCSF•
Isalsofoundinbileandgastricandpancreaticjuicesintheformofhydrochloricacid,whichaidsdigestionandenzymeactivation•
Helpsmaintainacid-basebalanceandcarbondioxidetransportinredbloodcells•
Normalrange:98to108mEq/L
Chloridebalance•
Regulationdependsonintakeandexcretionofchlorideandreabsorptionofchlorideionsbythekidneys.•
Chlorideisabsorbedintheintestines;GIdisordersmayaffectbalance.•
Sodiumlevelsarecloselylinkedwithchlorideandaffectedbyaldosteronesecretion.•
Theinverserelationshiptobicarbonateaffectsacid-basebalance.
Hypochloremia•
Canbecausedby:–
poorchlorideintakebecauseofasalt-restricteddiet,chloride-deficientinfantformula,orI.V.fluidreplacementwithoutelectrolytesupplementation–
excessivelossesfromtheGItract,skin,orkidneys–
sodiumorpotassiumdeficiencyormetabolicalkalosis,diabeticketoacidosis,Addison’sdisease,diuretics,rapidremovalofasciticfluid,andheartfailure
Signsandsymptoms•
Hyperactivedeeptendonreflexes•
Musclehypertonicityandcramps•
Signsandsymptomsofacid-baseimbalance(alkalosis)andelectrolyteimbalances(hyponatremia
andhypokalemia)•
Tetany
Treatment•
Increaseddietaryintake•
Treatmentofunderlyingcauseofmetabolicalkalosis•
I.V.salinesolutionwitheithersodiumchlorideorpotassiumchloride
Hyperchloremia•
Rarelyoccursonitsown;oftenassociatedwithotheracid-baseimbalances(suchasmetabolicacidosis)•
Chlorideandsodiumcloselyrelated;hypernatremiamaycausehyperchloremia•
Bicarbonateandchlorideinverselyrelated;hyperchloremiamayoccurifbicarbonatedecreases•
Alsomayresultfromincreasedchlorideanddecreasedwaterintake,decreasedabsorptionofchloridefromintestines,andcertainmedications
Signsandsymptoms•
Associatedwithmetabolicacidosis(whichrarelyproducessignsandsymptomsonitsown),suchastachypnea,lethargy,changesincognition,andweaknessSeveremetabolicacidosis•
Arrhythmias•
Kussmaul’srespirations•
Decreasedcardiacoutput•
DecreasedLOCthatmayprogresstocoma
Treatment•
I.V.fluidstospeedrenalexcretionofchloride•
Restrictedsodiumandchlorideintake•
I.V.sodiumbicarbonateforseverehyperchloremia
Quickquiz
1.Chlorideisprimarilyproducedbythe:A.brain.B.kidneys.C.heart.D.stomach.
Answer:D.Thechlorideionislargelyproducedbygastricmucosaandoccursintheformofhydrochloricacid.
2.Ifthelevelofbicarbonateionsincreases,thelevelofchlorideions:A.increases.B.decreases.C.staysthesame.D.isn’taffected.
Answer:B.Chlorideionsandbicarbonateionshaveaninverselyproportionalrelationship.Ifonelevelrises,theotherleveldrops.
3.Inapostoperativepatientwhohasachlorideimbalance,youwouldalsoexpecttoseeachangeintheelectrolyte:
A.calcium.B.potassium.C.sodium.D.phosphate.
Answer:C.Sodiumandchloridemovetogetherthroughthebody,soanimbalanceinoneusuallycausesanimbalanceintheother.
4.Ifapatienthasalowserumchloridelevel,whatacid-baseimbalancewouldyouexpecttosee?
A.RespiratoryacidosisB.MetabolicacidosisC.MetabolicalkalosisD.Respiratoryalkalosis
Answer:C.Adropinchlorideionscausesthebodytoretainbicarbonate—abase—and
resultsinhypochloremicmetabolicalkalosis.
5.Deep,rapidbreathingmayindicatea:A.serumchloridelevelgreaterthan108mEq/L.B.serumchloridelessthan98mEq/L.C.pHgreaterthan7.45.D.normalchloridelevels.
Answer:A.Deep,rapidbreathing,orKussmaul’srespirations,isthebody’sattempttoblowoffexcessacidintheformofcarbondioxide.Whenthisoccurs,suspectmetabolicacidosis,aconditionassociatedwithaserumchloridelevelgreaterthan108mEq/L.
ScoringIfyouansweredallfivequestionscorrectly,incredible!You’rethesaltoftheEarthwhenitcomestochlorideimbalances.Ifyouansweredfourquestionscorrectly,super!You’reobviouslyintheloopaboutchlorideimbalances.Ifyouansweredfewerthanfourquestionscorrectly,that’sokay.Yourchlorideintakefromthechapterisalittlelow,buttheimbalancecanbeeasilycorrectedbyreviewingthechapter.
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Hyperchloremiaafternoncardiacsurgeryisindependentlyassociatedwithincreasedmorbidityandmortality:Apropensity-matchedcohortstudy.AnesthesiaandAnalgesia,117(2),412–421.doi:10.1213/ANE.0b013e318293d81e
McIntosh,E.,&Andrews,P.J.(2013).Issodiumchlorideworthitssalt?CriticalCare,17(3),150.MedlinePlus.(2013).Chlorideindiet.Retrievedfrom
http://www.nlm.nih.gov/medlineplus/ency/article/002417.htmMiyahara,J.,AramakiS.,&Yokochi,K.(2009).Dietarychloridedeficiencyduetonewliquidnutritional
products.PediatricsInternational,51(2),197–200.doi:10.1111/j.1442-200X.2008.02670.xSeifter,J.R.(2011).Acid-basedisorders.InL.Goldman&A.I.Schafer(Eds.),CecilMedicine(24th
ed.,ch.120).Philadelphia,PA:Saunders.Tani,M.,Morimatsu,H.,Takatsu,F.,&Morita,K.(2012).Theincidenceandprognosticvalueof
hypochloremiaincriticallyillpatients.ScientificWorldJournal,2012,474185.doi:10.1100/2012/474185
Tutay,G.J.,Capraro,G.,Spirko,B.,Garb,J.,&Smithline,H.(2013).Electrolyteprofileofpediatricpatientswithhypertrophicpyloricstenosis.PediatricEmergencyCare,29(4),465–468.doi:10.1097/PEC.0b013e31828a3006
Yan,M.T.,Yang,S.S.,Chu,H.Y.,&Lin,S.H.(2009).Ataxiaassociatedwithspurioushyperchloremia:Theonebehindthescene.AmericanJournalofEmergencyMedicine,27(6),752.e1–752.e3.doi:10.1016/j.ajem.2008.09.044
Chapter11
Whenacidsandbasestipthebalance
JustthefactsInthischapter,you’lllearn:
♦thebody’smechanismsformaintainingacid-basebalance
♦conditionsthattriggeracid-baseimbalances
♦waystodifferentiatethefourrespiratoryandmetabolicacid-baseimbalances
♦propercareforthepatientwithanacid-baseimbalance.
Alookatacid-baseimbalancesThebodyconstantlyworkstomaintainabalance(homeostasis)betweenacidsandbases.Withoutthatbalance,cellscan’tfunctionproperly.Ascellsusenutrientstoproducetheenergytheyneedtofunction,twoby-productsareformed—carbondioxideandhydrogen.Acid-basebalancedependsontheregulationoffreehydrogenions.Theconcentrationofhydrogenionsinbodyfluidsdeterminestheextentofacidityoralkalinity,bothofwhicharemeasuredinpH.Remember,pHlevelsareinverselyproportionatetohydrogenionconcentration,whichmeansthatwhenhydrogenconcentrationincreases,pHdecreases(acidosis).Conversely,whenhydrogenconcentrationdecreases,pHincreases(alkalosis).(FormoreinformationaboutpH,seechapter3,Balancingacidsandbases.)
GasgivesgoodanswersBloodgasmeasurementsremainthemajordiagnostictoolforevaluatingacid-basestates.Anarterialbloodgas(ABG)analysisincludesthesetests:pH,whichmeasuresthehydrogenionconcentrationandisanindicationoftheblood’sacidityoralkalinity;partialpressureofarterialcarbondioxide(PaCO2),whichreflectstheadequacyofventilationbythelungs;andbicarbonatelevel,whichreflectstheactivityofthekidneysinretainingorexcretingbicarbonate.(SeeTheABCsofABGs.)
TheABCsofABGs
ThischartlistsnormalABGlevelsforadultpatients.pH 7.35to7.45PaCO2 35to45mmHg
Bicarbonate 22to26mEq/L
Normalfix-me-upsMostofthetime,thebody’scompensatorymechanismsrestoreacid-basebalance—oratleastpreventthelife-threateningconsequencesofanimbalance.Thosecompensatorymechanismsincludechemicalbuffers,certainrespiratoryreactions,andcertainkidneyreactions.Forexample,thebodycompensatesforaprimaryrespiratorydisturbancesuchasrespiratory
acidosisbyinducingmetabolicalkalosis.Unfortunately,notallattemptstocompensateareequal.Therespiratorysystemisefficientandcancompensateformetabolicdisturbancesquickly,whereasthemetabolicsystem,workingthroughthekidneys,cantakehoursordaystocompensate
foranimbalance,thereforeinterventioninnecessaryinordertofurtherpatientdeterioration.Thischaptertakesacloserlookateachofthefourmajoracid-baseimbalances.
RespiratoryacidosisAcompromiseinanyofthethreeessentialpartsofbreathing—ventilation,perfusion,ordiffusion—mayresultinrespiratoryacidosis.Thisacid-basedisturbanceischaracterizedbyalveolarhypoventilation,meaningthepulmonarysystemisunabletoridthebodyofenoughcarbondioxidetomaintainahealthypHbalance.Thisoccursbecauseofdecreasedrespirationorinadequategasexchange.
ThelackofefficientcarbondioxidereleaseleadstohypercapniainwhichPaCO2isgreaterthan45mmHg.Theconditioncanbeacute,resultingfromsuddenfailureinventilation,orchronic,resultingfromchronicpulmonarydisease.Inacuterespiratoryacidosis,pHdropsbelownormal(lowerthan7.35).Inchronicrespiratory
acidosis,commonlyduetochronicobstructivepulmonarydisease(COPD),pHstayswithinnormallimits(7.35to7.45)becausethekidneyshavehadtimetocompensatefortheimbalance.(Moreonthatcomplexphenomenonlater.)
HowithappensWhenapatienthypoventilates,carbondioxidebuildsupinthebloodstreamandpHdropsbelownormal—respiratoryacidosis.ThekidneystrytocompensateforadropinpHbyconservingbicarbonate(base)ions,orgeneratingtheminthekidneys,whichinturnraisesthepH.(SeeWhathappensinrespiratoryacidosis.)
WhathappensinrespiratoryacidosisThisseriesofillustrationsshowshowrespiratoryacidosisdevelopsatthecellularlevel.Whenpulmonaryventilationdecreases,retainedcarbondioxide(CO2)combineswithwater
(H2O)toformcarbonicacid(H2CO3)inlarger-than-normalamounts.Thecarbonicaciddissociatestoreleasefreehydrogenions(H+)andbicarbonateions(HCO3
−).TheexcessivecarbonicacidcausesadropinpH.LookforaPaCO2levelabove45mmHgandapHlevelbelow7.35.
AsthepHlevelfalls,hemoglobin(Hb)releaseoxygen(O2).ThealteredHb,nowstronglyalkaline,picksupH+andCO2,thuseliminatingsomeofthefreeH+andexcessCO2.Lookfordecreasedarterialoxygensaturation.
WheneverPaCO2increases,CO2buildsupinalltissuesandfluids,includingcerebrospinalfluidandtherespiratorycenterinthemedulla.TheCO2reactswithH2OtoformH2CO3,whichthenbreaksintofreeH+andHCO3
−.TheincreasedamountofCO2andfreeH+stimulatetherespiratorycentertoincreasetherespiratoryrate.AnincreasedrespiratoryrateexpelsmoreCO2andhelpstoreducetheCO2levelinbloodandtissues.Lookforrapid,shallowrespirationsandadecreasingPaCO2.
Eventually,CO2andH+causecerebralbloodvesselstodilate,whichincreasesbloodflowtothebrain.Thatincreasedflowcancausecerebraledemaanddepresscentralnervoussystemactivity.Lookforheadache,confusion,lethargy,nausea,diaphoresis,tachycardia,andvomiting.
Asrespiratorymechanismsfail,theincreasingPaCO2stimulatesthekidneystoconserveHCO3−
andsodiumions(Na)andtoexcreteH+,someintheformofammonium(NH4).TheadditionalHCO3−
andNacombinetoformextrasodiumbicarbonate(NaHCO3−),whichisthenabletobuffermorefree
H+.Lookforincreasedacidcontentintheurine;increasedserumpHandHCO3−levels;andshallow,depressedrespirations.
AstheconcentrationofH+overwhelmsthebody’scompensatorymechanisms,theH+moveintothecells,andpotassiumions(K)moveout.AconcurrentlackofO2causesanincreaseintheanaerobicproductionoflacticacid,whichfurtherskewstheacid-basebalanceandcriticallydepressesneurologicandcardiacfunctions.Lookforhyperkalemia,arrhythmias,increasedPaCO2,decreasedPaO2,decreasedpH,anddecreasedlevelofconsciousness.
Respiratoryacidosiscanresultfromneuromuscularproblems,depressionoftherespiratorycenterinthebrain,lungdisease,obesity,postoperativepain,oranairwayobstruction.
ThatbreathlessfeelingIncertainneuromusculardiseases—suchasGuillain-Barrésyndrome,myastheniagravis,andpoliomyelitis—therespiratorymusclesfailtorespondproperlytotherespiratorydrive,resultinginrespiratoryacidosis.Diaphragmaticparalysis,whichcommonlyoccurswithspinalcordinjury,worksthesamewaytocauserespiratoryacidosis.Hypoventilationfromcentralnervoussystem(CNS)traumaorbrainlesions—suchastumors,
vasculardisorders,orinfections—mayimpairthepatient’sventilatorydrive.Obesity(asinpickwickiansyndrome)orprimaryhypoventilation(asinOndine’scurse)maycontributetothisimbalanceaswell.Also,certaindrugs—includinganesthetics,hypnotics,opioids,andsedatives—candepresstherespiratorycenterofthebrain,leadingtohypercapnia.(SeeDrugsassociatedwithrespiratoryacidosis.)
DrugsassociatedwithrespiratoryacidosisThefollowingdrugsareassociatedwithrespiratoryacidosis:•
anesthetics•
hypnotics•
opioids•
sedatives.
ScantysurfaceLungdiseasesthatdecreasetheamountofpulmonarysurfaceareaavailableforgasexchangecanpromptrespiratoryacidosis.Lesssurfaceareadecreasestheamountofgasexchangethatcan
occur,thusimpedingcarbondioxideexchange.Examplesofpulmonaryproblemsthatcandecreasesurfaceareaincluderespiratoryinfections,COPD,acuteasthmaattacks,chronicbronchitis,latestagesofadultrespiratorydistresssyndrome,pulmonaryedema,conditionsinwhichthere’sincreaseddeadspaceinthelungs(hypoventilation),andphysiologicoranatomicshunts.Chestwalltrauma(leadingtopneumothoraxorflailchest)canalsocauserespiratoryacidosis.
Theventilatorydriveremainsintact,butthechestwallmechanicsofthecollapsedlungdon’tallowforsufficientalveolarventilationtomeetthebody’sneeds.Chestwallmechanicscanalsobeimpededasaresultoftheribcagedistortioncausedbyfibrothoraxorkyphoscoliosis.
Danger!ObstructionaheadRespiratoryacidosiscanalsobecausedbyairwayobstruction,whichleadstocarbondioxideretentioninthelungs.Airwayobstructioncanoccurasaresultofretainedsecretions,tumors,anaphylaxis,laryngealspasm,orlungdiseasesthatinterferewithalveolarventilation.Keepinmindthatchildrenareparticularlypronetoairwayobstruction,asareelderlyanddebilitatedpatients,whomaynotbeabletoeffectivelyclearsecretions.Otherfactorsalsoincreaseaninfant’sriskofdevelopingacidosis.(SeeInfantsandacidosis.)
Agesandstages
InfantsandacidosisInfantscommonlyhaveproblemswithacid-baseimbalances,particularlyacidosis.Becauseoflowresiduallungvolume,anyalterationinrespirationcanrapidlyanddramaticallychangepartialpressureofarterialcarbondioxide,leadingtoacidosis.Infantsalsohaveahighmetabolicrate,whichyieldslargeamountsofmetabolicwastesandacids
thatmustbeexcretedbythekidneys.Alongwiththeirimmaturebuffersystem,theseage-relateddifferencesleaveinfantspronetoacidosis.
RiskybusinessTreatmentscanalsoinducerespiratoryacidosis.Forinstance,mechanicalventilationthatunderventilatesapatientcancausecarbondioxideretention.Apostoperativepatientisatriskforrespiratoryacidosisiffearofpainpreventshimfromparticipatinginpulmonaryhygienemeasures,suchasusingtheincentivespirometerandcoughinganddeepbreathing.Also,analgesicsorsedativescandepressthemedulla(whichcontrolsrespirations),leadingtoinadequateventilationandsubsequentrespiratoryacidosis.
WhattolookforSignsandsymptomsofrespiratoryacidosisdependonthecauseofthecondition.Thepatientmaycomplainofaheadachebecausecarbondioxidedilatescerebralbloodvessels.(SeeSignsandsymptomsofrespiratoryacidosis.)
CAUTION!
SignsandsymptomsofrespiratoryacidosisThefollowingassessmentfindingscommonlyoccurinpatientswithrespiratoryacidosis:•
apprehension•
confusion•
decreaseddeeptendonreflexes•
diaphoresis•
dyspnea,withrapid,shallowrespirations•
headache•
nausea•
restlessness•
tachycardia•
tremors•
vomiting•
warm,flushedskin.
CNSdepressionmayresultinanalteredlevelofconsciousness(LOC),rangingfromrestlessness,confusion,andapprehensiontosomnolenceandcoma.Ifacidosisremainsuntreated,afineflappingtremoranddepressedreflexesmaydevelop.Thepatientmayalsoreportnauseaandvomiting,andtheskinmaybewarmandflushed.
Abreakdowninbreathing
Mostpatientswithrespiratoryacidosishaverapid,shallowrespirations;theymaybedyspneicanddiaphoretic.Auscultationrevealsdiminishedorabsentbreathsoundsovertheaffectedarea.However,ifacidosisstemsfromCNStraumaorlesionsordrugoverdose,therespiratoryrateisgreatlydecreased.Inapatientwithacidosis,hyperkalemia,andhypoxemia,youmaynotetachycardiaand
ventriculararrhythmias.Cyanosisisalatesignofthecondition.Resultingmyocardialdepressionmayleadtoshockand,ultimately,cardiacarrest.
WhattestsshowSeveraltestresultshelpconfirmadiagnosisofrespiratoryacidosisandguidetreatment:•ABGanalysisisthekeytestfordetectingrespiratoryacidosis.Typically,pHisbelow7.35,
andPaCO2isabove45mmHg.Thebicarbonatelevelvaries,dependingonhowlongtheacidosishasbeenpresent.Inapatientwithacuterespiratoryacidosis,bicarbonatemaybenormal;inapatientwithchronicrespiratoryacidosis,itmaybeabove26mEq/L.(SeeABGresultsinrespiratoryacidosis.)
•ChestX-rayscanhelppinpointsomecauses,suchasCOPD,pneumonia,pneumothorax,andpulmonaryedema.
•Serumelectrolytelevelswithpotassiumgreaterthan5mEq/Ltypicallyindicatehyperkalemia.Inacidosis,potassiumleavesthecell,soexpectserumleveltobeelevated.
•Drugscreeningmayconfirmasuspectedoverdose.
Howit’streatedTreatmentofrespiratoryacidosisfocusesonimprovingventilationandloweringPaCO2.Ifrespiratoryacidosisstemsfromnonpulmonaryconditions,suchasneuromusculardisordersoradrugoverdose,treatmentaimstocorrectorimprovetheunderlyingcause.Treatmentforrespiratoryacidosiswithapulmonarycauseincludes:
•abronchodilatortoopenconstrictedairways•supplementaloxygenasneeded•drugtherapytotreathyperkalemia
•antibiotictherapytotreatinfection•chestphysiotherapytoremovesecretionsfromthelungs•removalofaforeignbodyfromthepatient’sairwayifneeded(SeeWhenhypoventilationcan’tbecorrected.)
•painmedicationtocontrolpaintopromoteeffectivebreathing.
It'snotworking
Whenhypoventilationcan’tbecorrectedIfhypoventilationcan’tbecorrected,expectyourpatienttohaveanartificialairwayinsertedandthenreceivemechanicalventilation.Beawarethathemayrequirebronchoscopytoremoveretainedsecretions.
HowyouinterveneIfyourpatientdevelopsrespiratoryacidosis,maintainapatentairway.Helpremoveanyforeignbodiesfromhisairwayandestablishanartificialairway.Provideadequatehumidificationtokeepthepatient’ssecretionsmoist.Also,followthesemeasures:
•Monitorvitalsigns,andassesscardiacrhythm.Respiratoryacidosiscancausetachycardia,
alterationsinrespiratoryrateandrhythm,hypotension,andarrhythmias.•Continuetoassessrespiratorypatterns,andreportchangesquickly.Prepareformechanical
ventilationifindicated.•Institutemeasurestopreventventilator-associatedpneumonia.•Monitorthepatient’sneurologicstatus,andreportsignificantchanges.Alsomonitorcardiac
functionbecauserespiratoryacidosismayprogresstoshockandcardiacarrest.•ReportanyvariationsinABGlevels,pulseoximetry,orserumelectrolytelevels.•Givemedications,suchasanantibioticorabronchodilator,asprescribed.(SeeTeachingaboutrespiratoryacidosis.)
Teachingpoints
TeachingaboutrespiratoryacidosisWhenteachingapatientwithrespiratoryacidosis,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
descriptionoftheconditionandhowtopreventit•
reasonsforrepeatedABGanalyses•
deep-breathingexercises•
prescribedmedications•
homeoxygentherapyifindicated•
warningsignsandsymptomsandwhentoreportthem•
propertechniqueforusingbronchodilators,ifappropriate•
needforfrequentrest•
needforincreasedcaloricintakeifappropriate.
Oxygen:Toomuchofagoodthing•Administeroxygenasordered.Generally,patientswithCOPDshouldreceivelower
concentrationsofoxygen.ThemedullaofapatientwithCOPDisaccustomedtohighcarbondioxidelevels.Alackofoxygen,calledthehypoxicdrive,stimulatesthosepatientstobreathe.Toomuchoxygendiminishesthatdriveanddepressesrespiratoryefforts.
•Performtrachealsuctioning,incentivespirometry,posturaldrainage,andcoughinganddeepbreathingexercisesasindicated.
•Makesurethepatienttakesinenoughfluids,bothoralandI.V.,andmaintainaccurateintakeandoutputrecords.(SeeDocumentingrespiratoryacidosis.)
Chartsmart
DocumentingrespiratoryacidosisIfyourpatienthasrespiratoryacidosis,makesureyoudocumentthefollowinginformation:•
vitalsignsandcardiacrhythm•
intakeandoutput•
yourassessmentfindingsandinterventionsandthepatient’sresponse•
notificationofthepractitioner•
medicationsadministered•
oxygentherapyandventilatorsettings•
characterofpulmonarysecretions•
serumelectrolytelevelsandABGresults•
patientteaching.
•Providereassurancetothepatientandfamily.•Keepinmindthatanysedativesyougivetothepatientcandecreasehisrespiratoryrate.•Institutesafetymeasuresasneededtoprotectaconfusedpatient.
Asyoureevaluateyourpatient’scondition,considerthesequestions:•Havethepatient’srespiratoryrateandLOCreturnedtonormal?•Doesauscultationofthepatient’schestrevealreducedadventitiousbreathsounds?•Havetachycardiaandventriculararrhythmiasbeenstabilized?•Havethepatient’scyanosisanddyspneadiminished?•Havethepatient’sABGresultsandserumelectrolytelevelsreturnedtonormal?•DochestX-raysshowimprovementintheconditionofthepatient’slungs?
RespiratoryalkalosisTheoppositeofrespiratoryacidosis,respiratoryalkalosisresultsfromalveolarhyperventilationandhypocapnia.Inrespiratoryalkalosis,increasedeliminationofcarbondioxideoccurs;therefore,pHisgreaterthan7.45andPaCO2islessthan35mmHg.Acuterespiratoryalkalosisresultsfromasuddenincreaseinventilation.Chronicrespiratoryalkalosismaybedifficulttoidentifybecauseofrenalcompensation.
HowithappensAnyclinicalconditionthatincreasesrespiratoryrateordepthcancausethelungstoeliminate,or“blowoff,”carbondioxide.Becausecarbondioxideisanacid,eliminatingitcausesadecreaseinPaCO2alongwithanincreaseinpH—alkalosis.
Hyperventilation(gasp!)Themostcommoncauseofacuterespiratoryalkalosisishyperventilationstemmingfromanxietyorpanicattack.Itmayalsooccurduringcardiopulmonaryresuscitationwhenrescuers
hyperventilatethepatientat30to40breathsperminute.Paincanhavethesameeffect.Hyperventilationisalsoanearlysignofsalicylateintoxicationandcanoccurwiththeuseofnicotine,xanthinessuchasaminophylline,andotherdrugs.(SeeDrugsassociatedwithrespiratoryalkalosis.)
DrugsassociatedwithrespiratoryalkalosisDrugsassociatedwithrespiratoryalkalosisinclude:•
catecholamines•
nicotine•
salicylates•
xanthinessuchasaminophylline.
Hypermetabolicstates—suchasfever,liverfailure,andsepsis(especiallygram-negativesepsis)—canleadtorespiratoryalkalosis.Conditionsthataffecttherespiratorycontrolcenterinthemedullaarealsoadanger.Forexample,thehigherprogesteronelevelsduringpregnancymaystimulatethiscenter,whereasstrokeortraumamayinjureit,bothresultinginrespiratoryalkalosis.
Hypoxia(pant!)Acutehypoxia,secondarytohighaltitude,pulmonarydisease,severeanemia,pulmonaryembolus,orhypotension,cancauserespiratoryalkalosis.Suchconditionsmayoverstimulatetherespiratorycenterandcausethepatienttobreathefasteranddeeper.Overventilationduringmechanicalventilationcausesthelungstoblowoffmorecarbondioxide,resultinginrespiratoryalkalosis.
WhattolookforAnincreaseintherateanddepthofrespirationsisaprimarysignofrespiratoryalkalosis.It’salsocommonforthepatienttohavetachycardia.Thepatientmayappearanxiousandrestlessaswellascomplainoflightheadedness,muscleweakness,fear,ordifficultybreathing.(SeeWhathappensinrespiratoryalkalosis.)
WhathappensinrespiratoryalkalosisThisseriesofillustrationsshowshowrespiratoryalkalosisdevelopsatthecellularlevel.Whenpulmonaryventilationincreasesabovetheamountneededtomaintainnormalcarbon
dioxide(CO2)levels,excessiveamountsofCO2areexhaled.Thiscauseshypocapnia(afallinPaCO2),whichleadstoareductionincarbonicacid(H2CO3)production,alossofhydrogenions(H+)andbicarbonateions(HCO3
−),andasubsequentriseinpH.LookforapHlevelabove7.45,aPaCO2levelbelow35mmHg,andanHCO3
−levelbelow22mEq/L.
IndefenseagainsttherisingpH,H+arepulledoutofthecellsandintothebloodinexchangeforpotassiumions(K).TheH+enteringthebloodcombinewithHCO3
−toformH2CO3,whichlowerspH.LookforafurtherdecreaseinHCO3
−levels,afallinpH,andafallinserumpotassiumlevels(hypokalemia).
Hypocapniastimulatesthecarotidandaorticbodiesandthemedulla,whichcausesanincreaseinheartratewithoutanincreaseinbloodpressure.Lookforangina,electrocardiogramchanges,restlessness,andanxiety.
Simultaneously,hypocapniaproducescerebralvasoconstriction,whichpromptsareductionincerebralbloodflow.Hypocapniaalsooverexcitesthemedulla,pons,andotherpartsoftheautonomicnervoussystem.Lookforincreasinganxiety,fear,diaphoresis,dyspnea,alternatingperiodsofapneaandhyperventilation,dizziness,andtinglinginthefingersortoes.
Whenhypocapnialastsmorethan6hours,thekidneysincreasesecretionofHCO3−andreduce
excretionofH+.PeriodsofapneamayresultifthepHremainshighandthePaCO2remainslow.Lookforslowedrespiratoryrate,hypoventilation,andCheyne-Stokes’respirations.
.
ContinuedlowPaCO2increasescerebralandperipheralhypoxiafromvasoconstriction.Severealkalosisinhibitscalcium(Ca)ionization,whichinturncausesincreasednerveexcitabilityandmusclecontractions.Eventually,thealkalosisoverwhelmstheCNSandtheheart.LookfordecreasingLOC,hyperreflexia,carpopedalspasm,tetany,arrhythmias,seizures,andcoma.
InextremisInextremealkalosis,confusionorsyncopemayoccur.Becauseofthelackofcarbondioxideinthebloodanditseffectoncerebralbloodflowandtherespiratorycenter,youmayseealternatingperiodsofapneaandhyperventilation.Thepatientmaycomplainoftinglinginthefingersandtoes.
ECGexposéYoumayseeelectrocardiogram(ECG)changes,includingaprolongedPRinterval,aflattenedTwave,aprominentUwave,andadepressedSTsegment.(Formoreinformation,seechapter6,Whenpotassiumtipsthebalance.)
SignsoftroubleSignsandsymptomsworsenascalciumlevelsdropbecauseofvasoconstrictionofperipheralandcerebralvesselsresultingfromhypoxia.Youmayseehyperreflexia,carpopedalspasm,tetany,arrhythmias,aprogressivedecreaseinthepatient’sLOC,seizures,orcoma.(SeeSignsandsymptomsofrespiratoryalkalosis.)
CAUTION!
SignsandsymptomsofrespiratoryalkalosisThefollowingassessmentfindingscommonlyoccurinpatientswithrespiratoryalkalosis:•
anxiety•
diaphoresis•
dyspnea(increasedrespiratoryrateanddepth)•
ECGchanges•
hyperreflexia•
paresthesia•
restlessness•
tachycardia•
tetany.
WhattestsshowSeveraldiagnostictestresultsmayhelpdetectrespiratoryalkalosisandguidetreatment:•ABGanalysisisthekeydiagnostictestforidentifyingrespiratoryalkalosis.Typically,pHis
above7.45andPaCO2isbelow35mmHg.Thebicarbonatelevelmaybenormal(22to26mEq/L)whenalkalosisisacutebutusuallyfallsbelow22mEq/Lwhenalkalosisischronic.(SeeABGresultsinrespiratoryalkalosis.)
•Serumelectrolytelevelsmaypointtoametabolicdisorderthatiscausingcompensatoryrespiratoryalkalosis.Hypokalemiamaybeevident,signaledbydecreasedLOC.Theionizedserumcalciumlevelmaybedecreasedinthosewithsevererespiratoryalkalosis.
•ECGfindingsmayindicatearrhythmiasorthechangesassociatedwithhypokalemiaorhypocalcemia.
•Toxicologyscreeningmayrevealsalicylatepoisoning.
Howit’streatedTreatmentfocusesoncorrectingtheunderlyingdisorder,whichmayrequireremovingthecausativeagent,suchasasalicylateorotherdrug,ortakingstepstoreducefeverandeliminatethesourceofsepsis.Ifacutehypoxemiaisthecause,thepatientwillneedoxygentherapy.Ifanxietyisthecause,thepatientmayreceiveasedativeorananxiolytic.Ifthepatientishavingpain,thepatientmayreceiveananalgesic.
It’sinthebagTocounteracthyperventilation,thepatientcanbreatheintoapaperbagorintocuppedhands.Thisforcesthepatienttobreatheexhaledcarbondioxide,therebyraisingthecarbondioxidelevel.Ifapatient’srespiratoryalkalosisismedicallyinduced,mechanicalventilatorsettingsmaybeadjustedbydecreasingthetidalvolumeorthenumberofbreathsperminute.
HowyouinterveneMonitorpatientsatriskfordevelopingrespiratoryalkalosis.Ifyourpatientdevelopsthecondition,taketheseactions:•Allayanxietywheneverpossibletopreventhyperventilation.Recommendactivitiesthat
promoterelaxation.Helpthepatientbreathintoapaperbagorcuppedhandsifnecessary.•Monitorvitalsigns.Reportchangesinneurologic,neuromuscular,orcardiovascular
functioning.•MonitorABGandserumelectrolytelevels,andimmediatelyreportanyvariations.Remember,
twitchingandarrhythmiasmaypointtoalkalosisandelectrolyteimbalances.
•Ifthepatientisreceivingmechanicalventilation,checkventilatorsettingsfrequently.MonitorABGlevelsaftermakingchangesinsettings.
•Provideundisturbedrestperiodsafterthepatient’srespiratoryratereturnstonormal;hyperventilationmayresultinseverefatigue.
•Staywiththepatientduringperiodsofextremestressandanxiety.Offerreassurance,andmaintainacalm,quietenvironment.(SeeTeachingaboutrespiratoryalkalosis.)
•Institutesafetymeasuresandseizureprecautionsasneeded.•Documentallcare.(SeeDocumentingrespiratoryalkalosis.)
Teachingpoints
TeachingaboutrespiratoryalkalosisWhenteachingapatientwithrespiratoryalkalosis,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
explanationoftheconditionanditstreatment•
warningsignsandsymptomsandwhentoreportthem•
anxiety-reducingtechniquesifappropriate•
controlled-breathingexercisesifappropriate•
prescribedmedications.
Chartsmart
DocumentingrespiratoryalkalosisIfyourpatienthasrespiratoryalkalosis,makesureyoudocumentthefollowinginformation:•
vitalsigns•
intakeandoutput•
I.V.therapy•
interventions,includingmeasurestakentoalleviateanxiety•
patient’sresponsetointerventions•
serumelectrolytelevelsandABGresults•
safetymeasures•
notificationofthepractitioner•
patientteaching.
MetabolicacidosisMetabolicacidosisiscausedbyanincreaseinhydrogenionproductionandischaracterizedbyapHbelow7.35andabicarbonatelevelbelow22mEq/L.ThisdisorderdepressestheCNS.Leftuntreated,itmayleadtoventriculararrhythmias,coma,andcardiacarrest.
HowithappensTheunderlyingmechanismsinmetabolicacidosisarealossofbicarbonatefromextracellularfluid,anaccumulationofmetabolicacids,oracombinationofthetwo.Ifthepatient’saniongap
(measurementofthedifferencebetweentheamountofsodiumandtheamountofbicarbonateintheblood)isgreaterthan14mEq/L,thentheacidosisisaresultofanaccumulationofmetabolicacids(unmeasuredanions).Ifmetabolicacidosisisassociatedwithanormalaniongap(8to14mEq/L),lossof
bicarbonatemaybethecause.(SeeWhathappensinmetabolicacidosis,pages216and217.)
WhathappensinmetabolicacidosisThisseriesofillustrationsshowshowmetabolicacidosisdevelopsatthecellularlevel.Ashydrogenions(H+)starttoaccumulateinthebody,chemicalbuffers(plasmabicarbonate
[HCO3−]andproteins)inthecellsandextracellularfluidbindwiththem.Nosignsaredetectableat
thisstage.
ExcessH+thatcan’tbindwiththebuffersdecreasepHandstimulatechemoreceptorsinthemedullatoincreaserespiratoryrate.IncreasedrespiratoryratelowersPaCO2,whichallowsmoreH+
tobindwithHCO3−.Respiratorycompensationoccurswithinminutesbutisn’tsufficienttocorrectthe
imbalance.LookforapHlevelbelow7.35;anHCO3−levelbelow22mEq/L;adecreasingPaCO2
level;andrapid,deeperrespirations.
HealthykidneystrytocompensateforacidosisbysecretingexcessH+intotherenaltubules.Thoseionsarebufferedbyphosphateorammoniaandthenareexcretedintotheurineintheformofaweakacid.Lookforacidicurine.
EachtimeaH+issecretedintotherenaltubules,asodiumion(Na)andanHCO3−areabsorbed
fromthetubulesandreturnedtotheblood.LookforpHandHCO3−levelsthatslowlyreturnto
normal.
ExcessH+intheextracellularfluiddiffuseintocells.Tomaintainthebalanceofthechargeacrossthemembrane,thecellsreleasepotassiumions(K)intotheblood.Lookforsignsandsymptomsofhyperkalemia,includingcolicanddiarrhea,weaknessorflaccidparalysis,tinglingandnumbnessintheextremities,bradycardia,atallTwave,aprolongedPRinterval,andawideQRScomplex.
ExcessH+alterthenormalbalanceofK,Na,andcalciumions(Ca),leadingtoreducedexcitabilityofnervecells.LookforsignsandsymptomsofprogressiveCNSdepression,includinglethargy,dullheadache,confusion,stupor,andcoma.
Acidsanteup,basesbottomoutMetabolicacidosisischaracterizedbyagaininacidsoralossofbasesfromtheplasma.Theconditionmayberelatedtoanoverproductionofketonebodies.Thisoccurswhenthebodyhasusedupitsglucosesuppliesanddrawsonitsfatstoresforenergy,convertingfattyacidstoketonebodies.Conditionsthatcauseanoverproductionofketonebodiesincludediabetesmellitus,chronicalcoholism,severemalnutritionorstarvation,poordietaryintakeofcarbohydrates,hyperthyroidism,andsevereinfectionwithaccompanyingfever.Lacticacidosiscancauseorworsenmetabolicacidosisandcanoccursecondarytoshock,
heartfailure,pulmonarydisease,hepaticdisorders,seizures,orstrenuousexercise.
KidneyculpritMetabolicacidosiscanalsostemfromadecreasedabilityofthekidneystoexcreteacids,asoccursinrenalinsufficiencyorrenalfailurewithacutetubularnecrosis.
GutreactionsMetabolicacidosisalsooccurswithexcessivegastrointestinal(GI)lossesfromdiarrhea,intestinalmalabsorption,adrainingfistulaofthepancreasorliver,oraurinarydiversiontotheileum.Othercausesincludehyperaldosteronismanduseofapotassium-sparingdiureticsuchasacetazolamide,whichinhibitsthesecretionofacid.
PoisonpillsAtparticularriskformetabolicacidosisarepatientswithpoisoningoratoxicreactiontoadrug.Thiscanoccurfollowinginhalationoftolueneoringestionofasalicylate(suchasaspirinoranaspirin-containingmedication),methanol,ethyleneglycol,paraldehyde,hydrochloricacid,orammoniumchloride.
WhattolookforMetabolicacidosistypicallyproducesrespiratory,neurologic,andcardiacsignsandsymptoms.Asacidbuildsupinthebloodstream,thelungscompensatebyblowingoffcarbondioxide.Hyperventilation,especiallyincreaseddepthofrespirations,isthefirstcluetometabolic
acidosis.CalledKussmaul’srespirations,thebreathingisrapidanddeep.ApatientwithdiabeteswhoexperiencesKussmaul’srespirationsmayhaveafruitybreathodor.Theodorstemsfromcatabolismoffatsandexcretionofacetonethroughthelungs.
SodepressingAspHdrops,theCNSisfurtherdepressed,asismyocardialfunction.Cardiacoutputandbloodpressuredrop,andarrhythmiasmayoccurifthepatientalsohashyperkalemia.Initially,theskiniswarmanddryasaresultofperipheralvasodilationbut,asshockdevelops,
theskinbecomescoldandclammy.Thepatientmaycomplainofweaknessandadullheadacheasthecerebralvesselsdilate.Thepatient’sLOCmaydeterioratefromconfusiontostuporandcoma.Aneuromuscular
examinationmayshowdiminishedmuscletoneanddeeptendonreflexes.MetabolicacidosisalsoaffectstheGIsystem,causinganorexia,nausea,andvomiting.(SeeSignsandsymptomsofmetabolicacidosis.)
CAUTION!
SignsandsymptomsofmetabolicacidosisThefollowingassessmentfindingscommonlyoccurinpatientswithmetabolicacidosis:•
confusion•
decreaseddeeptendonreflexes•
dullheadache•
hyperkalemicsignsandsymptoms,includingabdominalcramping,diarrhea,muscleweakness,andECGchanges•
hypotension•
Kussmaul’srespirations•
lethargy•
warm,dryskin•
nausea•
fruitybreath•
coma.
WhattestsshowSeveraltestresultsmayhelpdiagnoseandtreatmetabolicacidosis:•ABGanalysisisthekeydiagnostictestfordetectingmetabolicacidosis.Typically,pHis
below7.35.PaCO2maybelessthan35mmHg,indicatingcompensatoryattemptsbythelungstoridthebodyofexcesscarbondioxide.(SeeABGresultsinmetabolicacidosis.)
•Serumpotassiumlevelsareusuallyelevatedashydrogenionsmoveintothecellsandpotassiummovesouttomaintainelectroneutrality.
•Bloodglucoseandserumketonelevelsriseinpatientswithdiabeticketoacidosis(DKA).•Plasmalactatelevelsriseinpatientswithlacticacidosis.(SeeAlookatlacticacidosis.)
AlookatlacticacidosisLactate,producedasaresultofcarbohydratemetabolism,ismetabolizedbytheliver.Thenormallactatelevelis0.93to1.65mEq/L.Withtissuehypoxia,however,cellsareforcedtoswitchtoanaerobicmetabolismandmorelactateisproduced.Whenlactateaccumulatesinthebodyfasterthanitcanbemetabolized,lacticacidosisoccurs.Itcanhappenanytimethedemandforoxygeninthebodyisgreaterthanitsavailability.Thecausesoflacticacidosisincludesepticshock,cardiacarrest,pulmonarydisease,seizures,and
strenuousexercise.Thelattertwocausetransientlacticacidosis.Hepaticdisorderscanalsocauselacticacidosis
becausethelivercan’tmetabolizelactate.
TreatmentTreatmentfocusesoneliminatingtheunderlyingcause.IfpHisbelow7.1,sodiumbicarbonateoranotheralkalinizingagentsuchastromethaminemaybegiven.Usecautionwhenadministeringsuchagentsbecausealkalosismayresult.
•Theaniongapisincreased.Thismeasurementiscalculatedbysubtractingtheamountofnegativeions(chlorideplusbicarbonate)fromtheamountofthepositiveion(sodium).Sometimes,theamountofpotassiumionisaddedtotheamountofpositiveion,buttheamountofpotassiumionisusuallysosmallthatthecalculationdoesn’tchange.Thenormalaniongapis8to14mEq/L.
•ECGchangesassociatedwithhyperkalemia—suchastallTwaves,prolongedPRintervals,andwideQRScomplexes—maybefound.
Howit’streatedTreatmentaimstocorrecttheacidosisasquicklyaspossiblebyaddressingboththesymptomsandtheunderlyingcause.Respiratorycompensationisusuallythefirstlineoftherapy,includingmechanicalventilationifneeded.
PutpotassiuminitsplaceForpatientswithdiabetes,expecttoadministerrapid-actinginsulintoreverseDKAanddrivepotassiumbackintothecell.Foranypatientwithmetabolicacidosis,monitorserumpotassiumlevels.Eventhoughthepatientinitiallyhashighserumpotassiumlevels,thelevelsdropasacidosisiscorrected,andthepatientmayendupwithhypokalemia.Anyotherelectrolyteimbalancesshouldbeevaluatedandcorrected.
BumpupthebicarbonateExpecttoadministerI.V.sodiumbicarbonatetoneutralizebloodacidityinpatientswithbicarbonatelossandapHlowerthan7.1.Fluidsarereplacedparenterallyasrequired.Dialysismaybeinitiatedinpatientswithrenalfailureoratoxicreactiontoadrug.Suchpatientsmayreceiveanantibiotictotreatsourcesofinfectionoranantidiarrhealtotreatdiarrhea-induced
bicarbonateloss.
AlwaysonthealertWatchforsignsofworseningCNSstatusordeterioratinglaboratoryandABGtestresults.Thepatientmayneedventilatorysupport,soprepareforintubation.Apatientwithrenalfailuremayneeddialysis,especiallywhenthisconditioniscomplicatedbydiabetes.MaintainapatentI.V.linetoadministeremergencydrugs,andflushthelinewithnormalsalinesolutionbeforeandafteradministeringsodiumbicarbonatebecausethebicarbonatemayinactivateorcauseprecipitationofmanydrugs.(SeeAcidosisanddopamine.)
It'snotworking
AcidosisanddopamineIfyou’readministeringdopaminetoapatientanditisn’traisinghisbloodpressureasyouexpected,investigateyourpatient’spH.ApHlevelbelow7.1(ascanhappeninseveremetabolicacidosis)causesresistancetovasopressortherapy.CorrectthepHlevel,anddopaminemayprovetobemoreeffective.
HowyouinterveneIfyourpatientisatriskformetabolicacidosis,carefulmonitoringcanhelppreventitfromdeveloping.Ifyourpatientalreadyhasmetabolicacidosis,nursingcareincludesimmediateemergency
interventionsandlong-termtreatmentoftheconditionanditsunderlyingcauses.Observethefollowingguidelines:•Monitorvitalsigns,andassesscardiacrhythm.•Prepareformechanicalventilationordialysisasrequired.•Closelymonitorthepatient’sneurologicstatusbecausechangescanoccurrapidly.Notifythe
practitionerofanychangesinthepatient’scondition.•InsertanI.V.lineasordered,andmaintainpatentI.V.access.Havealarge-borecatheterin
placeforemergencysituations.AdministerI.V.fluid,avasopressor,anantibiotic,andothermedicationsasprescribed.
•Administersodiumbicarbonateasordered.RemembertoflushtheI.V.linewithnormalsalinesolutionbeforeandaftergivingbicarbonatebecausethechemicalcaninactivatemanydrugsorcausethemtoprecipitate.Keepinmindthattoomuchbicarbonatecancausemetabolicalkalosisandpulmonaryedema.
•Positionthepatienttopromotechestexpansionandeasebreathing.Ifthepatientisstuporous,turnhimfrequently.(SeeTeachingaboutmetabolicacidosis.)
Teachingpoints
Teachingpoints
TeachingaboutmetabolicacidosisWhenteachingapatientwithmetabolicacidosis,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
basicsoftheconditionanditstreatment•
testingofbloodglucoselevelsifindicated•
needforstrictadherencetoantidiabetictherapyifappropriate•
avoidanceofalcohol•
warningsignsandsymptomsandwhentoreportthem•
prescribedmedications•
avoidanceofingestionoftoxicsubstances.
•Takestepstohelpeliminatetheunderlyingcause.Forexample,administerinsulinandI.V.fluidsasprescribedtoreverseDKA.
•Watchforanysecondarychanges,suchasdecliningbloodpressure,thathypovolemiamaycause.
•Monitorthepatient’srenalfunctionbyrecordingintakeandoutput.(SeeDocumentingmetabolicacidosis.)
Chartsmart
DocumentingmetabolicacidosisIfyourpatienthasmetabolicacidosis,makesureyoudocumentthefollowinginformation:•
assessmentfindings,includingresultsofneurologicexaminations•
intakeandoutput•
notificationofthepractitioner•
prescribedmedicationsandI.V.therapyandpatient’sresponse•
safetymeasuresimplemented•
serumelectrolytelevelsandABGresults•
ventilatorordialysisdata•
vitalsignsandcardiacrhythm•
patientteaching.
•Watchforchangesinserumelectrolytelevels,andmonitorABGresultsthroughouttreatmenttocheckforovercorrection.
•Orientthepatientasneeded.Ifhe’sconfused,takestepstoensurehisorhersafety,suchaskeepingthebedinthelowestposition.
•Investigatereasonsforthepatient’singestionoftoxicsubstances.
Q&AtimePhysicalexaminationandfurtherdiagnostictestsmayprovidemoreinformationaboutyourpatient’smetabolicacidosis.Asyoureevaluatethepatient’scondition,considerthesequestions:•Hasthepatient’sLOCreturnedtonormal?•Havevitalsignsstabilized?
•HaveABGresults,bloodglucoselevels,andserumelectrolytelevelsimproved?•Iscardiacoutputnormal?•Hasthepatientregainedanormalsinusrhythm(orhispreviouslystableunderlyingrhythm)?•Isthepatientventilatingadequately?
MetabolicalkalosisMetabolicalkalosisiscausedbyadecreaseinhydrogenionproduction,characterizedbyabloodpHabove7.45,andaccompaniedbyabicarbonatelevelabove26mEq/L.Inacutemetabolicalkalosis,bicarbonatemaybeashighas50mEq/L.Withearlydiagnosisandprompttreatment,theprognosisforeffectivetreatmentisgood.Leftuntreated,metabolicalkalosiscanresultincoma,arrhythmias,anddeath.
HowithappensInmetabolicalkalosis,theunderlyingmechanismsincludealossofhydrogenions(acid),againinbicarbonate,orboth.APaCO2levelgreaterthan45mmHg(possiblyashighas60mmHg)indicatesthatthelungsarecompensatingforalkalosis.Renalcompensationismoreeffectivebutslower.Metabolicalkalosisiscommonlyassociatedwithhypokalemia,particularlyfromtheuseofthiazides,furosemide,ethacrynicacid,andotherdiureticsthatdepletepotassiumstores.Inhypokalemia,thekidneysconservepotassium.Atthesametime,thekidneysalsoincreasetheexcretionofhydrogenions,whichpromptsalkalosisfromthelossofacid.Metabolicalkalosismayalsooccurwithhypochloremiaandhypocalcemia.(SeeWhathappensinmetabolicalkalosis.)
WhathappensinmetabolicalkalosisThisseriesofillustrationsshowshowmetabolicalkalosisdevelopsatthecellularlevel.Asbicarbonateions(HCO3
−)starttoaccumulateinthebody,chemicalbuffers(inextracellularfluidandcells)bindwiththem.Nosignsaredetectableatthisstage.
ExcessHCO3−thatdoesn’tbindwithchemicalbufferselevatesserumpHlevels,whichinturn
depresseschemoreceptorsinthemedulla.Depressionofthosechemoreceptorscausesadecreaseintherespiratoryrate,whichincreasesPaCO2.Theadditionalcarbondioxide(CO2)combineswithwater(H2O)toformcarbonicacid(H2CO3).Note:Loweredoxygenlevelslimitrespiratorycompensation.LookforaserumpHlevelabove7.45;anHCO3
−levelabove26mEq/L;arisingPaCO2;andslow,shallowrespirations.
WhentheHCO3−levelexceeds28mEq/L,therenalglomerulicannolongerreabsorbexcess
amounts.TheexcessHCO3−isexcretedinurine;hydrogenions(H+)areretained.Lookforalkaline
urineandpHandHCO3−levelsthatslowlyreturntonormal.
Tomaintainelectrochemicalbalance,thekidneysexcreteexcesssodiumions(Na),H2O,and
HCO3−.Lookforpolyuriainitially,thensignsandsymptomsofhypovolemia,includingthirstand
drymucousmembranes.
LoweredH+levelsintheextracellularfluidcausestheionstodiffuseoutofthecells.Tomaintainthebalanceofchargeacrossthecellmembrane,extracellularpotassiumions(K)moveintothecells.Lookforsignsandsymptomsofhypokalemia,includinganorexia,muscleweakness,andlossofreflexes.
AsH+levelsdecline,calcium(Ca)ionizationdecreases.ThatdecreaseinionizationmakesnervecellsmorepermeabletoNa.ThemovementofNaintonervecellsstimulatesneuralimpulsesandproducesoverexcitabilityoftheperipheralsystemandCNS.Lookfortetany,belligerence,irritability,disorientation,andseizures.
GIgriefMetabolicalkalosiscanresultfrommanycauses,themostcommonofwhichisexcessiveacidlossfromtheGItract.Vomitingcauseslossofhydrochloricacidfromthestomach.Childrenwho
havepyloricstenosiscandevelopthisdisorder.Alkalosisalsoresultsfromprolongednasogastric(NG)suctioning,presentingariskforsurgicalpatientsandpatientswithGIdisorders.
DiureticdangerDiuretictherapypresentsanotherriskofmetabolicalkalosis.Thiazideandloopdiureticscanleadtoalossofhydrogen,potassium,andchlorideionsfromthekidneys.Hypokalemiacausesthekidneystoexcretehydrogenionsastheytrytoconservepotassium.Potassiummovesoutofthecellsashydrogenmovesin,resultinginalkalosis.Withthefluidlossfromdiuresis,thekidneysattempttoconservesodiumandwater.Forsodium
tobereabsorbed,hydrogenionsmustbeexcreted.Inaprocessknownascontractionalkalosis,bicarbonateisreabsorbedandmetabolicalkalosisresults.
MoremetabolicmishapsCushing’sdiseasecanleadtometabolicalkalosisbycausingretentionofsodiumandchlorideandurinarylossofpotassiumandhydrogen.Reboundalkalosisfollowingcorrectionoforganicacidosis,suchasaftercardiacarrestandadministrationofsodiumbicarbonate,canalsocausemetabolicalkalosis.Posthypercapnicalkalosisoccurswhenchroniccarbondioxideretentioniscorrectedbymechanicalventilationandthekidneyshaven’tyetcorrectedthechronicallyhighbicarbonatelevels.Metabolicalkalosiscanalsoresultfromkidneydisease,suchasrenalarterystenosis,orfrom
multipletransfusions.Certaindrugs,suchascorticosteroidsandantacidsthatcontainsodiumbicarbonate,canalsoleadtometabolicalkalosis.(SeeDrugsassociatedwithmetabolicalkalosis.)ContinuousNGtubesuctioncanalsocausemetabolicalkalosisduetotheremovalofacidandelectrolytes.
Drugsassociatedwithmetabolicalkalosis•
Thefollowingdrugsarecommonlyassociatedwithmetabolicalkalosis:•
antacids(sodiumbicarbonate,calciumcarbonate)•
corticosteroids•
thiazideandloopdiuretics.
Whattolookfor
Initially,yourpatientmayhaveslow,shallowrespirationsashypoventilation,acompensatorymechanism,occurs.However,thismechanismislimitedbecausehypoxemiasoondevelops,whichstimulatesventilation.Thesignsandsymptomsofmetabolicalkalosisarecommonlyassociatedwithanunderlyingcondition.CharacteristichypokalemicorhypocalcemicECGchangesmayoccur,aswellassignsofhypotension.
AneurologicnightmareMetabolicalkalosisresultsinneuromuscularexcitability,whichcausesmuscletwitching,weakness,andtetany.Thepatientdevelopshyperactivereflexes.Hemayalsoexperiencenumbnessandtinglingofthefingers,toes,andmoutharea.Neurologicsymptomsincludeapathyandconfusion.Seizures,stupor,andcomamayresultifsevere.
KeeptrackofthesetractsIfhypokalemiaaffectstheGItract,thepatientislikelytoexperienceanorexia,nausea,andvomiting.Ifitaffectsthegenitourinary(GU)tract—thatis,ifthekidneysareaffected—polyuriamayresult.Ifleftuntreated,metabolicalkalosiscanresultinarrhythmiasanddeath.(SeeSignsandsymptomsofmetabolicalkalosis.)
CAUTION!
SignsandsymptomsofmetabolicalkalosisThefollowingassessmentfindingscommonlyoccurinpatientswithmetabolicalkalosis:•
anorexia•
apathy•
confusion•
cyanosis•
hypotension•
lossofreflexes•
muscletwitching•
nausea•
paresthesia•
polyuria•
vomiting•
weakness•
seizures•
coma.
Whattestsshow
Thesetestsmaybehelpfulinthediagnosisandtreatmentofmetabolicalkalosis:•ABGanalysismayrevealabloodpHabove7.45andabicarbonatelevelabove26mEq/L.If
theunderlyingcauseisexcessiveacidloss,thebicarbonatelevelmaybenormal.ThePaCO2levelmaybeabove45mmHg,indicatingrespiratorycompensation.(SeeABGresultsinmetabolicalkalosis,page226.)
•Serumelectrolytelevelsusuallyindicatelowpotassium,calcium,andchloridelevels.Bicarbonatelevelsareelevated.
•ECGchangesmayoccur,suchasalowTwavethatmergeswiththePwave.
Howit’streatedTreatmentaimstocorrecttheacid-baseimbalancebyprovidingthepatient’sbodysufficienttimetoriditselfofexcessbicarbonateandincreaseitshydrogenconcentration.Treatmentmayinclude:•I.V.administrationofammoniumchlorideorargininemonohydrochloride;rarelydonebut
sometimesnecessaryinseverecases•discontinuationofthiazidediureticsandNGsuctioning•administrationofanantiemetictotreatunderlyingnauseaandvomiting•additionofacetazolamide(Diamox)toinhibitcalciumandincreaserenalexcretionof
bicarbonate.
HowyouinterveneIfyourpatientisatriskformetabolicalkalosis,carefulmonitoringcanhelppreventitsdevelopment.Ifyourpatientalreadyhasmetabolicalkalosis,followtheseguidelines:
•Monitorvitalsigns,includingcardiacrhythmandrespiratorypattern.•Assessthepatient’sLOCwhentakingthehealthhistoryorbytalkingwiththepatientwhile
you’reperformingthephysicalexamination.Forinstance,apathyandconfusionmaybeevidentinapatient’sconversation.
•Administeroxygenasorderedtotreathypoxemia.•Instituteseizureprecautionswhenneeded,andexplainthemtothepatientandfamily.(SeeTeachingaboutmetabolicalkalosis.)
Teachingpoints
TeachingaboutmetabolicalkalosisWhenteachingapatientwithmetabolicalkalosis,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
basicsoftheconditionanditstreatment•
needtoavoidoveruseofalkalineagentsanddiuretics•
prescribedmedications,especiallyadverseeffectsofpotassium-wastingdiureticsorpotassiumchloridesupplements•
warningsignsandsymptomsandwhentoreportthem.
•MaintainpatentI.V.accessasordered.•Administerdilutedpotassiumsolutionswithaninfusiondevice.•Monitorintakeandoutput.(SeeDocumentingmetabolicalkalosis.)
Chartsmart
DocumentingmetabolicalkalosisIfyourpatienthasmetabolicalkalosis,makesureyoudocumentthefollowinginformation:•
vitalsigns•
I.V.therapy•
interventionsandthepatient’sresponse•
medications•
intakeandoutput•
oxygentherapy•
notificationofthepractitioner•
safetymeasures•
serumelectrolytelevelsandABGresults•
patientteachingperformedandthepatient’sresponse.
•Infuse0.9%ammoniumchloridenofasterthan1Lover4hours.Fasteradministrationmaycausehemolysisofredbloodcells.Don’tadministerthedrugtoapatientwhohashepaticorrenaldisease.
•IrrigateanNGtubewithnormalsalinesolutioninsteadoftapwatertopreventlossofgastricelectrolytes.
•Assesslaboratorytestresults,suchasABGandserumelectrolytelevels.Notifythepractitionerofanychanges.
•Watchcloselyforsignsofmuscleweakness,tetany,ordecreasedactivity.
That'sawrap!
Acid-baseimbalancesreview
Acid-basebasics•
Acid-basebalancedependsontheregulationoffreehydrogenions.•
Balanceismaintainedbychemicalbuffers,respiratoryreactions,andkidneyreactions.•
ABGanalysisisthemajordiagnostictoolforevaluatingacid-basestates:–
pH:determinestheextentofacidityoralkalinity,bothofwhicharemeasured–
PaCO2:reflectstheadequacyofventilationbythelungs–
Bicarbonatelevel:reflectstheactivityofthekidneysinretainingorexcretingbicarbonate.•
Ifhydrogenionconcentrationincreases,pHdecreases(acidosis).•
Ifhydrogenionconcentrationdecreases,pHincreases(alkalosis).
Respiratoryacidosis•
Resultsfromcompromiseinbreathing•
Characterizedbyalveolarhypoventilation(bodycan’tgetridofcarbondioxide)•
Leadstohypercapnia
Causes•
HypoventilationfromCNStraumaortumorthatdepressestherespiratorycenter•
Neuromusculardisordersthataffectrespiratorydrive•
Lungdiseasesthatdecreaseamountofsurfaceareaavailableforgasexchange•
Airwayobstruction•
Chestwalltrauma•
Drugsthatdepresstherespiratorycenter
Treatment•
Ventilation,bronchodilator,supplementaloxygen,andchestphysiotherapy•
Antibioticstotreatinfection•
Drugtherapytotreathyperkalemia•
Removalofforeignbodiesfromairwayifneeded•
Painmanagement
Respiratoryalkalosis•
Occurswhencarbondioxideeliminationincreases
Causes•
Conditionsthatincreaserespiratoryrateanddepth•
Hyperventilation•
Hypercapnia•
Hypermetabolicstates•
Liverfailure•
Certaindrugs•
Conditionsthataffectthebrain’srespiratorycontrolcenter•
Acutehypoxiasecondarytohighaltitude,pulmonarydisease,severeanemia,pulmonaryembolus,andhypotension
Treatment•
Removalofcausativeagent•
Feverreduction•
Sepsistreatment•
Oxygentherapy(ifacutehypoxemiaisthecause)•
Rebreathingexhaledcarbondioxide
Metabolicacidosis•
Occurswhenhydrogenproductionincreases•
DepressestheCNSand,ifuntreated,mayleadtoventriculararrhythmias,coma,andcardiacarrest
Causes•
Lossofbicarbonate(base)•
Accumulationofmetabolicacids(acid)•
Overproductionofketonebodies•
Decreasedabilityofkidneystoexcreteacids
•ExcessiveGIlossesfromdiarrhea,intestinalmalabsorption,orurinarydiversiontoileum•
Hyperaldosteronism•
Useofpotassium-sparingdiuretics•
Poisoningortoxicdrugreaction
Treatment•
Correctionofacidosisasquicklyaspossible•
Respiratorycompensation(mechanicalventilationifneeded)•
Rapid-actinginsulin(fordiabetics)•
I.V.bicarbonateandI.V.fluids•
Dialysis(forpatientswithrenalfailure)
Metabolicalkalosis•
Commonlyassociatedwithhypokalemia•
Resultsfromdecreaseinhydrogenproduction,againinbicarbonate,orboth
Causes•
ExcessiveacidlossfromtheGItract•
Diuretictherapy(kidneylossofhydrogen,potassium,andchloride)•
Cushing’sdisease(fromsodiumandchlorideretentionandpotassiumandhydrogenexcretion)
Treatment•
I.V.fluidsandacetazolamidetoincreaserenalexcretion•
Correctionofunderlyingacid-baseimbalance•
DiscontinuationofthiazidediureticsandNGsuctioning
Forseverecases•
I.V.ammoniachloride
ThischartshowspH,PaCO2,andbicarbonatevaluesinrespiratoryandmetabolicalkalosisandacidosis.
Quickquiz
1.Thebodycompensatesforchronicrespiratoryalkalosisby:A.increasingexcretionofbicarbonate.B.decreasingexcretionofbicarbonate.C.increasingPaCO2.D.decreasingPaCO2.
Answer:A.Whenhypocapnialastsmorethan6hours,thebodydevelopsmetabolicacidosisandthekidneyscompensatebyincreasingexcretionofbicarbonateandreducingexcretionofhydrogenions.HydrogenionsreturntothebloodtodecreasepH,causingchemoreceptorsinthemedullatodecreasetherespiratoryrate.
2.You’retakingcareofapatientwithobesity-hypoventilationsyndrome.Youexpecttoseesignsofchronicrespiratoryacidosisinthepatient’sABGresults.Whatdoyoulookfor?
A.IncreasingpHB.IncreasedPaCO2C.Increasedbicarbonate
D.DecreasedbicarbonateAnswer:C.Asrespiratorymechanismsfail,thebodycompensatesbyusingtheincreasedPaCO2toexcretehydrogenandtostimulatethekidneystoretainbicarbonateandsodiumions.Asaresult,moresodiumbicarbonate(thusanincreasedbicarbonate)isavailabletobufferfreehydrogenions(metabolicalkalosis).Ammoniumionsarealsoexcretedtoremovehydrogen.
3.Ifyourpatient’sNGtubeisattachedtosuction,youknowthepatientmaydevelopmetabolicalkalosis.YouexpectthathisABGresultswillshow:
A.decreasedpH,increasedPaCO2,anddecreasedbicarbonate.B.increasedpH,increasedPaCO2,andincreasedbicarbonate.C.decreasedpH,decreasedPaCO2,anddecreasedbicarbonate.D.increasedpH,decreasedPaCO2,andnochangeinbicarbonate.
Answer:B.Metabolicacidosisiscausedbyalossinhydrogenionproductionandagaininbicarbonate,causingincreasedpHandbicarbonatelevels.Ifrespiratorycompensationoccurs,PaCO2willincreaseabove45mmHg.
4.WhenassessingapatientwithDKA,youdetectKussmaul’srespirations.Yourealizethebodyisin:
A.respiratoryalkalosiswithcompensation.B.respiratoryacidosiswithcompensation.C.metabolicalkalosiswithcompensation.D.metabolicacidosiswithcompensation.
Answer:D.ApatientwithDKAwilldevelopmetabolicacidosis.Whenexcesshydrogencan’tbebuffered,thehydrogenreducesbloodpHandstimulateschemoreceptorsinthemedulla,whichinturnincreasestherespiratoryrate(leadingtorespiratoryalkalosis).Thismechanismlowerscarbondioxidelevelsandallowsmorehydrogentobindwithbicarbonate.
5.InapatientwithCOPD,theprimaryimbalanceislikelytobe:A.respiratoryalkalosis.B.respiratoryacidosis.C.metabolicalkalosis.D.metabolicacidosis.
Answer:B.COPDresultsindestructionofthealveoli,therebydecreasingthesurfaceareaofthelungsavailableforgasexchange.Withalveolarventilationdecreased,thePaCO2increases.Thecarbondioxidecombineswithwatertoformexcessiveamountsofcarbonicacid.Thecarbonicaciddissociatestoreleasefreehydrogenandbicarbonateions,therebydecreasingthepH(respiratoryacidosis).
6.YourbedriddenpatienthastheseABGresults:pH,7.5;PaCO2,26mmHg;bicarbonate,
24mEq/L.He’sdyspneicandhasaswollenrightcalf.Thepatientmostlikelyissufferingfrom:
A.apulmonaryembolus.B.heartfailure.C.dehydration.D.hyperaldosteronism.
Answer:A.Unexplainedrespiratoryalkalosismaymeanapulmonaryembolus(inthiscase,mostlikelyathrombusinthelegasaresultofimmobility).
7.Ifadministeringdopaminetoapatientwithhypotensionprovesineffective,howshouldyouproceed?
A.Changetodobutamine.B.Investigatethepatient’spH.C.Checkthepatient’sserumpotassiumlevel.D.Increasetherateofdopamineinfusion.
Answer:B.Ifyou’readministeringdopaminetoapatientanditisn’televatinghisbloodpressureasyouexpected,youshouldinvestigatethepatient’spH.ApHlevelbelow7.1causesresistancetovasopressortherapy.
8.Beforeandafteryouadministersodiumbicarbonate,youshouldflushtheI.V.linewith:A.heparin.B.sterilewater.C.normalsalinesolution.D.potassium.
Answer:C.YoushouldflushtheI.V.linewithnormalsalinesolutionbeforeandaftergivingbicarbonate.
ScoringIfyouansweredalleightquestionscorrectly,wow!TestthepHofthenearestpool,andjumpinforarefreshingswim!Ifyouansweredfivetosevencorrectly,excellent!You’rejustaboutreadytodoyourfirstsolobalancingact!Ifyouansweredfewerthanfivecorrectly,takeheart.You’restillaboffobufferinourbook.(Buffer,getit?Forchemicalbuffers?Ohwell,can’twin‘emall.)
ReferencesBronfenbrenner,R.(2013).Acid-baseinterpretation.Retrievedfrom
http://emedicine.medscape.com/article/2058760-overviewLippincott’svisualnursing:Aguidetodiseaseskillsandtreatment(2nded.).(2012).Philadelphia,PA:
LippincottWilliams&Wilkins.Williamson,M.A.,&Snyder,L.M.(2009).Wallach’sinterpretationofdiagnostictests(9thed.).
Philadelphia,PA:LippincottWilliams&Wilkins.
PartIII
Disordersthatcauseimbalances
12 Heat-relatedhealthalterations
13 Heartfailure
14 Respiratoryfailure
15 ExcessiveGIfluidloss
16 Acutepancreatitis
17 Renalfailure
18 Burns
Chapter12
Heat-relatedhealthalterations
JustthefactsInthischapter,you’lllearn:
♦thedifferencesamongthefivetypesofheat-relatedhealthalterations
♦signsandsymptomsofheat-relatedhealthalterations
♦properwaystomanageheat-relatedhealthalterations.
Alookatheat-relatedhealthalterationsHeat-relatedhealthalterationsareamajorcauseofpreventabledeathsworldwide,especiallyinregionswithhightemperatures.Heat-relatedhealthalterationsdevelopwhenthebodycan’toffsetitsrisingtemperature,thusretainingtoomuchheat(hyperthermia).Whenthebodygetstoohottooquickly(temperatureabove99°F[37.2°C]),heat-relatedhealthalterationsoccur.
Justcoolit!Althoughthebodyinitiallytriestocoolitselfdownwhenit’sexposedtotoomuchheat,themechanismsthatregulatebodyheatcanfailifthestressbecomestoogreat.Normally,thebodyadjuststoexcessivetemperaturesthroughcomplexcardiovascularandneurologicchangescoordinatedbythehypothalamus.Heatlossoffsetsheatproductiontoregulatebodytemperature.
ToandfroHeattransfertoandfromthebodyoccursinfourways:
Conductionisthetransferofheatthroughdirectphysicalcontactandaccountsforlessthan2%ofthebody’sheatloss.
Inconvection,heatistransferredfromthebodytotheairandwatervaporsurroundingthebody.Itaccountsforlessthan10%ofthebody’sheatloss.Whenairtemperatureishigherthanbodytemperature,thebodygainsheatenergy.
Radiationisthetransferofheatviaelectromagneticwavesandaccountsformostheatloss.Aslongastheairtemperatureislessthanthebodytemperature,about65%ofthebody’sheatislostbyradiation.
Inevaporation,heatistransferredwhenaliquidchangesintoavapor.Itaccountsforabout30%ofthebody’sheatloss.
Ifyoucan’ttaketheheat...Inhottemperatures,thebodylosesheatmainlybyradiationandevaporation.However,whenairtemperatureishigherthan95°F(35°C),radiationofheatfromthebodystopsandevaporationbecomestheonlymeansofheatloss.Whenairtemperaturesincreaseandapersonisexercising,hecansweat1to2Leveryhour.
However,ifhumidityreaches100%,evaporationofsweatisnolongerpossibleandthebodylosesitsabilitytoloseheat.
HowtheyhappenSweatisthebody’smainwaytogetridofextraheat.Whenapersonsweats,waterevaporatesfromtheskin.Theheatthatmakesthisevaporationpossiblecomesfromtheheatcreatedbybloodflowingthroughtheskin.Aslongasbloodisflowingproperly,extraheatfromthecoreofthebodyis“pumped”totheskinandremovedbysweatevaporation.
WeatherforecastTheeffectivenessofsweatsometimesdependsontheweather.Iftheairishumid,it’sharderforsweattoevaporate.Thismeansit’seasiertosweat(andforthebodytoriditselfofexcessheat)whenit’srelativelydrythanwhenit’shumid.
Don’tsweatthesmallstuffBecausetheevaporationthatoccursduringsweatingcauseswaterloss,it’simportantforapersontodrinkwaterwhensweating.Ifthebodydoesn’thaveenoughwater,dehydrationcanoccur.Thisconditionmakesitharderforthebodytocoolitselfbecauselesswaterisavailableforthebodytouseduringevaporation.
Heat-relatedhealthalterationsareeasytopreventwithadequatehydration.Discusswithyourpatientstheimportanceofdrinkingwater,especiallywhenexertingthemselvesinhotweather(U.S.DepartmentofLabor,n.d.).
WhatcausesthemHeat-relatedhealthalterationsresultwhenthebody’sproductionofheatincreasesatafasterratethanthebody’sabilitytodissipateit(heatloss).Heatproductionincreaseswithexercise,fever,
infection,andtheuseofcertaindrugs,suchasamphetamines.Heatlossdecreaseswithhightemperaturesorhumidity,lackofacclimatization,lackofairconditioningorproperventilation,excessclothing,obesity,decreasedfluidintake,dehydration,extensiveburns,cardiovasculardisease,skindiseases,sweatglanddysfunction,endocrinedisorders(suchashyperthyroidism,diabetes,andpheochromocytoma),ingestionofalcohol,anduseofcertainmedications.(SeeDrugsthatcancauseheat-relatedhealthalterations.)
Drugsthatcancauseheat-relatedhealthalterationsDrugsthatmaycausedecreasedheatlossinclude:•
anticholinergics•
antihistamines•
beta-adrenergicblockers•
cyclicantidepressants•
diuretics•
ethanol•
lithium•
phenothiazines•
salicylates•
sympathomimetics(e.g.,cocaineandamphetamines)thatcausevasodilation.
Whenthebodyusesallitstricksandstillcan’tkeepitstemperaturedown,theexcessheatisretainedandheat-relatedhealthalterationscandevelop.
Typesofheat-relatedhealthalterationsHeat-relatedhealthalterationsfallintofivecategories:heatrash,heatcramps,heatexhaustion,heatsyncope,andheatstroke.
Heatrash
Heatrashisaskinirritationthatcandevelopfromexcessivesweatingduringhotweather.Itisusuallyfoundontheneckoruppertorso,orinskinfoldssuchastheaxillae,groin,orbreastcreases,andlookslikeredpimplesortinyblisters.
HeatcrampsHeatcrampsaremusclecontractionsthattypicallyoccurinthegastrocnemiusorhamstringmuscles.Thesepainfulcontractionsarecausedbyadeficiencyofwaterandsodiumandaregenerallyattributedtodehydrationandpoormuscleconditioning.Crampsusuallyoccurafterexertioninhightemperatures(>100°F[37.8°C])withprofusesweatingandwaterintakewithoutadequateelectrolytereplacement.Heatcrampsarecommoninmanuallaborers,athletes,andskierswhooverdressforthecoldaswellasinthosewhoaren’tusedtohot,dryclimatesinwhichexcessivesweatingisalmostundetectedbecauseofrapidevaporation.Symptomsusuallyimprovewithrest,waterconsumption,andacoolenvironment.
HeatexhaustionHeatexhaustioniscausedbyheatandfluidlossfromexcessivesweatingwithoutfluidreplacement.Rest,water,icepacks,andacoolenvironmentmayhelpinmildheatexhaustion.MoreseverelyexhaustedpatientsmayneedI.V.fluids,especiallyifvomitingkeepsthemfromdrinkingenough.Circulatorycollapsemayoccurifthisconditionisn’tpromptlytreated.
HeatsyncopeHeatsyncope(faintingordizziness)occurswhenapatientstandsupquicklyorhasbeenstandingforaprolongedperiodoftime.Dehydrationisoftentoblameforheatsyncope.
HeatstrokeHeatstroke,alsoknownassunstroke,isthemostsevereformofheat-relatedhealthalteration.Itcommonlyoccursinpatientswhoexerciseinhotweather.
Elderlypatientsandpatientstakingcertainmedicationsarealsoatriskforheatstrokeinhotweather,evenintheabsenceofexercise.Signstolookforincludewarm,flushedskinandlackofsweating.Somepatientsmayhavesymptomsthatresemblearegularstroke,suchasslurredspeech,bizarrebehavior,confusion,ordizziness.(Athleteswhohaveheatstrokeaftervigorousexerciseinhotweathermaystillsweatconsiderably.)Whetherexercise-relatedornot,apersonwithheatstrokeusuallyhasaveryhightemperature
(104°F[40°C]orhigher)andmaybedeliriousorunconsciousorhavingseizures.
CoolmovesPatientssufferingfromheatstrokeneedtohavetheirtemperaturereducedquickly(oftenwithicepacks)andmustalsobegivenI.V.fluidsforrehydration.Becausemanybodyorganscanfailinheatstroke,patientsaretypicallyhospitalizedforobservation.Thebody’sattempttoregulateitstemperatureduringheat-relatedhealthalterationscausesalossofexcessiveamountsofwaterandelectrolytes.Thesemustbereplacedtocounteractthehyperthermia.Extremelyhighbodytemperaturemaydamagetissues,includingmuscleandbraintissues,andmayleadtopermanentdisabilityandevendeath.
WhattolookforSignsandsymptomsofheat-relatedhealthalterationsvarydependingontheseverityofthesyndrome.(SeeSignsandsymptomsofheat-relatedhealthalterations.)
Signsandsymptomsofheat-relatedhealthalterationsHeat-relatedhealthalterationsmaybeclassifiedasmild(heatcrampsorheatrash),moderate(heatexhaustionorheatsyncope),orcritical(heatstroke).Thistablehighlightsthemajorassessmentfindingsassociatedwitheachclassification.
Classification AssessmentfindingsMildhyperthermiaHeatrashHeatcramps
•Redpimplesortinyblistersonuppertorsoorinskinfolds(heatrashonly)•
Mildagitation(centralnervoussystemfindingsotherwisenormal)•
Mildhypertension•
Moist,coolskinandmuscletenderness;involvedmusclegroups
possiblyhardandlumpy•
Muscletwitchingandspasms•
Nauseaandabdominalcramps•
Reportofprolongedactivityinaverywarmorhotenvironmentwithoutadequatesaltintake•
Tachycardia•
Temperaturerangingfrom99°to102°F(37.2°to38.9°C)
ModeratehyperthermiaHeatexhaustionHeatsyncope
•Dizziness•
Headache•
Hypotension•
Musclecramping•
Nauseaandvomiting•
Oliguria•
Pale,moistskin•
Rapid,threadypulse•
Syncopeorconfusion•
Temperatureelevatedupto104°F(40°C)•
Thirst•
Weakness
CriticalhyperthermiaHeatstroke
•Atrialorventriculartachycardia•
Confusion,combativeness,anddelirium
•Bizarrebehavior•
Fixed,dilatedpupils•
Hot,dry,reddenedskin•
Lossofconsciousness•
Seizures•
Tachypnea•
Temperaturegreaterthan104°F(40°C)
Risksofheat-relatedhealthalterationsThepresenceofcertainfluidandelectrolyteimbalancesisassociatedwithincreasedriskofheat-relatedhealthalterations.Theseimbalancesincludedehydration,hyponatremia,andhypokalemia.
DryideaSignsandsymptomsofdehydrationincludethirst;drymucousmembranes;hot,dryskin;decreasedurineoutput;confusion;dizziness;posturalhypotension;tachycardia;andeventuallyanhidrosis(absenceofsweating).
Passthesalt,please
Signsandsymptomsofhyponatremia(decreasedserumsodiumlevels)includelethargy,nauseaandvomiting,musclecrampsandweakness,muscletwitching,andseizures.
SpecialKSignsandsymptomsofhypokalemia(decreasedserumpotassiumlevels)includefatigue,paresthesia,hypoactivereflexes,ileus,cardiacarrhythmias,andelectrocardiogramchanges(flattenedTwaves,thedevelopmentofUwaves,ST-segmentdepression,andprolongedPRintervals).
Who’satrisk?Patientswhoaremostatriskforfluidandelectrolytelosswithheat-relatedillnessincludeelderlypeople,youngchildren,peoplewithchronicanddebilitatingdiseases,thosenotacclimatedtoheat,alcoholics,andpeopletakingcertainmedications(suchasanticholinergics,diuretics,andbeta-adrenergicblockers).(SeeAge-relatedheat-relatedhealthalterationrisk.)Fluidandelectrolytelossalsooccursinhealthypeoplewhoworkorexerciseinextremeheatandhumidityandinthosewhodon’tincreasetheirfluidintakeaccordingly.Footballplayersarepronetoheat-relatedhealthalterationsbecausetheiruniformscovernearlyallofthebodyandpracticeusuallybeginsinlatesummer,whenthetemperatureoutsideishighest.Athletesshouldpaycarefulattentiontothefluidstheydrinkandloseandshouldwearlightweightclothingwhenpossible.
Agesandstages
Agesandstages
Age-relatedheat-relatedhealthalterationriskWithaging,anindividual’sthirstmechanismandabilitytosweatdecrease.Thesefactorsputelderlypatientsatriskforheat-relatedhealthalterations,especiallyduringhotsummerdays.Heatstrokeisamedicalemergencyandmustbetreatedrapidlytopreventseriouscomplicationsor
death.Tohelppreventheatstroke,teachyourolderpatienttofollowtheseinstructions:•
Reduceactivityinhotweather,especiallyoutdooractivity.•
Wearlightweight,loose-fittingclothingduringhotweather;whenoutdoors,wearahatandsunglassesandavoidwearingdarkcolorsthatabsorbsunlight.•
Drinkplentyoffluids,especiallywater,andavoidtea,coffee,andalcoholbecausetheycancausedehydration.•
Stayinsidewhenpossible,anduseairconditioningoropenwindows(makingsurethatasecurescreenisinplace).Teachthepatienttouseafantohelpcirculateair.(Ifthepatientdoesn’thaveairconditioningathome,suggestthatheorshegoestocommunityresourcesthathaveairconditioningduringperiodsofexcessiveheat,suchasseniorcenters,libraries,andchurches.Somecommunitycentersmayevenprovidetransportationforthepatient.)
Littleones,tooNeonatesarealsoatincreasedriskforheat-relatedhealthalterations.Inpart,thisisduetotheirbodies’poorlydevelopedheat-regulatingabilities.
WhattestsshowThesetestresultscanhelpdiagnoseheat-relatedhealthalterationsanddeterminetheirseverity:•Serumsodiumandpotassiumlevelswillbedecreased.•Urinespecificgravitywillbeincreased.•Alaninetransaminaselevelswillbeelevated(almostuniversalinheatstroke).Otherlaboratorytestsareusedtodetectend-organdamage(especiallyinpatientswith
heatstroke)ortoruleoutotherdisorders.
Howthey’retreated
Thegoaloftreatmentforheat-relatedhealthalterationsistolowerthepatient’sbodytemperatureasquicklyaspossible.Elderlypatientsmayrequiremoreaggressivetreatmentandshouldbeevaluatedforeventhemildestcasesofheat-relatedhealthalterations.
ForheatrashPatientscanavoidheatrashbystayingincoolenvironmentswithlowhumiditywheneverpossible.Treatmentofheatrashincludeskeepingtheaffectedareadryandpowderingwithcornstarchtodecreasediscomfort.
ForheatcrampsHospitalizationforheatcrampsisrare,andthesignsandsymptomsareusuallyself-limiting.Treatmentincludesrest,intakeofelectrolyte-richfluids(sportsdrinks),andingestionofsaltyfoods.Clothingcanberemovedorloosened,andstretchingordirectpressureonthemusclesmaydecreasecramping.Ifthepatientcan’teatordrink,hemayneedanI.V.infusionofnormalsalinesolution(U.S.DepartmentofLabor,n.d.).
ForheatexhaustionHospitalizationusuallyisn’tnecessaryforheatexhaustion.It’stypicallytreatedbyhavingthepatientrestinacoollocationanddrinkwater,slightlysaltyfluids,orelectrolyte-richsportsdrinkseveryfewminutes.Clothingcanberemovedorloosenedandthefeetcanbeelevated120(30.5cm).Forseverecases,isotonicI.V.fluidsmaybegivenifavailableandifnecessary.Rarely,cardiacstimulantsandplasmavolumeexpanders(suchasalbuminanddextran)aregiven;theseshouldbeusedcautiouslytoavoidvolumeoverload.Untreatedheatexhaustionmayleadtoheatstroke(CentersforDiseaseControlandPrevention,2014;U.S.DepartmentofLabor,n.d.).
ForheatsyncopeTeachyourpatientstoavoidheatsyncopebystayinghydrated,remainingincoolerenvironments
whenpossible,andtoimmediatelysitorliedowniftheybegintofeellight-headed.Dependingonthecircumstances,patientswhoexperienceheatsyncopemayneed
hospitalizationormedicalattention,particularlyiftheyhavesustainedaninjuryduringthesyncopalepisode(U.S.DepartmentofLabor,n.d.).
ForheatstrokeHospitalizationorimmediatemedicalattentionisrequiredforpatientswithheatstroke.Treatmentfocusesoncoolingthebodyasquicklyaspossible.Icepacksshouldbeplacedonthepatient’sneck,armpits,andgroin.Heshouldremainundressedandshouldbespongedwithwater,sprayedwithtepidwater,ordabbedwithwettowels.Afanmayalsobeusedtoblowcoolairoverthepatient.Thiscausesevaporativecooling—thebestcoolingmethodforpatientswithheatstroke.He’llalsoneedcoolI.V.fluids.Otherwaystosupportthecoolingprocessmayincludeoxygentherapyand,inseverecases,endotrachealintubation.Ifthepatienthasuncontrollableseizures,he’llneedI.V.diazepamandbarbiturates(CentersforDiseaseControlandPrevention,2014;U.S.DepartmentofLabor,n.d.).
Beatingtheheat—carefullyOtheroptionsforcoolingthepatientincludecoveringhimwithiceandimmersinghiminanicebath.Althougheffectiveatrapidlyloweringbodytemperature,thesemethodscancreatecomplicationssuchasperipheralvasoconstriction,whichcanleadtolessheatdissipation.Thesetechniquesalsoareuncomfortableforthepatient,limittheabilitytomonitorthepatient’svitalsignsandcardiacstatus,mayresultinhypothermia,andeventuallymaycausethepatienttoshiver.Shiveringslowsthecoolingprocessbecauseitincreasescorebodytemperature.
Saynoto(these)drugsForalltypesofheat-relatedhealthalterations,patientsshouldn’ttakesalicylatestodecreasebodytemperaturebecausesalicylatesincreasetheriskofcoagulopathy.Patientsshouldn’talsotakeacetaminophenbecauseitdoesn’treducebodytemperatureduringheat-relatedhealthalterations.Takingacetaminophenmayactuallyworsenexistinghepaticdamagebecausethelivermetabolizesacetaminophen.
HowyouinterveneTreatmentofheat-relatedhealthalterationsrequiresfrequentmonitoringoflaboratoryvalues(centralvenousandpulmonarywedgepressures),institutingrehydrationmeasures,replacingsodiumandpotassium,andstartingcoolingmeasurestodecreasebodytemperature.Alsoinstitutetheinterventionsdiscussedhere.
Forheat-relatedhealthalterations•Replacefluidandelectrolytesbyencouragingfluidintakewithabalancedelectrolytedrink;
givesalttablets.•Loosenthepatient’sclothing.•Askthepatienttoliedowninacoolplace.•Massagehismuscles.•Ifheatcrampsaresevere,startanI.V.infusionwithnormalsalinesolution.•Ifthepatienthasheatexhaustion,hemayrequireoxygenadministration.
Forheatstroke•InitiatetheABCs(airway,breathing,andcirculation)oflifesupport.•Quicklylowerthepatient’sbodytemperatureusinghypothermiablanketsandicepackson
arterialpressurepoints.•Monitorthepatient’stemperaturecontinuously.Temperaturesshouldn’tbeallowedtofall
below101°F(38.3°C)orthepatientmaydevelophypothermia.•ReplacefluidsandelectrolytesI.V.•Whennecessary,givediazepamtocontrolseizures,chlorpromazineI.V.toreduceshivering,or
mannitolI.V.tomaintainurineoutputasordered.•Insertanasogastrictubetopreventaspirationasordered.•Monitortemperature,intake,output,andcardiacstatus.Assistwiththeinsertionofacentral
venouscatheterorapulmonaryarterycatheter.GivedobutamineI.V.tocorrectcardiogenicshock.Vasoconstrictorsshouldn’tbeused.(SeeDocumentingheat-relatedhealthalterations.)
Chartsmart
Documentingheat-relatedhealthalterationsIfyourpatienthasaheat-relatedhealthalteration,makesureyoudocumentthefollowinginformation:•
prescribedmedications•
coolingproceduresandtheireffect•
intakeandoutput•
levelofconsciousness•
cardiacoutput•
vitalsigns•
heartsounds•
lungsounds•
centralvenouspressureandpulmonaryarterywedgepressureifcentrallineinplace•
oxygenadministration•
patientteaching.
•Avoidstimulantsandsedatives.•Encouragebedrestforafewdays.•Warnthepatientthathistemperaturemayfluctuateforweeks.
Preventingheat-relatedhealthalterationsPreventionofheat-relatedhealthalterationsispossible.Byencouragingyourpatienttokeepwell
hydratedandbesensibleaboutexertioninhot,humidweather,you’rehelpinghimtostayontherighttrack.Remembertotellhimthatwateristhebestfluidtodrinkwhenhe’ssweating,notanelectrolytedrink.(SeeTeachingaboutheat-relatedhealthalterations.)
Teachingpoints
Teachingaboutheat-relatedhealthalterationsHeat-relatedhealthalterationsareeasilypreventable,soit’simportanttoeducateindividualsaboutthevariousfactorsthatcausethem.Thisinformationisespeciallyvitalforathletes,laborers,andsoldiersinfieldtraining.Besuretofollowtheseguidelineswhenperformingpatientteaching:•
Advisepatientstotaketheseprecautionsinhotweather:restfrequently,avoidhotplaces,drinkadequatefluids,andwearloose-fitting,lightweightclothing.•
Advisepatientswhoareobese,elderly,ortakingdrugsthatimpairheatregulationtoavoidoverheating.•
Tellpatientswhohavehadheatcrampsorheatexhaustiontoincreasetheirsaltandwaterintake.Theyshouldalsorefrainfromexercisinguntilsignsandsymptomsresolveandresumeexercisesgradually,makingsuretodrinkplentyofelectrolyte-containingfluids.Advisethemtotakeprecautionstopreventoverheating.•
Warnpatientswithheatstrokethatresidualhypersensitivitytohightemperaturesmaypersistforseveralmonths.•
Teachparentshowtotakestepstopreventyoungchildrenandinfantsfromoverheatinginhotweather.
That'sawrap!
Heat-relatedhealthalterationsreview
Heat-relatedhealthalterationsbasics•
Developwhenthebodycan’toffsetrisingtemperatureandretainstoomuchheat•
Resultfromfailureofthemechanismsthatregulatebodytemperature•
Areeasilypreventedwithadequatehydration
Heattransfer•
Fourmethods:conduction,convection,radiation,andevaporation•
Bodyheatlostmainlythroughradiationandevaporation;ifairtemperature>95°F(35°C),evaporationisonlymeansofheatloss
Sweat•
Body’smainwaytogetridofextraheat•
Heatcreatedbybloodflowingthroughtheskinevaporateswaterfromtheskin’ssurface.•
Weatheranddehydrationinfluencetheeffectivenessofsweating.
Typesofheat-relatedhealthalterations•
Heatrash(mild)•
Heatcramps(mild)•
Heatexhaustion(moderate)•
Heatsyncope(moderate)•
Heatstroke(critical)
Heatrash•
Developsfromexcessivesweatingduringhotweather•
Usuallyfoundontheneckoruppertorsoorinskinfolds•
Lookslikeredpimplesortinyblisters
Heatcramps•
Causedbydeficiencyofwaterandsodium•
Generallyattributedtodehydrationandpoormuscleconditioning
Heatexhaustion•
Causedbyheatandfluidlossfromexcessivesweatingwithoutfluidreplacement•
Canresultincirculatorycollapseifnottreatedpromptly
Heatsyncope(fainting)•
Occurswhenapatientstandsupquicklyorhasbeenstandingforaprolongedperiodoftime•
Dehydrationisoftentoblameforheatsyncope!
Heatstroke•
Causedbyrisingbodytemperature•
Leadstodamageofinternalorgans•
Consideredamedicalemergency
Causes•
Fever•
Infection•
Dehydration•
Burns•
Cardiovasculardisease•
Skindiseases•
Sweatglanddysfunction•
Diabetes•
Hyperthyroidism•
Pheochromocytoma•
Obesity•
Hightemperaturesorhumidity•
Lackofacclimatization•
Drugs(suchasamphetamines)andalcohol
Treatment•
Institutecoolingmeasurestolowerbodytemperature.•
Removeorloosenclothing.•
Instituterehydrationmeasuresandreplacesodiumandpotassiumlosses.•
TreatheatstrokeasamedicalemergencybyinitiatingtheABCsoflifesupportifneeded.•
Forheatstroke,monitortemperature,intake,output,andcardiacstatus.•
Patientsexperiencingheatstrokemayrequireadministrationofbenzodiazepinestocontrolseizures,dobutamineI.V.tocorrectcardiogenicshock,chlorpromazineI.V.toreduceshivering,ormannitolI.V.tomaintainurineoutput(CentersforDiseaseControlandPrevention,2014;U.S.DepartmentofLabor,n.d.).
Quickquiz
1.Whichmechanismaccountsformostofthebody’sheatlossundertypicalenvironmentalconditions?
A.ConvectionB.ConductionC.RadiationD.Evaporation
Answer:C.Radiationaccountsforapproximately65%ofthebody’sheatlosswhentheoutsidetemperatureislessthanthebody’stemperature.
2.Aftercoolingapatientwithheatstroke,hebeginstoshiver.Youexpecttoadminister:A.aspirin.B.acetaminophen.C.diazepam.D.chlorpromazine.
Answer:D.Chlorpromazineshouldbeusedwhenapatientisshiveringtopreventsignificantheatproduction.
3.Whichfeaturecanhelpyoudeterminewhetherapatienthasheatexhaustionorheatstroke?
A.Temperaturehigherthan102°F(38.9°C)B.AlteredCNSfunctionC.DehydrationD.Elevatedlivertransaminaselevels
Answer:B.AlteredCNSfunction(includingseizures,coma,delirium,bizarrebehavior,anddilatedpupils)isthehallmarkofheatstroke.Heatexhaustioncausesfatigueandweakness;however,thepatientisusuallyaware.Heatexhaustion,ifitissevereandleftuntreated,mayprogresstoheatstroke.
4.Whentreatingapatientwithheatstroke,youneedtomonitortemperaturecontinuouslytomakesurethatitdoesn’tfallbelow:
A.101°F(38.3°C).B.98.6°F(37°C).C.104°F(40°C).D.99°F(37.2°C).
Answer:A.Forpatientswithheatstroke,arapiddecreaseinbodytemperaturebelow101°F(38.3°C)cancausehypothermia.
5.Thebestcoolingmethodforheatstrokeis:A.waterimmersion.B.icedperitoneallavage.C.evaporativecooling.D.I.V.fluids.
Answer:C.Evaporativecooling,whichincludesundressingthepatient,sprayingtepidwateronhim,andusingcoolfanstomaximizeevaporation,isthebestcoolingmethodforapatientwithheatstroke.
Scoring
Ifyouansweredallfivequestionscorrectly,grababottleofwater!You’rehot,hot,hot!Ifyouansweredfourquestionscorrectly,goodjob!You’veworkedupasweatinthischapter.Nowmoveontothenextone.Ifyouansweredfewerthanfourquestionscorrectly,don’tworry!You’resuretohitahotstroke—err,streak—soon.
ReferencesCentersforDiseaseControlandPrevention.(2014).Heatstress.Retrievedfrom
http://www.cdc.gov/niosh/topics/heatstress/U.S.DepartmentofLabor.(n.d.).Heatrelatedillnessesandfirstaid.Retrievedfrom
https://www.osha.gov/SLTC/heatstress/heat_illnesses.html
Chapter13
Heartfailure
JustthefactsInthischapter,you’lllearn:
♦conditionsthatleadtoheartfailure
♦signsandsymptomsofheartfailure
♦imbalancesthatcanoccurasaresultofheartfailureoritstreatmentandwaystomanagethem.
AlookatheartfailureHeartfailureisacomplexclinicalsyndromethatresultsfromanystructuralorfunctionalimpairmentofventricularfillingorejectionthatcausesdiminishedcardiacoutput.Fromthesubtlelossofnormalventricularfunctiontothepresenceofsignsandsymptomsthatnolongerrespondtomedicaltherapy,heartfailureoccurswhentheheartcan’tpumpenoughbloodtomeetthebody’smetabolicneeds.Thereisnosinglediagnostictestforheartfailurebecauseitisclinicallydiagnosedbasedonsymptomsandphysicalexam.Howtheventriclesfunctiondependsontheinteractionamongthefourfactorsthatregulatethe
cardiacoutput:•preload(volume)•afterload(pressure)•contractility(squeeze)•heartrate.(Woods,2010)
CyclesurveyIt’simportanttorememberthattwoperiods—diastoleandsystole—makeupthenormalcardiaccycle.Diastoleistheportionofthecyclewhentheheartisatrest,fillingtheventricleswith
blood.Systoleistheportionofthecyclewhentheventriclescontract,ejectingtheirvolumeofblood.
ChainreactionWhenanyofthefourinterrelatedfactorsarealtered,cardiacoutputmaybeaffected.Forexample,whenthepreload(volume)deliveredtotheventriclesduringdiastoleisinadequate,cardiacoutputmaybecompromised,andheartfailuremayresult.Furthermore,whentheafterload(pressure)againstwhichtheventriclesmustcontractiselevatedduringsystole,cardiacoutputmaybecompromised,leadingtoheartfailure.Heartfailuremayresultwhenthebalanceofthesefourinterrelatedfactorsisalteredduring
eitherdiastoleorsystole.Whenheartfailurestemsfrominadequatefillingoftheventricles,thesyndromeisdescribedasdiastolicheartfailure.Whenheartfailurestemsfrominadequatecontraction,thesyndromeisdescribedassystolicheartfailure.Thisventriculardysfunctionmayoccurineithertheleftorrightventricle(Woods,2010;Yancyetal.,2013).
HowithappensNormally,thepumpingactionsoftherightandleftsidesoftheheartcomplementeachother,producingasynchronizedandcontinuousbloodflow.However,whenanunderlyingdisorderispresent,onesidemayfailwhiletheothercontinuestofunctionnormallyforsometime.Becauseoftheprolongedstrain,thefunctioningsideeventuallyfails,resultingintotalheartfailure(Eckman,2011).
TheleftleadsoffUsually,theheart’sleftsidefailsfirst.Left-sidedheartfailuretypicallyleadstoandisthemaincauseofright-sidedheartfailure.
Here’swhathappens:Diminishedleftventricularfunctionallowsbloodtopoolintheventricleandatriumandeventuallybackupintothepulmonaryveinsandcapillaries.(SeeLeft-sidedheartfailure,page250.)
Left-sidedheartfailureThisillustrationshowswhathappenswhenleft-sidedheartfailuredevelops.Theleftsideoftheheartnormallyreceivesoxygenatedbloodreturningfromthelungsandthenpumpsbloodthroughtheaortatoalltissues.Left-sidedheartfailurecausesbloodtobackupintothelungs,whichresultsinsuchrespiratorysymptomsastachypneaandshortnessofbreath.
Asthepulmonarycirculationbecomesengorged,risingcapillarypressurepushessodiumandwaterintotheinterstitialspace,causingpulmonaryedema.Therightventriclebecomesstressedbecauseit’spumpingagainstgreaterpulmonaryvascularresistanceandleftventricularpressure,leadingtopulmonarycongestion,dyspnea,andcardiomegaly(Eckman,2011;Woods,2010).
TherightrespondsAstherightventriclestartstofail,signsandsymptomsworsen.Bloodpoolsintherightventricleandrightatrium.Thebacked-upbloodcausespressureandcongestioninthevenaecavaeandsystemiccirculation.(SeeRight-sidedheartfailure,page251.)
Right-sidedheartfailureThisillustrationshowswhathappenswhenright-sidedheartfailuredevelops.Therightsideoftheheartnormallyreceivesdeoxygenatedbloodreturningfromthetissuesandthenpumpsthatbloodthroughthepulmonaryarteryintothelungs.Right-sidedheartfailurecausesbloodtobackuppastthevenacavaandintothesystemiccirculation.This,inturn,causesenlargementoftheabdominalorgansandtissueedema.
Bloodalsodistendsthevisceralveins,especiallythehepaticvein.Astheliverandspleenbecomeengorged,theirfunctionisimpaired.Risingcapillarypressureforcesexcessfluidfromthecapillariesintotheinterstitialspace.Thiscausestissueedema,especiallyinthelowerextremitiesandabdomen.
CompensatoryresponsesWhentheheartbeginstofail,thebodyrespondswiththreecompensatorymechanismstomaintainbloodflowtothetissues.Thesemechanismsincludesympatheticnervoussystemactivation,increasedpreload,andhypertrophyofthecardiaccells.Initially,thecompensatorymechanismsincreasethecardiacoutput.However,thesemechanismseventuallycontributetoheartfailure.
ThesympatheticnervoussystemDiminishedcardiacoutputactivatesthesympatheticnervoussystem,whichincreasesheartrate
andcontractility.Thisinitiallyincreasescardiacoutput.However,thisincreasedheartrateandcontractilitycausetheheart’sdemandforoxygentorise,therebyincreasingtheworkthattheheartmustdotomeetthisdemand.(Overtime,thisdemandcontributestoheartfailureratherthancompensatingforit.)(Eckman,2011;Woods,2010)Withincreaseddemand,bloodthenshuntsawayfromareasoflowpriority(suchastheskinand
kidneys)toareasofhighpriority(suchastheheartandbrain).Pulmonarycongestion,acomplicationofheartfailure,canleadtopulmonaryedema,alife-
threateningcondition.Decreasedperfusiontomajororgans,particularlythebrainandkidneys,maycausetheseorganstofail,necessitatingdialysisforkidneyfailure.Thepatient’slevelofconsciousness(LOC)maydecrease,possiblyleadingtocoma.Myocardialinfarction(MI)mayoccurbecausemyocardialoxygendemandscan’tbesufficientlymet.
IncreasedpreloadWhenbloodisshuntedawayfromareasoflowpriority,thekidneys,sensingareducedrenalbloodflow,activatetherenin-angiotensin-aldosteronesystem.Thisresultsinsodiumandwaterretention,whichincreasesbloodvolume(preload).Again,initially,thisservestoincreasecardiacoutput.However,overtime,theheartcan’tpumpthisincreasedvolumeeffectively,makingheartfailureworse,notbetter.
CardiachypertrophyWhentheheartisunderstrain,itrespondsbyincreasingitsmusclemass,aconditioncalledcardiachypertrophy.Asthecardiacwallthickens,theheart’sdemandforbloodandoxygengrows.Thepatient’sheartmaybeunabletomeetthisdemand,furthercompromisingthepatient’scondition.
AllstretchedoutWhenpressureinsidethechambers(usuallytheleftventricle)risesforasustainedperiod,theheartcompensatesbystretching,aconditioncalledcardiacdilation.Eventually,stretchedmusclefibersbecomeoverstrained,reducingtheheart’sabilitytopump.
ImbalancescausedbyheartfailureSeveralimbalancesmayresultfromtheheart’sfailuretopumpbloodandperfusetissuesadequately.Imbalancesalsomayresultfromstimulationoftherenin-angiotensin-aldosteronesystemorfromcertaintreatments,suchasdiuretictherapy.Fluid,electrolyte,andacid-baseimbalancesassociatedwithheartfailureinclude:•hypervolemiaandhypovolemia•hyperkalemiaandhypokalemia•hypochloremia,hypomagnesemia,andhyponatremia•metabolicacidosisandalkalosis•respiratoryacidosisandalkalosis.
AfloodoffluidHypervolemia—themostcommonfluidimbalanceassociatedwithheartfailure—resultsfromtheheart’sfailuretopropelbloodforward,consequentvascularpooling,andsodiumandwaterreabsorptiontriggeredbytherenin-angiotensin-aldosteronesystem.Excessextracellularfluidvolumecommonlycausesperipheraledema.Hypovolemiaisusuallyassociatedwithoverlyaggressivediuretictherapyandcanbe
especiallydangerousinelderlypatientsbecauseitcausesconfusionandhypotension.
LowdownonlowsodiumHyponatremiamayresultfromsodiumlossduetodiureticabuse.Insomecases,itmayresultfromadilutionaleffectthatoccurswhenwaterreabsorptionisgreaterthansodiumreabsorption.
OtherelectrolytehighsandlowsInpatientswithheartfailure,prolongeduseofadiureticwithoutadequatepotassiumreplacementcancausehypokalemia.Likewise,useofapotassium-sparingdiureticcancausehyperkalemia.Bothhypokalemiaandhyperkalemiacanleadtolife-threateningarrhythmias.Therefore,potassiumlevelsrequirecarefulmonitoringwheneverapatientreceivesanykindofdiuretic,oralorI.V.Hypomagnesemiamayaccompanyhypokalemia,particularlyifthepatientisreceivinga
diuretic(manydiureticscausethekidneystoexcretemagnesium).Hypochloremiamayalsoresultfromexcessivediuretictherapy.
LacticacidontheriseWhencellsdon’treceiveenoughoxygen,theyproducemorelacticacid.Poortissueperfusioninapatientwithheartfailureallowslacticacidtoaccumulate,whichinturnleadstometabolicacidosis.Metabolicalkalosismaybecausedbyexcessivediureticuse,whichcausesbicarbonate
retention.Intheearlystagesofheartfailure,asrespiratoryrateincreases,morecarbondioxideisblown
offfromthelungs,whichraisespHandleadstorespiratoryalkalosis.Asheartfailureprogresses,gasexchangeisfurtherimpaired.Carbondioxideaccumulates,resultinginrespiratoryacidosis.
WhatcausesheartfailureAwiderangeofpathophysiologicprocessescancauseheartfailure,includingconditionsthatdirectlydamagetheheart,suchasMI,myocarditis,myocardialfibrosis,andventricularaneurysm.Thedamagefromthesedisorderscausesasubsequentdecreaseinthecontractilityoftheheart.Ventricularoverloadcanalsocauseheartfailure.Thisoverloadmaybecausedbyincreased
bloodvolumeintheheart(calledincreasedpreload)asaresultofaorticinsufficiencyoraventricularseptaldefect.Systemicorpulmonaryhypertensionoranelevationinpressureagainstwhichtheheartmustpump(calledincreasedafterload)asaresultofaorticorpulmonicstenosiscanalsocausethisoverload.
Restrictedventriculardiastolicfilling,characterizedbythepresenceofsolittlebloodthattheventriclecan’tpumpiteffectively,canalsocauseheartfailure.Suchdiastolicfillingistriggeredbyconstrictivepericarditisorcardiomyopathy,tachyarrhythmias,cardiactamponade,ormitraloraorticstenosisandusuallyoccursinolderpatients.
RiskraisersCertainconditionscanpredisposeapersontoheartfailure,especiallyifthereisanunderlyingdisease.Theyinclude:•anemia,whichcausestheheartratetospeeduptomaintaintissueoxygenation•pregnancyandthyrotoxicosis,whichincreasethedemandforcardiacoutput•infections,whichincreasemetabolicdemandsandfurtherburdentheheart
•increasedphysicalactivity,emotionalstress,greatersodiumorwaterintake,orfailuretocomplywiththeprescribedtreatmentregimenforunderlyingheartdisease
•pulmonaryembolism,whichelevatespulmonaryarterialpressuresandcancauseright-sidedheartfailure
•connectivetissuedisorders(sarcoidosis).
WhattolookforSignsandsymptomsofheartfailurevaryaccordingtothesiteoffailureandstageofthedisease.Expecttoencounteracombinationofthefindingsdiscussedhere.
Left-sidedheartfailureIfyourpatienthasleft-sidedheartfailureandtissuehypoxia,theywillprobablycomplainoffatigue,weakness,orthopnea,andexertionaldyspnea.Thepatientmayalsoreportparoxysmalnocturnaldyspnea.Thepatientmayusetwoorthreepillowstoelevatehisheadtosleepormayhavetosleep
sittingupinachair.Shortnessofbreathmayawakenthepatientshortlyaftertheyfallasleep,forcingthemtoquicklysituprighttocatchhisbreath.Thepatientmayhavedyspnea,coughing,andwheezingevenwhensittingup.Tachypneamayoccur,andyoumaynotecracklesoninspiration.Coughingmayprogresstothepointwherethepatientproducespink,frothysputumashedevelopspulmonaryedema.Thepatientmaybetachycardic.Auscultationofheartsoundsmayrevealthirdandfourthheart
soundsasthemyocardiumbecomeslesscompliant.Hypoxiaandhypercapniacanaffectthecentralnervoussystem,causingrestlessness,confusion,andaprogressivedecreaseinthepatient’sLOC.Later,withcontinueddecreaseincardiacoutput,thekidneysmaybeaffected,andoliguriamaydevelopasaresultofhypoperfusion.
Right-sidedheartfailureInspectionofapatientwithright-sidedheartfailuremayrevealvenousengorgement.Whenthepatientsitsupright,neckveinsmayappeardistended,feelrigid,andexhibitexaggeratedpulsations.Edemamaydevelop,andthepatientmayreportaweightgain.Nailbedsmayappearcyanotic.Anorexiaandnauseamayoccur.Thelivermaybeenlargedandslightlytender.Thisconditionmayprogresstocongestivehepatomegaly,ascites,andjaundice.
AdvancedheartfailureInapatientwithadvancedheartfailure,pulsepressuremaybediminished,reflectingreducedstrokevolume.Occasionally,diastolicpressurerisesfromgeneralizedvasoconstriction.Thepatient’sskinfeelscoolandclammy.Progressionofheartfailuremayleadtopalpitations,chesttightness,andarrhythmias.Cardiacarrestmayoccur.(SeeRecognizingadvancedheartfailure.)
CAUTION!
RecognizingadvancedheartfailureThefollowingassessmentfindingscommonlyoccurinpatientswithheartfailure:•
cool,clammyskin•
diminishedpulsepressure•
elevateddiastolicpressure•
chesttightness•
arrhythmias.
WhattestsshowSeveraltestsmayhelpconfirmthediagnosisofheartfailure:•Electrocardiogramscandetectarrhythmias,MI,orthepresenceofcoronaryarterydisease.•ChestX-raysshowcardiomegaly,alveolaredema,pleuraleffusion,andpulmonaryedema.
•Atwo-dimensionalechocardiogramwithDopplershouldbeperformedduringinitialevaluationtoassessventricularfunction,size,wallthickness,wallmotion,andvalvefunction.
•Cardiaccatheterizationsandechocardiogramsrevealenlargedheartchambers,changesinventricularfunction,andthepresenceofvalvulardisease.Echocardiogram,thegoldstandardfordetectingheartfailure,showsleftventriculardysfunction.
•Hemodynamicpressurereadingsrevealincreasedcentralvenousandpulmonaryarterywedgepressures.
•MeasurementofB-typenatriureticpeptide(BNP)orN-terminalprohormoneofbrainnatriureticpeptide(NT-proBNP)tosupportdiagnosisofacutelydecompensatedheartfailure.
•Measurementofcardiactroponintodeterminediseaseseverityinacutelydecompensatedcases(Yancyetal.,2013).
Howit’streatedHeartfailureisamedicalemergency.Relievingdyspneaandimprovingarterialoxygenationaretheimmediatetherapeuticgoals.Secondarygoalsincludeminimizingoreliminatingtheunderlyingcause,reducingsodiumandwaterretention,optimizingcardiacpreloadandafterload,andenhancingmyocardialcontractility.
ThestartinglineupOneormoredrugs—suchasadiuretic,avasodilator,oraninotropicagent—areusuallyneededtomanageheartfailure.Diuretictherapy,thestartingpointofthistreatment,increasessodiumandwatereliminationbythekidneys.Byreducingfluidoverload,diureticsdecreasetotalbloodvolumeandrelievecirculatorycongestion.Formostdiureticstoworkeffectively,thepatientmustcontrolhissodiumintake.Typesofdiureticsincludethiazideandloopdiuretics,suchasfurosemide,torsemide,and
bumetanide.Becausethiazideandloopdiureticsworkatdifferentsitesinthenephron,theyproduceasynergisticeffectwhengivenincombination.Potassium-sparingdiuretics,suchasamiloride,spironolactone,andtriamterene,mayalsobeused.Anypatientwhotakesadiureticneedscarefulmonitoringbecausethesedrugscandisturbthe
electrolytebalanceandleadtometabolicalkalosis,metabolicacidosis,orothercomplications.
TheotherplayersOtherdrugsalsohelpmanageheartfailure:•Vasodilatorscanreducepreloadorafterloadbydecreasingarterialandvenous
vasoconstriction.Reducingpreloadandafterloadhelpsincreasestrokevolumeandcardiacoutput.
•Angiotensin-convertingenzyme(ACE)inhibitorsdecreasebothafterloadandpreload.BecauseACEinhibitorspreventpotassiumloss,hyperkalemiamaydevelopinpatientswhoarealsotakingapotassium-sparingdiuretic,sothesepatientsneedclosemonitoring.
•Angiotensin-receptorblocker(ARB)isrecommendedforpatientswhoareACEinhibitorintolerant.Itdecreasesbothafterloadandpreload.
•Nitrates,primarilyvasodilators,alsodilatearterialsmoothmuscleathigherdoses.Mostpatientswithheartfailuretoleratenitrateswell.Nitratescomeinseveralforms,suchasI.V.,oral,andtopicalointments.
•Beta-adrenergicblockerssuchascarvediloldecreaseafterloadthroughtheirvasodilatingaction.Specifically,theycauseperipheralvasodilation,decreasingsystemicpressuredirectlyandcardiacworkloadindirectly.Beta-adrenergicblockertherapyalsoenhanceslongevity.
•Inotropicdrugssuchasdigoxinincreasecontractilityinthefailingheartmuscleandslowconductionthroughtheatrioventricularnode.However,there’sanarrowmarginofsafetybetweentherapeuticandtoxiclevels.Aconcurrentelectrolyteimbalance,suchashypokalemia,maycontributetodigoxintoxicitybecauseitdecreasesdigoxinexcretionfromthebody.Thistoxicitymayleadtofatalcardiacarrhythmias,muscleweakness,andrespiratorydistress.
•Otherdrugs—suchasdopamine,dobutamine,milrinone,andinamrinone—maybeindicatedforpatientswithacuteheartfailuretoincreasemyocardialcontractilityandcardiacoutput.Hydralazineandnitroprussidemayalsobeusedtotreatheartfailure.
•Morphineiscommonlyusedinpatientswithheartfailurewhoalsohaveacutepulmonaryedema.Besidesreducinganxiety,itdecreasespreloadandafterloadbydilatingveins(Eckman,2011;Nettina,2010;Woods,2010;Yancyetal.,2013).
UrgencymaycallforsurgeryPatientswithsevereheartfailuremayrequiresurgery.Incardiomyoplasty,amuscleiswrappedaroundthefailinghearttoboostitspumpingaction.Inleftventriculectomy,asectionofnonviablemyocardiumisremovedtoreduceventricularsize,whichallowsthehearttopumpmoreeffectively.Tohelptheventriclespropelbloodthroughthevascularsystem,anintra-aorticballooncounterpulsationorotherventricularassistdevice,suchasabiventricularpacemakeroranimplantablecardioverterdefibrillator(sometimesnecessarybecauseapatientwithheart
failuremayhaveaconcurrentlife-threateningarrhythmia),maybeimplanted.Hearttransplantisusedonlyasalastresort.
HowyouinterveneToproperlycareforapatientwithheartfailure,you’llneedtoinvestigatethepatient’ssignsandsymptomsandperformanumberofspecificinterventions:•Assessthepatient’svitalsignsandmentalstatusandimmediatelyreportanychanges.•Assessthepatientforsignsandsymptomsofimpendingcardiacfailure,suchasfatigue;
restlessness;hypotension;rapidrespiratoryrate;shortnessofbreath;orthopnea;dyspnea;coughing;decreasedurineoutput;liverenlargement;andarapid,threadypulse.
•Assessthepatientforedema.Notetheamountandlocationofedemaandthedegreeofpitting,ifpresent.(SeeDocumentingheartfailure.)
Chartsmart
DocumentingheartfailureIfyourpatienthasheartfailure,makesureyoudocumentthefollowinginformation:•
prescribedmedications•
dailyweight,intake,andoutput(anyweightgainover2lb[0.9kg]inlessthan24hoursputsthepatientatriskforfluidoverload)•
edema•
dietrestrictions•
vitalsigns•
lungsounds•
heartsounds•
skinconditions•
patientpositioningandresponse•
mentalstatus•
toleranceofactivity•
safetymeasuresimplemented•
notificationofpractitioner•
patientteaching.
•Monitorsodiumandfluidintakeasprescribed.Hyponatremiaandfluidvolumedeficitcan
stimulatetherenin-angiotensin-aldosteronesystemandexacerbateheartfailure.Usually,mildsodiumrestriction(noaddedsaltallowed)isprescribed.
•Checkthepatient’sweightandfluidintakeandoutputdailyforsignificantchangestodetermineifthepatientisinastateoffluidoverload.Ifthepatienthasgained2lb(0.9kg)ormoreover24hours,he’llneedfurtherdiuretictherapy.(SeeTeachingaboutheartfailure,page258.)
Teachingpoints
TeachingaboutheartfailureWhenteachingapatientwithheartfailure,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
basicsoftheconditionanditstreatment•
needforadequaterest•
properskincare•
prescribedmedications•
dietaryrestrictions•
needtoreducestressandanxietylevel•
needforregularexercise•
needfordailyweights•
warningsignsandsymptomsandwhentoreportthem•
importanceoffollow-up.
•Monitorvitalsigns,includingbloodpressure,pulse,respirations,andheartandbreathsounds,forabnormalitiesthatmightindicateafluidexcessordeficit.
•Monitorserumelectrolytelevels—especiallysodiumandpotassium—forchangesthatmayindicateanimbalance.Rememberthathypokalemiacanleadtodigoxintoxicity.Monitorarterialbloodgasresultstoassessadequacyofventilation.
•Maintaincontinuouscardiacmonitoringduringacuteandadvancedstagesofthediseasetoidentifyarrhythmiaspromptly.
•Administerprescribedmedications—suchasdigoxin,diuretics,ACEinhibitors,ARB,andpotassiumsupplements—tosupportcardiacfunctionandminimizesymptoms.
•Administeroralpotassiumsupplementsinorangejuiceorwithmealstopromoteabsorptionandpreventgastricirritation.
•Placethepatientinsemi-Fowler’sorFowler’spositionastolerated,andgivesupplementaloxygenasorderedtohelphimbreathemoreeasily.
•Encourageindependentactivitiesofdailylivingastolerated,althoughsomepatientsmayrequirebedrest.Repositionthepatientasneededevery1to2hours.Edematousskinispronetobreakdown.
•Instructthepatientandhisfamilytonotifythestaffofanychangesinthepatient’scondition,suchasincreasedshortnessofbreath,chestpain,ordizziness.
•Instructthepatienttocallthepractitionerifhispulserateisirregular;ifitmeasuresfewerthan60beats/minute;orifheexperiencesdizziness,blurredvision,shortnessofbreath,apersistentdrycough,palpitations,increasedfatigue,nocturnaldyspneathatcomesandgoes,swollenankles,ordecreasedurineoutput(Eckman,2011;Nettina,2010;Woods,2010;Yancyetal.,2013).
That'sawrap!
Heartfailurereview
Heartfailure
•Clinicalsyndromeofmyocardialdysfunctionthatcausesdiminishedcardiacoutput•
Occurswhentheheartcan’tpumpenoughbloodtomeetthebody’smetabolicneeds
Left-sidedheartfailure•
Typicallyleadstoandisthemaincauseofright-sidedheartfailure•
Causespulmonaryedema,hypoxia,andhypercapnia•
Clinicalsymptoms:fatigue;weakness;orthopnea;exertionaldyspnea;pulmonaryedema;paroxysmalnocturnaldyspnea;tachycardia;thirdandfourthheartsounds;tachypnea;shortnessofbreath;oliguria;andcoughingwithpink,frothysputum
Right-sidedheartfailure•
Causesenlargementoftheabdominalorgansandtissueedema•
Clinicalsignsandsymptoms:venousengorgement,edema,weightgain,anorexia,nausea,cyanosisofnailbeds,coolandclammyskin,chesttightness,palpitations,neckveindistentionandrigidity,cardiacarrest,andhepatomegaly
Causes•
MI•
Myocarditis•
Myocardialfibrosis•
Ventricularaneurysm•
Ventricularoverloadasaresultofaorticinsufficiencyorventricularseptaldefect•
Systemicorpulmonaryhypertensionasaresultofaorticorpulmonicstenosis•
Restrictedventriculardiastolicfillingtriggeredbyconstrictivepericarditisorcardiomyopathy,tachyarrhythmias,cardiactamponade,ormitraloraorticstenosis
Imbalancescausedbyheartfailure•
Hypervolemiaorhypovolemia•
Hyperkalemiaorhypokalemia•
Hypochloremia,hypomagnesemia,andhyponatremia•
Metabolicacidosisoralkalosis•
Respiratoryacidosisoralkalosis
Hypervolemia•
Mostcommonfluidimbalanceassociatedwithheartfailure•
Resultsfromheart’sfailuretopropelbloodforward,resultinginvascularpoolingandsodiumandwaterreabsorption•
Commonlycausesperipheraledema
Hypovolemia•
Associatedwithoveruseofdiuretics•
Causesconfusionandhypotensioninelderlypatients•
Maycauseelectrolyteimbalances
Hyponatremia•
Mayresultfromsodiumlossduetodiureticabuse•
Mayresultfromadilutionaleffectwhenwaterreabsorptionisgreaterthansodiumreabsorption•
Maycauseconfusion
Otherelectrolyteimbalances•
Hypokalemia—resultsfromprolongeduseofadiureticwithoutadequatepotassiumreplacement•
Hyperkalemia—occurswithuseofpotassium-sparingdiuretics•
Hypokalemiaandhyperkalemia—leadtolife-threateningarrhythmias
•Hypomagnesemia—occurswithhypokalemia,especiallywithdiureticuse•
Hypochloremia—resultsfromexcessivediuretictherapy
Metabolicandrespiratoryacidosisandalkalosis•
Metabolicacidosis—occurswhenpoortissueperfusionallowslacticacidtoaccumulate•
Metabolicalkalosis—occurswithexcessivediureticuse,whichcausesbicarbonateretention•
Respiratoryalkalosis—occursearlyinheartfailurewhenincreasedrespirationscausemorecarbondioxidetobeblownoffandpHtorise•
Respiratoryacidosis—occursasheartfailureprogresses,gasexchangeisimpaired,andcarbondioxideaccumulates
Treatment•
Medicalemergency•
Reliefofdyspnea•
Improvedarterialoxygenation•
Diureticstorelievefluidoverload,vasodilatorstoreducepreloadandafterload,orinotropicstoincreaseheartcontractility•
Possiblysurgeryforsevereheartfailure(hearttransplantaslastresort)•
Patientandfamilyeducationaboutthediseaseanditsmanagement
Quickquiz
1.Whenassessingapatientwithleft-sidedheartfailure,youwouldexpecttodetect:A.distendedneckveins.B.edemaofthelowerextremities.
C.dyspneaonexertion.D.hepatomegaly.
Answer:C.Diminishedleftventricularfunctionallowsbloodtopoolintheventricleandatriumandeventuallybackupintothepulmonaryveinsandcapillaries.Asthepulmonarycirculationbecomesengorged,risingcapillarypressurepushessodiumandwaterintotheinterstitialspace,causingpulmonaryedema.Reasonsforseekingcareincludefatigue,exertionaldyspnea,orthopnea,weakness,andparoxysmalnocturnaldyspnea.
2.Themostcommonfluidimbalanceassociatedwithheartfailureis:A.hypervolemia.B.hypovolemia.C.hyperkalemia.D.hypokalemia.
Answer:A.Extracellularfluidvolumeexcessresultsfromtheheart’sfailuretopropelbloodforward,whichcausesvascularpooling,andfromthesodiumandwaterreabsorptiontriggeredbytherenin-angiotensin-aldosteronesystem.
3.Apatientwithheartfailureismorelikelytodevelopatoxicreactiontodigoxinifhehasconcurrent:
A.hyponatremia.B.hyperkalemia.C.hypernatremia.D.hypokalemia.
Answer:D.Hypokalemia,whichcanoccurwithdiuretictherapy,mayleadtodigoxintoxicity.
4.Whichdrugclassgiventotreatheartfailurehasbeenshowntoincreaselongevity?A.ACEinhibitorsB.NitratesC.Beta-adrenergicblockersD.Digoxin
Answer:C.Beta-adrenergicblockertherapyenhanceslongevity.
ScoringIfyouansweredallfourquestionscorrectly,wesaluteyourheartfelteffort!Ifyouansweredthreequestionscorrectly,great!Weapplaudyourboisterousbravado!Ifyouansweredfewerthanthreequestionscorrectly,relax.Westillcommendyourveritablevalor!
References
Woods,S.(Ed.).(2010).Cardiacnursing(6thed.).Philadelphia,PA:LippincottWilliams&Wilkins.Eckman,M.(Ed.).(2011).Professionalguidetopathophysiology(3rded.).Philadelphia,PA:Lippincott
Williams&Wilkins.Nettina,S.M.(2010).Lippincottmanualofnursingpractice(9thed.).Philadelphia,PA:Lippincott
Williams&Wilkins.Yancy,C.W.,Jessup,M.,Bozkurt,B.,Butler,J.,Casey,D.E.,Jr.,Drazner,M.H.,...Wilkoff,B.L.
(2013).ACCF/AHAguidelinesforthemanagementofheartfailure.JournaloftheAmericanCollegeofCardiology,62(16),e147–e239.
Chapter14
Respiratoryfailure
JustthefactsInthischapter,you’lllearn:
♦conditionsthatleadtorespiratoryfailure
♦signsandsymptomsofrespiratoryfailure
♦imbalancesthatoccurwithrespiratoryfailureandwaystomanagethem.
AlookatrespiratoryfailureWhenthelungscan’tsufficientlymaintainarterialoxygenationoreliminatecarbondioxide,acuterespiratoryfailureresults.Uncheckedanduntreated,thisconditioncanleadtodecreasedoxygenationofthebodytissuesandmetabolicacidosis.
Inpatientswithessentiallynormallungtissue,respiratoryfailureusuallyproduceshypercapnia(anabove-normalamountofcarbondioxideinthearterialblood)andhypoxemia(adeficiencyofoxygeninthearterialblood).Inpatientswithchronicobstructivepulmonarydisease(COPD),respiratoryfailuremaybesignaledonlybyanacutedropinarterialbloodgas(ABG)levelsandclinicaldeterioration.ThisisbecausesomepatientswithCOPDconsistentlyhavehighpartialpressureofarterialcarbondioxide(PaCO2)levelsandlowpartialpressureofarterialoxygen(PaO2)levelsbutareabletocompensateandmaintainanormal,ornear-normal,pHlevel.
HowithappensInpatientswithacuterespiratoryfailure,gasexchangeisdiminishedbyanycombinationofthesemalfunctions:•alveolarhypoventilation•ventilation-perfusion( )mismatch•intrapulmonaryshunting.Imbalancesassociatedwithrespiratoryfailureincludehypervolemia,hypovolemia,
hypokalemia,hyperkalemia,respiratoryacidosis,respiratoryalkalosis,andmetabolicacidosis.Let’slookateachoneindividually.(SeeWhathappensinacuterespiratoryfailure.)
WhathappensinacuterespiratoryfailureThreemajormalfunctionsaccountforimpairedgasexchangeandsubsequentacuterespiratoryfailure:alveolarhypoventilation,ventilation-perfusion( )mismatch,andintrapulmonary(righttoleft)shunting.
AlveolarhypoventilationInalveolarhypoventilation(shownbelowastheresultofairwayobstruction),theamountofoxygenbroughttothealveoliisdiminished,whichcausesadropinthepartialpressureofarterialoxygenandanincreaseinalveolarcarbondioxide(CO2).TheaccumulationofCO2inthealveolipreventsdiffusionofadequateamountsofCO2fromthecapillaries,whichincreasesthepartialpressureofarterialCO2.
( )mismatch( )mismatch,theleadingcauseofhypoxemia,occurswheninsufficientventilationexistswithanormalflowofbloodorwhen,asshownbelow,normalventilationexistswithaninsufficientflowofblood.
IntrapulmonaryshuntingIntrapulmonaryshuntingoccurswhenbloodpassesfromtherightsideofthehearttotheleftsidewithoutbeingoxygenated,asshownbelow.Shuntingcanresultfromuntreatedventilationorperfusionmismatches.
Hypervolemia
Prolongedrespiratorytreatments,suchasnebulizeruse,canleadtoinhalationandabsorptionofwatervapor.Excessivefluidabsorptionmayalsoresultfromincreasedlungcapillarypressureorpermeability,whichtypicallyoccursinacuterespiratorydistresssyndrome(ARDS).Theexcessivefluidabsorptionmayprecipitatepulmonaryedema.
HypovolemiaBecausethelungsremovewaterdailythroughexhalation,anincreasedrespiratoryratecanpromoteexcessivelossofwater.Excessivelosscanalsooccurwithfeveroranyotherconditionthatincreasesthemetabolicrateandthustherespiratoryrate.(SeeCausesofrespiratoryfailure,page264.)
CausesofrespiratoryfailureProblemswiththebrain,lungs,muscles,andnervesorwithpulmonarycirculationcanimpairgasexchangeandcauserespiratoryfailure.Here’salistofconditionsthatcancauserespiratoryfailure.
Brain
•Anesthesiaorcertainmedications(opioids)
•Cerebralhemorrhage
•Cerebraltumor
•Drugoverdose
•Headtrauma
•Skullfracture
Lungs
•Acuterespiratorydistresssyndrome(ARDS)
•Asthma
•Chronicobstructivepulmonarydisease(COPD)
•Cysticfibrosis
•Flailchest
•Massivebilateralpneumonia
•Sleepapnea
•Trachealobstruction
Musclesandnerves
•Amyotrophiclateralsclerosis
•Guillain-Barrésyndrome
•Multiplesclerosis
•Musculardystrophy
•Myastheniagravis
•Polio
•Spinalcordtrauma
Pulmonarycirculation
•Heartfailure
•Pulmonaryedema
•Pulmonaryembolism
HypokalemiaIfapatientbeginstohyperventilateandalkalosisresults,hydrogenionswillmoveoutofthecellsandpotassiumionswillmovefromthebloodintothecells.Thatshiftcancausehypokalemia.
HyperkalemiaInacidosis,excesshydrogenionsmoveintothecell.Potassiumionsthenmoveoutofthecellandintothebloodtobalancethepositivechargesbetweenthetwofluidcompartments.Hyperkalemiamayresult.
RespiratoryacidosisRespiratoryacidosis,whichisduetohypoventilation,resultsfromtheinabilityofthelungstoeliminatesufficientquantitiesofcarbondioxide.Theexcesscarbondioxidecombineswithwatertoformcarbonicacid.IncreasedcarbonicacidlevelsresultindecreasedpH,whichcontributestorespiratoryacidosis.
RespiratoryalkalosisRespiratoryalkalosisdevelopsfromanexcessivelyrapidrespiratoryrate,orhyperventilation,andcausesexcessivecarbondioxideelimination.Lossofcarbondioxidedecreasestheblood’sacid-formingpotentialandresultsinrespiratoryalkalosis.
MetabolicacidosisConditionsthatcausehypoxiacausecellstouseanaerobicmetabolism.Thatmetabolismcreatesanincreaseintheproductionoflacticacid,whichcanleadtometabolicacidosis.
WhattolookforHypoxemiaandhypercapnia,whicharecharacteristicofacuterespiratoryfailure,stimulatestrongcompensatoryresponsesfromallbodysystems,especiallytherespiratory,cardiovascular,andcentralnervoussystems(CNS).
LeadingwiththelungsWhenthebodysenseshypoxemiaorhypercapnia,therespiratorycenterrespondsbyincreasingrespiratorydepthandthenrespiratoryrate.Signsoflaboredbreathing—flarednostrils,pursed-lipexhalation,andtheuseofaccessorybreathingmuscles,amongothers—maysignifyrespiratoryfailure.Asrespiratoryfailureworsens,muscleretractionsbetweentheribs,abovetheclavicle,and
abovethesternummayalsooccur.Thepatientisdyspneicandmaybecomecyanotic.Auscultationofthechestrevealsdiminishedorabsentbreathsoundsovertheaffectedarea.Youmayalsohearwheezes,crackles,orrhonchi.Respiratoryarrestmayoccur.
TheheartheatsupThesympatheticnervoussystemusuallycompensatesbyincreasingtheheartrateandconstrictingbloodvesselsinanefforttoimprovecardiacoutput.Thepatient’sskinmaybecomecool,pale,andclammy.Eventually,asmyocardialoxygenationdiminishes,cardiacoutput,bloodpressure,andheartratedrop.Arrhythmiasdevelop,andcardiacarrestmayoccur.
Memoryjogger
Whenyouauscultateapatientwithworseningrespiratoryfailure,certainsignsmaystickinyourCRAW:
Crackles
Rhonchi
Absentbreathsounds
Wheezes.
S.O.S.fromtheCNSEvenaslightdisruptioninoxygensupplyandcarbondioxideeliminationcanaffectbrainfunctionandbehavior.Hypoxiainitiallycausesearlysignsofanxietyandrestlessness,whichcanprogresstomarkedconfusion,agitation,andlethargy.Theprimaryindicatorofhypercapnia,headache,occursascerebralvesselsdilateinanefforttoincreasethebrain’sbloodsupply.Ifthecarbondioxidelevelcontinuestorise,thepatientwilldisplayfatigueandbeatriskforseizuresandcoma.(SeeRecognizingworseningrespiratoryfailure,page266.)
CAUTION!
RecognizingworseningrespiratoryfailureThefollowingassessmentfindingscommonlyoccurinpatientswithworseningrespiratoryfailure:
•arrhythmias
•bradycardia
•cyanosis
•diminishedorabsentbreathsoundsoveraffectedareaand,possibly,wheezes,crackles,orrhonchi
•dyspnea
•airhunger
•hypotension
•muscleretractions.
WhattestsshowThefollowingdiagnostictestresultscanhelpdiagnoserespiratoryfailureandguideitstreatment:•ABGchangesindicaterespiratoryfailure.(AlwayscompareABGresultswithyourpatient’s
baselinevalues.Forapatientwithpreviouslynormallungs,theABGchangesmayrevealthepHusuallylessthan7.35,thePaO2lessthan50mmHg,andthePaCO2greaterthan50mmHg.InapatientwithCOPD,anacutedropinthePaO2levelof10mmHgormoreindicatesrespiratoryfailure.KeepinmindthatpatientswithCOPDhaveachronicallylowPaO2,increasedPaCO2,increasedbicarbonatelevels,butanormalpH.)
•ChestX-raysmayidentifyanunderlyingpulmonarycondition.
•Electrocardiogram(ECG)changesmayshowarrhythmias.•Changesinserumpotassiumlevelsmayberelatedtoacid-basebalance.
Howit’streatedTheunderlyingcauseofrespiratoryfailuremustbeaddressedandoxygenandcarbondioxidelevelsimproved.
Uptheoxygen—butnottoomuchOxygenisgivenincontrolledconcentrations,oftenusingaVenturimask.AVenturimaskmixesoxygenwithroomair,creatinghigh-flowenrichedoxygenofasettableconcentration.Itprovidesanaccurateandconstantdeliveryofoxygen(AmericanThoracicSociety,2014).Thegoalofoxygentherapyistopreventoxygentoxicitybyadministeringthelowestdoseofoxygenfortheshortestperiodoftimewhileachievinganoxygensaturationof90%ormoreoraPaO2levelofatleast60mmHg.Oxygentherapymustbeusedcautiouslyinpatientswithchroniclungdisease.
Intubate,ventilate,saturateIntubationandmechanicalventilationareindicatedifconservativetreatmentfailstoraiseoxygensaturationabove90%.Thepatientmayalsobeintubatedandventilatedifacidemiacontinues,ifhebecomesexhausted,orifrespiratoryarrestoccurs.Intubationprovidesapatentairway.Mechanicalventilationdecreasestheworkofbreathing,ventilatesthelungs,andimprovesoxygenation.Positiveend-expiratorypressure(PEEP)therapymaybeorderedduringmechanicalventilation
orwithabilevelpositiveairwaypressure(BiPAP)masktoimprovegasexchange.PEEPmaintainspositivepressureattheendofexpiration,thuspreventingtheairwaysandalveolifromcollapsingbetweenbreaths.BiPAPisapressure-controlledventilationsystemwithtwocyclesthatsupportsspontaneousbreathing.
KeeptheairwaysopenforbusinessBronchodilators,especiallyinhalants,areusedtoopentheairways.Ifthepatientcan’tinhaleeffectivelyorisonamechanicalventilator,hemayreceiveabronchodilatorviaanebulizer.Acorticosteroid,theophylline,andanantibioticmayalsobeordered.Thepatientmayalsoneedchestphysiotherapy,includingposturaldrainage,chestpercussion,andchestvibrationandpossiblysuctioningtocleartheairways.I.V.fluidsmaybeorderedtocorrectdehydrationandtohelpthinsecretions.Adiureticmayhelpifthepatientisexperiencingfluidoverload.
HowyouinterveneTocareeffectivelyforapatientwithrespiratoryfailure,followtheseguidelines:
•Assessrespiratorystatus;monitorrate,depth,andcharacterofrespirations,checkingbreathsoundsforabnormalities.
•Monitorvitalsignsfrequently.•Monitorthepatient’sneurologicstatus;itmaybecomedepressedasrespiratoryfailure
worsens.•Makesureyourongoingrespiratoryassessmentincludesskinandmucousmembranecolor;
accessorymuscleuse;changesinbreathsounds;ABGanalysis;secretionproductionandclearance;andrespiratoryrate,depth,andpattern.Notifythepractitionerifinterventionsdon’timprovethepatient’scondition.
•Monitorfluidstatusbymaintainingaccuratefluidintakeandoutputrecords.Obtaindailyweights.
•Evaluateserumelectrolytelevelsforabnormalitiesthatcanoccurwithacid-baseimbalances.•EvaluateECGresultsforarrhythmias.•Monitoroxygensaturationvalueswithapulseoximeter.•Interveneasneededtocorrectunderlyingrespiratoryproblemsandassociatedalterationsin
acid-basestatus.•Keepahandheldresuscitationbagatthebedside.•MaintainpatentI.V.accessasorderedformedicationandI.V.fluidadministration.•Administeroxygenasorderedtohelpmaintainadequateoxygenationandrestorenormal
respiratoryrate.•UsecautionwhenadministeringoxygentoapatientwithCOPD.Increasedoxygenlevelscan
depressthebreathingstimulus.•Makesuretheventilatorsettingsareattheorderedparameters.•Performchestphysiotherapyandposturaldrainageasneededtopromoteadequateventilation.•Ifthepatientisretainingcarbondioxide,encourageslowdeepbreathswithpursedlipsto
preventalveolarcollapse.Urgetothecoughingupofsecretions.Ifthepatientcan’tmobilizesecretions,suctionwhennecessary.
•Unlessthepatientisretainingfluidorhasheartfailure,increasehisfluidintaketo2qt(2
L)/daytohelpliquefysecretions.•Repositiontheimmobilizedpatientevery1to2hours.•Positionthepatientforoptimumlungexpansion.Sittheconsciouspatientuprightastoleratedin
asupported,forward-leaningpositiontopromotediaphragmmovement.Supplyanoverbedtableandpillowsforsupport.
•Ifthepatientisn’tonaventilator,avoidgivingnarcoticsoranotherCNSdepressantbecauseeithermayfurthersuppressrespirations.
•Limitcarbohydrateintakeandincreaseproteinintakebecausecarbohydratemetabolismcausesmorecarbondioxideproductionthanproteinmetabolism.
•Calmandreassurethepatientwhilegivingcare.Anxietycanraiseoxygendemands.•Pacecareactivitiestomaximizethepatient’senergylevelandtoprovideneededrest.Limitthe
needtorespondverbally.Talkingmaycauseshortnessofbreath.•Implementsafetymeasuresasneededtoprotectthepatient.Reorienttheconfusedpatient.•Stresstheimportanceofreturningforroutinefollow-upappointmentswiththedoctor.•Explainhowtorecognizesignsandsymptomsofoverexertion,fluidretention,andheartfailure.
Thesemayincludeaweightgainof2to3lb(0.9to1.4kg)/day,edemaofthefeetorankles,nausea,lossofappetite,shortnessofbreath,orabdominaltenderness.(SeeTeachingaboutrespiratoryfailure.)
Teachingpoints
Teachingpoints
TeachingaboutrespiratoryfailureWhenteachingapatientwithrespiratoryfailure,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:
•basicsofrespiratoryfailureanditstreatment
•properpulmonaryhygieneandcoughingtechniques
•needforproperrest
•needtoquitsmoking,ifappropriate
•prescribedmedications
•warningsignsandsymptomsandwhentoreportthem
•importanceoffollow-upappointments
•dietrestrictions,ifappropriate.
•Helpthepatientdeveloptheknowledgeandskillsheneedstoperformpulmonaryhygiene.Encourageadequatehydrationtothinsecretions—butinstructthepatienttonotifythedoctorofanysignsorsymptomsoffluidretentionorheartfailure.
•Documentallinstructionsgivenandcareprovided.(SeeDocumentingrespiratoryfailure.)
Chartsmart
DocumentingrespiratoryfailureIfyourpatienthasrespiratoryfailure,makesureyoudocumentthefollowinginformation:
•breathsounds
•lungsecretions
•laboratoryresults
•breathingexercisesandthepatient’sresponse
•colorandtemperatureofskin
•dailyweight
•intakeandoutput
•measurestakentopromoteventilationandthepatient’sresponse
•neurologicstatus
•notificationofdoctor
•oxygentherapy
•safetymeasures
•patientteaching.
That'sawrap!
Respiratoryfailurereview
Respiratoryfailurebasics
•Occurswhenthelungscan’tsufficientlymaintainarterialoxygenationoreliminatecarbondioxide
•Usuallyproduceshypercapniaandhypoxemiainpatientswithnormallungtissue
•MaybesignaledonlybyanacutedropinABGlevelsandclinicaldeteriorationinpatientswithCOPD
•Gasexchangediminishedbythreemajormalfunctions:alveolarhypoventilation,( )mismatch,andintrapulmonaryshunting
ImbalancesassociatedwithrespiratoryfailureHypervolemia
•Maybecausedbyexcessivefluidabsorptionasaresultofprolongedrespiratorytreatmentsorincreasedlungcapillarypressureorpermeability
•Mayprecipitatepulmonaryedema
Hypovolemia
•Maybecausedbyincreasedrespiratoryrate,whichcanpromoteexcessivewaterloss
•Mayalsooccurwithfeveroranyotherconditionthatincreasesthemetabolicrateandthustherespiratoryrate
Hypokalemia
•Maybecausedbyhyperventilationandresultingalkalosis,whichcauseshydrogenionstomoveoutofthecellsandpotassiumionstoshiftfromthebloodandintothecells
Hyperkalemia
•Maybecausedbyacidosis,inwhichexcesshydrogenionsmoveintothecellswhilepotassiumionsshiftfromthecellsandintotheblood
Respiratoryacidosis
•Resultsfromhypoventilation(lungscan’teliminatecarbondioxide;carbondioxidecombineswithwatertoformcarbonicacid)
•ContributedtobydecreasedpHlevelsthatresultfromincreasedcarbonicacid
Respiratoryalkalosis
•Resultsfromhyperventilation(rapidrespirationcausesexcessivecarbondioxideelimination,whichdecreasestheblood’sacid-formingpotential,resultinginalkalosis)
Metabolicacidosis
•Resultsfromhypoxia,whichcausescellstouseanaerobicmetabolism
•Producesanincreaseinlacticacid,leadingtometabolicacidosis
Signsandsymptoms
•Increasedrespiratorydepthandrate
•Muscleretractionbetweentheribs,abovetheclavicle,andabovethesternum
•Increasedheartrateandarrhythmias
•Constrictionofbloodvessels
•Anxietyandrestlessness,progressingtofatigue,confusion,agitation,andlethargy
•Headaches
•
Changesinserumpotassiumlevels
Treatment
•Lowestpossibledoseofoxygenfortheshortestamountoftimetopreventoxygentoxicity
•Intubationandventilationifunabletoachieveoxygensaturationabove90%
•Bronchodilatorsasorderedtoopenairways
•Corticosteroids,theophylline,antibiotics,chestphysiotherapy,andsuctioningasordered
•I.V.fluidsfordehydrationordiureticsforafluidoverloadasordered
Quickquiz
1.Whenthebodysenseshypoxemiaorhypercapnia,thebrain’srespiratorycenterrespondsby:
A.slowingdowntherespiratoryrate.B.decreasingtheheartrate.C.increasingthedepthandrateofrespirations.D.increasingtheheartrate.
Answer:C.Thebrain’srespiratorycenterinitiallycausesanincreaseinrespiratoryrate.Itthencausesanincreaseinrespiratorydepthinanefforttoblowoffexcesscarbondioxide.
2.Respiratoryalkalosiscandevelopfrom:A.hyperventilation.B.excessivevomiting.C.prolongeduseofantacids.D.decreasedrespiratoryrate.
Answer:A.Respiratoryalkalosisdevelopsfromanexcessivelyrapidrespiratoryrate—hyperventilation—whichcausesexcessivecarbondioxideelimination.
3.Prolongedrespiratorytreatment,suchasnebulizeruse,canleadtowhichofthefollowingconditions?
A.HypovolemiaB.RespiratoryalkalosisC.RespiratoryacidosisD.Hypervolemia
Answer:D.Prolongedrespiratorytreatments,suchasnebulizeruse,canleadtotheinhalationandabsorptionofwatervapor,whichcanleadtohypervolemia.
4.You’reconcernedaboutpossiblerespiratoryfailureinyournewlyadmittedpatient.Whenadministeringdrugtherapy,youshouldavoidgivinghimwhichofthefollowingagents?
A.AnticholinergicsB.CorticosteroidsC.OpioidsD.Antihypertensives
Answer:C.Opioidsdepresstherespiratorycenterofthebrainandmayhastenthedevelopmentofrespiratoryfailure.
5.Apatientwithrespiratoryfailureshouldlimithisintakeof:A.protein.B.carbohydrates.C.water.D.sodium.
Answer:B.Apatientwithrespiratoryfailureshouldlimitcarbohydrateintakeandincreaseproteinintakebecausecarbohydratemetabolismcausesmorecarbondioxideproductionthanproteinmetabolism.
Scoring
Ifyouansweredallfivequestionscorrectly,outstanding!You’reaninspirationwhenitcomestorespiration!Ifyouansweredfourquestionscorrectly,great!Breathedeeplyandappreciateyouraccomplishment!Ifyouansweredfewerthanfourquestionscorrectly,don’tworry.Keepyourheadupandcatchyourbreath;youhavemorechapterstorunthrough!
ReferencesAmericanThoracicSociety.(2014).Oxygendeliverymethods.Retrievedfrom
https://www.thoracic.org/clinical/copd-guidelines/for-health-professionals/exacerbation/inpatient-oxygen-therapy/oxygen-delivery-methods.php
Chapter15
ExcessiveGIfluidloss
JustthefactsInthischapter,you’lllearn:
♦causesofexcessivegastrointestinal(GI)fluidloss
♦fluid,electrolyte,andacid-baseimbalancesthatoccurwithexcessiveGIfluidlossandwaystotreatthem
♦signsandsymptomsofexcessiveGIfluidloss
♦teachingpointsforpatientswithexcessiveGIfluidloss.
AlookatexcessiveGIfluidlossNormally,verylittlefluidislostfromtheGIsystem.Mostfluidisreabsorbedintheintestines.However,thepotentialforsignificantlossexistsbecauselargeamountsoffluids—isotonicandhypotonic—passthroughtheGIsysteminthecourseofaday.IsotonicfluidsthatmaybelostfromtheGItractincludegastricjuices,bile,pancreaticjuices,
andintestinalsecretions.Theonlyhypotonicfluidthatmaybelostissaliva,whichhasalowersoluteconcentrationthanotherGIfluids.
HowithappensExcessiveGIfluidlossmaycomefromphysicalremovalofsecretionsasaresultofvomiting,suctioning,orincreasedordecreasedGItractmotility.Excessivefluidscanbeexcretedaswasteproductsorsecretedfromtheintestinalwallintotheintestinallumen,bothofwhichleadtofluidandelectrolyteimbalances.(SeeImbalancescausedbyexcessiveGIfluidloss.)
ImbalancescausedbyexcessiveGIfluidlossExcessiveGIfluidlosscanleadtoanumberoffluid,electrolyte,andacid-baseimbalances.Here’sabreakdownofthoseimbalances.
Fluidimbalances•
Hypovolemiaanddehydration—Largeamountsoffluidcanbelostduringprolonged,uncorrectedvomitinganddiarrhea.Hypovolemiacanalsoresultifgastricandintestinalsuctioningoccurwithoutpropermonitoringofintakeandoutputtomakesurelostfluidandelectrolytesareadequatelyreplaced.
Electrolyteimbalances•
Hypokalemia—Theexcessivelossofgastricfluidsrichinpotassiumcanleadtohypokalemia.•
Hypomagnesemia—Althoughgastricsecretionscontainlittlemagnesium,severalweeksofvomiting,diarrhea,orgastricsuctioningcanresultinhypomagnesemia.Becausehypomagnesemiaitselfcancausevomiting,thepatient’sconditionmaybeself-perpetuating.•
Hyponatremia—Prolongedvomiting,diarrhea,orgastricorintestinalsuctioningcandepletethebody’ssupplyofsodiumandleadtohyponatremia.•
Hypochloremia—Anylossofgastriccontentscausesthelossofchloride.Prolongedgastricfluidlosscanleadtohypochloremia.
Acid-baseimbalances•
Metabolicacidosis—Anyconditionthatpromotesintestinalfluidlosscanresultinmetabolicacidosis.Intestinalfluidcontainslargeamountsofbicarbonate.Withthelossofbicarbonate,pHfalls,creatinganacidiccondition.•
Metabolicalkalosis—LossofgastricfluidsfromvomitingortheuseofdrainagetubesintheupperGItractcanleadtometabolicalkalosis.Gastricfluidscontainlargeamountsofacidsthat,whenlost,leadtoanincreaseinpHandalkalosis.Excessiveuseofantacidscanalsoworsentheimbalancebyaddingtothealkaloticstate.
Osmoticdiarrheamayoccurintheintestineswhenahighsoluteloadintheintestinallumenattractswaterintothecavity.BothacidsandbasescanbelostfromtheGItract.
VomitingandsuctioningVomitingormechanicalsuctioningofstomachcontents,aswithanasogastrictube,causestheloss
ofhydrogenionsandelectrolytes,suchaschloride,potassium,andsodium.Vomitingalsodepletesthebody’sfluidvolumesupplyandcauseshypovolemia.Dehydrationoccurswhenmorewaterthanelectrolytesislost.Whenassessingacid-basebalance,rememberthatthepHoftheupperGItractislowandthatvomitingcausesthelossofthoseacidsandraisestheriskofalkalosis.(SeeCharacteristicsandcausesofvomiting,page274.)
CharacteristicsandcausesofvomitingVomitingmayleadtoseriousfluid,electrolyte,andacid-basedisturbancesandcanoccurforavarietyofreasons.Bycarefullyobservingthecharacteristicsofthevomitusand,asneeded,questioningthepatient,youmaygaincluesastotheunderlyingdisorder.Here’swhatthevomitusmayindicate.
Bile-stained(greenish)Obstructionbelowthepylorus,asfromaduodenallesion
BloodyUpperGIbleeding,asfromgastritisorpepticulcer(ifbrightred)orfromgastricoresophagealvarices(ifdarkred)
BrownwithafecalodorIntestinalobstructionorinfarction
Burning,bitter-tastingExcessivehydrochloricacidingastriccontents
Coffee-groundconsistencyDigestedbloodfromslowlybleedinggastricorduodenallesions
UndigestedfoodGastricoutletobstruction,asfromgastrictumororulcer
BowelmovementsAnincreaseinthefrequencyandamountofbowelmovementsandachangeinthestooltowardawateryconsistencycancauseexcessivefluidloss,resultinginhypovolemiaanddehydration.Inadditiontofluidloss,diarrheacancausealossofpotassium,magnesium,andsodium.FluidslostfromthelowerGItractcarryalargeamountofbicarbonatewiththem,whichlowerstheamountofbicarbonateavailabletocountertheeffectsofacidsinthebody.
LaxativesandenemasLaxativesandenemasmaybeusedbypatientstotreatconstipation,ortheymaybegiventopatientsbeforeabdominalsurgeryordiagnosticstudiestocleanthebowel.Excessiveuseoflaxatives—suchasmagnesiumsulfate,milkofmagnesia,andFleetPhospho-soda—cancausehighmagnesium(hypermagnesemia)andphosphorus(hyperphosphatemia)levels.Excessiveuseofcommerciallypreparedenemascontainingsodiumandphosphate,suchas
Fleetenemas,cancausehighphosphorusandsodium(hypernatremia)levelsiftheenemasareabsorbedbeforetheycanbeeliminated.Excessiveuseoftapwaterenemascancauseadecreaseinsodiumlevelsbecausewaterabsorbedbythecoloncanhaveadilutionaleffectonsodium.
FactorinfluidlossExcessiveGIfluidlosscanresultfromseveralotherfactors,too.BacterialinfectionsoftheGItracttypicallycausevomitinganddiarrhea.Antibioticadministrationremovesthenormalfloraandpromotesdiarrhea.Agecanalsoplayarole;infantsandyoungchildrenareespeciallyvulnerabletodiarrhea.Pregnancy,pancreatitis,hepatitisand,inyoungchildren,pyloricstenosiscanallbeaccompaniedbyvomiting.
AnabundanceofimbalancesImbalancescanalsoresultfromfecalimpaction,poorabsorptionoffoods,poordigestion,anorexianervosa,orbulimiaaswellasexcessiveintakeofalcoholicsubstancesandsomeillicitdrugs.Suchdisordersasanorexianervosaandbulimia,whichprimarilyaffectyoungwomen,typicallyinvolvetheuseoflaxativesandvomitingasameansofcontrollingweight.Thiscanleadtonumerousfluid,electrolyte,andacid-baseimbalances.(SeeAdolescentsandexcessiveGIfluidloss.)Otherdisordersthatcancausedisturbancesinfluid,electrolyte,oracid-basebalanceincludethepresenceoffistulasinvolvingtheGItract,GIbleeding,intestinalobstruction,andparalyticileus.
Agesandstages
AdolescentsandexcessiveGIfluidlossWhentreatinganadolescent,especiallyafemale,forexcessiveGIfluidloss,assessforsignsandsymptomsofanorexiaandbulimia.Teeththatappearyellowandwornawayandahistoryoflaxativeordietpillusearetwoobvioussigns.Also,assessthepatientforuseofalternativediettherapies,particularlypillscontainingmahuang
orephedrine,whichspeedthemetabolismbymimickingtheeffectsofadrenalineontheGIsystem.Otheragentssuchasorlistat(Xenical)bindtogastricandpancreaticenzymestopreventdigestionoffatsandmayproduceGIfluidlossaswellasdecreasedabsorptionofvitamins.
Memoryjogger
Remember,laxativesandenemascanmakeapatientHYPER:
Excessivelaxativeusecancausehypermagnesemiaandhyperphosphatemia.
Excessiveuseofenemasthatcontainsodiumandphosphatecancausehypernatremiaandhyperphosphatemia.
Theuseofenteraltubefeedingsandostomies(especiallyileostomies)mayalsoleadtoimbalances.Enteraltubefeedingsmaycausediarrheaorvomiting,dependingontheircomposition,concentration,andthepatient’scondition.Suctioningofgastricsecretionsthroughtubesmaydepletethebodyofvitalfluids,electrolytes,andacids.Dysphagiarelatedtoextensiveheadandneckcancerandotherconditionsthatinterferewithswallowingmayresultinsalivaloss.
WhattolookforWithexcessiveGIfluidloss,thepatientmayshowsignsofhypovolemia.Lookforthesesignsandsymptoms:•Tachycardiaoccursasthebodytriestocompensateforhypovolemiabyincreasingtheheart
rate.Bloodpressurealsofallsasintravascularvolumeislost.•Thepatient’sskinmaybecoolanddryasthebodyshuntsbloodflowtomajororgans.Skin
turgormaybedecreasedortheeyeballsmayappeartobesunken,asoccurswithdehydration.Urineoutputdecreasesaskidneystrytoconservefluidandelectrolytes.
•Cardiacarrhythmiasmayoccurfromelectrolyteimbalances,suchasthoserelatedtopotassiumandmagnesium.Thepatientmaybecomeweakandconfused.Mentalstatusmaydeteriorateasfluid,electrolyte,andacid-baseimbalancesprogress.
Takingadeepbreath•Respirationsmaychangeaccordingtothetypeofacid-baseimbalancethepatientdevelops.
Forinstance,acidosiswillcauserespirationstobedeeperasthepatienttriestoblowoffacid.•Thepatientwillalsohavesignsandsymptomsrelatedtotheunderlyingdisorder—forinstance,
pancreatitis.(SeeRecognizingexcessiveGIfluidloss.)
CAUTION!
RecognizingexcessiveGIfluidlossInadditiontothesignsandsymptomsrelatedtotheunderlyingdisorder,apatientwithexcessiveGIfluidlossmayshowthesesignsandsymptomsofhypovolemia:•
changesinrespiration•
weightloss•
confusionordeterioratedmentalstatus•
cool,dry,paleskin•
musclecramps•
decreasedbloodpressure•
decreased/tentingskinturgororsunkeneyeballs•
decreasedoutputwithconcentratedurine•
possiblearrhythmias•
tachycardia•
weakness.
WhattestsshowDiagnostictests,suchasendoscopy,ultrasound,computerizedtomography,ormagneticresonanceimaging,mayrevealthecauseandextentofthedisorder.Inaddition,diagnostictestresultsrelatedtothefluid,electrolyte,andacid-baseimbalancesassociatedwithexcessiveGIfluidlosscanhelpdirectyournursinginterventions.Suchresultsinclude:
•changesinarterialbloodgaslevelsrelatedtometabolicacidosisormetabolicalkalosis•alterationsinthelevelsofcertainelectrolytes,suchaspotassium,magnesium,and/orsodium•hematocritthatmaybefalselyelevatedinavolume-depletedpatient•culturesofbodyfluidsamplesthatmayhelptoidentifybacteriaresponsiblefortheunderlying
disorder.
Howthey’retreatedTreatmentisaimedattheunderlyingcauseoftheimbalancetopreventfurtherfluidandelectrolyteloss.Forinstance,anantiemeticandanantidiarrhealmaybegivenforvomitinganddiarrhea,respectively.Inanotherinstance,GIdrainagetubesandthesuctionappliedtothemshouldbediscontinuedassoonaspossible.ThepatientshouldalsoreceiveI.V.ororalfluidreplacement,dependingonhistoleranceand
thecauseofthefluidloss.Hemayalsoneedelectrolytesreplacedifhisserumlevelsaredecreased.Long-termparenteralnutritionmaybeneeded.Ifinfectionistheunderlyingcauseoffluidloss,thepatientmayneedantibiotics.
HowyouinterveneApatientwithaconditionthataltersfluidandelectrolytebalancethroughGIlossesrequiresclosemonitoring.You’llneedtoreportanyincreaseintheamountofdrainageorchangeindrainagecharacteristicsfromGItubesorincreaseinthefrequencyofvomitingordiarrhea.FollowtheseinterventionswhencaringforapatientwithGIfluidlosses:•Measureandrecordtheamountoffluidlostthroughvomiting,diarrhea,orgastricorintestinal
suctioning.RemembertoincludeGIlossesaspartofthepatient’stotaloutput.SignificantincreasesinGIlossplacesthepatientatincreasedriskforfluidandelectrolyteimbalancesandmetabolicalkalosisoracidosis.
•Assessthepatient’sfluidstatusbymonitoringintakeandoutput,dailyweight,andskinturgor.•Assessvitalsignsandreportanychangesthatmayindicatefluiddeficits,suchasadecreased
bloodpressureorincreasedheartrate.•Reportvomitingtokeepimbalancesfrombecomingsevereandtoinitiateprompttreatment.•Administeroralfluidscontainingwaterandelectrolytes,suchasGatoradeorPedialyte,ifthe
patientcantoleratefluids.(SeeTeachingaboutexcessiveGIfluidloss.)
Teachingpoints
Teachingpoints
TeachingaboutexcessiveGIfluidlossWhenteachingapatientwithexcessiveGIfluidloss,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
basicsoftheconditionanditstreatment•
needtoreportprolongedvomitingordiarrhea•
importanceofavoidingrepeateduseofenemasandlaxatives•
propertechniqueforirrigatingagastrictube,ifappropriate•
propertechniqueformonitoringI.V.infusion,ifappropriate.
•Performoralcareandprovidelipbalmbecausethemucousmembranesandlipsmaybedryandcracked.
•MaintainpatentI.V.accessasordered.AdministerI.V.replacementfluidsasprescribed.Monitortheinfusionrateandvolumetopreventhypervolemia.(SeeDon’tgotoofastwithfluids.)
Agesandstages
Agesandstages
Don’tgotoofastwithfluidsElderlypatientscandevelopheartfailureifI.V.fluidsareinfusedtoorapidly.Therefore,usecautionwhenadministeringI.V.fluidstoreplacefluidlossesinthesepatients.
•Ifthepatientisundergoinggastricsuctioning,monitorGItubeplacementoftentopreventfluidaspirationortubemigration.
•Irrigatethesuctiontubewithisotonicnormalsalinesolutionasordered.Remember,neveruseplainwaterforirrigation.Itdrawsmoregastricsecretionsintothestomachinanattempttomakethefluidisotonicforabsorption.Also,thefluidissuctionedoutofthestomach,causingfurtherdepletionoffluidsandelectrolytes.
•Whenthepatientisconnectedtogastricsuction,restricttheamountoficechipsgivenbymouthandexplainthereasonfortherestriction.Gastricsuctioningoficechipscandepletefluidandelectrolytesfromthestomach.
•Administermedications,suchasanantiemeticorantidiarrheal,asprescribedtocontrolthepatient’sunderlyingcondition.
•EvaluateserumelectrolytelevelsandpHtodetectabnormalitiesandtomonitortheeffectivenessoftherapy.
•Chartallinstructionsgivenandcareprovided.(SeeDocumentingexcessiveGIfluidloss.)
Chartsmart
DocumentingexcessiveGIfluidlossIfyourpatienthasexcessiveGIfluidloss,makesureyoudocumentthefollowinginformation:•
vitalsigns•
intakeandoutput•
dailyweight•
presenceandcharacteristicsofvomitus,diarrhea,and/orGIfluiddrainage•
skinturgor•
correctplacementofGItube,ifpresent,pluscarerelatedtothetube•
interventionsusedtodecreaseGIfluidloss•
I.V.ororalfluidandelectrolytereplacementtherapyandthepatient’sresponse.
That'sawrap!
ExcessiveGIfluidlossreview
ExcessiveGIfluidloss•
Mayresultfromvomiting,suctioning,orincreasedordecreasedGItractmotility•
Maybeexcretedaswasteproductsorsecretedfromtheintestinalwallintotheintestinallumen,leadingtofluidandelectrolyteimbalances
Causes•
Anorexianervosa•
Antibioticuse•
BacterialGIinfections•
Bulimia•
Enteraltubefeedingsandostomies•
Excessiveintakeofalcoholandillicitdrugs•
Excessiveuseofenemasandlaxatives•
Fecalimpaction•
GIbleeding•
GIfistulas•
Intestinalobstruction•
Pancreatitisorhepatitis•
Paralyticileus
•Poorabsorptionoffoods•
Poordigestion•
Pyloricstenosisinyoungchildren
Signsandsymptoms•
Alteredrespirations•
Arrhythmias•
Cool,dryskinordecreasedskinturgor•
Decreased,concentratedurineoutput•
Falselyelevatedhemoglobinlevelandhematocrit•
Increasedheartrateanddecreasedbloodpressure•
Sunkeneyeballs•
Musclecramps•
Weaknessandconfusion
ImbalancesassociatedwithexcessiveGIfluidlossHypovolemiaanddehydration•
Canoccurwithprolongedvomitinganddiarrheaorifgastricandintestinalsuctioningoccurwithoutpropermonitoringofintakeandoutput
Hypokalemia•
Canoccurwithexcessivelossofgastricfluidsrichinpotassium
Hypomagnesemia•
Canoccurwithprolonged(lastingseveralweeks)vomiting,diarrhea,orgastricsuctioning
Hyponatremia•
Canoccurwithprolongedvomiting,diarrhea,orgastricsuctioning•
Canalsooccurwithexcessiveuseoftapwaterenemasbecausewaterabsorbedbythecoloncanhaveadilutionaleffectonsodium
Hypochloremia•
Canbecausedbyanylossofgastriccontents
Metabolicacidosis•
Causedbyalossofintestinalfluid,whichcauseslossofbicarbonate,leadingtodecreasedpHandanacidicstate
Metabolicalkalosis•
Causedbyalossofgastricfluids,includingacid,whichincreasespHandcreatesanalkaloticstate
Hypermagnesemiaandhyperphosphatemia•
Maybecausedbyexcessiveuseoflaxatives,suchasmagnesiumsulfate,milkofmagnesia,andFleetPhospho-soda
Hypernatremiaandhyperphosphatemia•
Maybecausedbyexcessiveuseofenemascontainingsodiumandphosphorus,suchasFleetenemas
Treatment•
Preventionoffurtherfluidandelectrolyteloss•
Antiemeticsfornauseaandvomitingifindicated•
Antidiarrhealsifdiarrheaisthecause•
I.V.ororalfluidreplacement,dependingontheseverity•
Electrolytereplacement•
Long-termparenteralnutritionifneeded•
Antibioticsifinfectionistheunderlyingcause
Quickquiz
1.WhichofthefollowingfluidandelectrolyteimbalancescanoccurwithexcessiveGIfluidloss?
A.Hypomagnesemia,hypermagnesemia,andhyponatremiaB.Hypomagnesemia,hypernatremia,andhyperchloremiaC.Hypervolemia,hyponatremia,andhypernatremiaD.Hypervolemia,hypomagnesemia,andhyperkalemia
Answer:A.Hypomagnesemia,hypermagnesemia,andhyponatremia—andothers—mayoccurwithvaryingtypesofGIfluidloss.
2.ApatientwithfluidlossesfromtheupperGItractislikelytosufferfromwhichofthefollowingimbalances?
A.MetabolicalkalosisB.MetabolicacidosisC.RespiratoryacidosisD.Metabolicacidosis
Answer:A.FluidlossesfromtheupperGItractcanresultinmetabolicalkalosis;lossesfromthelowerGItractcanresultinmetabolicacidosis.
3.WarningsignsofhypovolemiaassociatedwithGIlossesinclude:A.bradycardia,decreasedbloodpressure,anddecreasedurineoutput.B.tachycardia,increasedbloodpressure,andincreasedurineoutput.C.decreasedbloodpressure;increasedurineoutput;andwarm,flushedskin.D.tachycardia,decreasedbloodpressure,anddecreasedurineoutput.
Answer:D.Tachycardia,decreasedbloodpressure,anddecreasedurineoutputindicatethatthepatientisexperiencinghypovolemiafromGIlosses.
4.Youcarefullyobservethecharacteristicsofthepatient’svomitusanddocumentyourfindingasbrownwithfecalodor.Thistypeofvomitusmayindicate:
A.excessivehydrochloricacidingastriccontents.B.intestinalobstruction.C.obstructionbelowthepylorus.D.gastricoutletobstruction.
Answer:B.Brownvomitusthathasafecalodormayindicateintestinalobstructionorinfarction.
Scoring
Ifyouansweredallfourquestionscorrectly,here’sahighfive!You’reaGIgenius!Ifyouansweredthreequestionscorrectly,wewanttoshakeyourhand!You’recertainlynotatalossfortherightanswers!Ifyouansweredfewerthanthreecorrectly,don’tfret!Withalittle(certainlynotexcessive!)review,you’llgetthisdownjustfine.
ReferenceHinkle,J.,&Cheever,K.(2014).Brunner&Suddarth’stextbookofmedical-surgicalnursing(13th
ed.).Philadelphia,PA:LippincottWilliams&Wilkins.
Chapter16
Acutepancreatitis
JustthefactsInthischapteryou’lllearn:
♦typesandcausesofacutepancreatitis
♦signsandsymptomsofacutepancreatitis
♦fluidandelectrolyteimbalancesthatcanoccurwithacutepancreatitis
♦treatmentsforacutepancreatitis
♦nursinginterventionsforpatientswithacutepancreatitis.
AlookatacutepancreatitisPancreatitisisaninflammationofthepancreas.Anaccessoryorganofthegastrointestinal(GI)tract,thepancreasliesintheleftupperabdomenbehindthestomachandbetweenthespleenandduodenum.Itfunctionsasbothanexocrineandendocrinegland,producingenzymesthatpromotedigestionandhormonesthataidinglucosebalance.(SeeFunctionsofthepancreas.)
FunctionsofthepancreasThepancreasworksintwoways.Asanexocrinegland,itsecretesitsproductsthroughducts—inthiscase,enzymesandbicarbonatethatpromotedigestion.Asanendocrinegland,thepancreassecreteshormonesdirectlyintothebloodstream.Thesehormoneshelpmaintainglucosebalance.
ExocrinefunctionWithinthepancreas,groupsofacinarcellsproduceprecursordigestiveenzymesthatthepancreas
secretesintotheintestinethroughthemainpancreaticduct.Theseenzymesplayacrucialroleinbreakingdownandmetabolizingcarbohydrates,proteins,andfats.Whentheseenzymesfirstcomefromtheacinarcells,theyaren’tactive;thatdoesn’thappenuntil
theycombinewithenzymesintheintestinalmucosaoftheduodenum.Thecombinedenzymesthenconvertpartiallydigestedfoodintosubstancesthebodycanuseforenergy.Thepancreasproducesthreemaintypesofenzymes:amylase,whichdigestscarbohydrates;trypsinogenandchymotrypsinogen,whichdigestprotein;andpancreaticlipase,whichcombineswithbileacidstodigesttriglycerides,amajorcomponentofdietaryfats.Pancreaticsecretionsalsocontainbicarbonate,whichcomesfromtheepithelialcellsliningthe
smallerpancreaticducts.Thebicarbonatehelpsindigestionbyneutralizingtheacidicchymethatthestomachreleasesintothesmallintestine.
EndocrinefunctionThepancreasalsosecreteshormonesdirectlyintothebloodstream,wherethey’recarriedtodifferentcellsinthebody.ItproducesthesehormonesintheisletsofLangerhans,aspecializedgroupofcells.Isletcellsaredispersedthroughoutthepancreas,althoughthetailofthepancreashasthehighestconcentration.FourdifferenttypesofcellsintheisletsofLangerhansproducehormones.Betacells,which
compose65%to80%ofisletcells,produceinsulin,amylin,andC-peptide.Insulinregulatestheuseandstorageofglucose.Itactsbyforcingmanybodycellstoabsorbanduseglucose,whichdecreasesbloodglucoselevels.Whenbloodglucoselevelsriseagain,thepancreassecretesmoreinsulin.Amylinsupplementsinsulin’sactionsbyreducingbloodglucoselevels.Italsoinhibitsthesecretionofglucagon,slowstheemptyingofthestomach,andsendsasatietysignaltothebrain.C-peptideisabyproductofinsulinproduction.Levelsofthishormonehelptoidentifyviablebetacellmass.Alphacells—15%to20%ofisletcells—produceglucagon.Thishormonehelpsmaintainasteady
bloodglucoselevel.Itdoesthisbyforcingmanybodycellstoreleaseorproduceglucose.Lowbloodglucoselevelsstimulateitssecretion;highglucoseandamylinlevelsinhibititssecretion.Deltacells,whichmakeup3%to10%ofisletcells,producesomatostatin.Thishormone
decreasestherateofnutrientabsorption,inhibitsthesecretionofmanyotherhormones—includinggrowthhormone,insulin,glucagon,andotherGIhormones—andsuppressespancreaticexocrinesecretions.Italsohasvariouscomplexeffectsonthenervoussystem.Gammaorpancreaticpolypeptidecellsmakeupamere1%ofisletcells.Thesecellsproduce
pancreaticpolypeptide.Althoughitsfunctionisunknown,it’sthoughttoinhibitappetite.Secretionofthishormoneincreasesafteraproteinmeal,fasting,exercise,andacutehypoglycemia.SomatostatinandI.V.glucosedecreaseitsproduction.
Adultsofanyagecandevelopacutepancreatitis;however,childrenrarelydevelopthedisorder.Itcanoccurineitheredematous(interstitial)ornecrotizingform.Bothtypescauseinflammationthatbeginsintheacinarcells.(SeeEdematousvs.necrotizing,page284.)Mostcasesofacutepancreatitisaremild;however,about15%ofpatientsexperienceasevereformofthediseasethatcancauselife-threateningcomplications,includingfluidandelectrolyte
disturbances.
Edematousvs.necrotizingAcutepancreatitisoccursintwoforms:edematous(orinterstitial)andnecrotizing.Bothformsbeginintheacinarcells,causinginflammation.Theseverityofthediseasedependsonthedegreeoftheinflammatoryresponseandresultingcelldamage.
Edematouspancreatitis•
Usuallymild•
Eighty-fivepercentofcases•
Self-limiting,typicallyresolvingin5to7days•
Triggersaninflammatoryresponse•
Causesfluidaccumulationandswelling•
Resultsinminimalorgandamage•
Maycausescatteredareasoffatnecrosis
Necrotizingpancreatitis•
Severe•
Fifteenpercentofcases•
Progressive•
Triggersahyperinflammatoryresponse•
Causestissuedamageandcelldeath•
Resultsinorganfailure•
Maycauselife-threateningcomplications
Acutepancreatitisthatoccursontwoormoreoccasionsisclassifiedasacuterecurrentpancreatitis.Whenprogressiverecurringepisodesofinflammationcausestructuraldamageandlossofglandularfunction,pancreatitisbecomeschronic.(SeeChronicpancreatitis,page285.)
ChronicpancreatitisInchronicpancreatitis,widespreadscarringanddestructionofpancreatictissueoccurs.Inabout80%ofcases,thedisorderresultsfromprolongedandexcessivealcoholintake.Chronicpancreatitistypicallyaffectstheexocrinefunctionsofthepancreasfirstandresultsin
weightlossbecauseoftheintestines’inabilitytodigestfoodandabsorbnutrition.Patientswithchronicpancreatitisareatriskfordeveloping:•
calculithatcanblockorcausestenosisofbileducts•
diabetesmellitus•
gastricbleeding•
pancreaticcancer•
portalhypertension•
pseudocysts•
severe,chronicpain.
HowithappensGallstonesarethemostcommoncauseofacutepancreatitis,accountingfor45%ofallcasesintheUnitedStates(Fernandez&Kerman,2013).Theypassintothebileductandtemporarilyblocktheopeningintotheduodenumatthepointwhereit’sjoinedbythepancreaticduct.Thisobstructspancreaticjuicesfromflowingoutofthepancreasintotheduodenum.Thebackflowofthesedigestivejuicescauseslysis(dissolving)ofpancreaticcellsandsubsequentpancreatitis.Thistypicallymildtypeofpancreatitisresolveswiththepassageorremovalofthegallstones.
EvilspiritsIt’sbelievedthatethylalcohol,thesecondmostcommoncauseofacutepancreatitis,cancausethediseaseinseveralways.Ethylalcoholisimplicatedasthecausativefactorin35%ofallpancreatitiscasesandisthemostcommoncauseofpancreatitisinmalesworldwide(Fernandez&Kerman,2013).AlcoholcanaffectthemotilityofthesphincterofOddi,havedirecttoxicandmetaboliceffectsonthepancreas,andformproteinplugsthatobstructsmallductsinthepancreas.It’salsobelievedthatalcoholproducesatemporarybutsignificantreductioninbloodflowtothepancreas.Whentheseepisodesoccurrepeatedly,theyresultinischemicdamagetothecells.Theseeffectscanoccurfromlong-termabuseorfromasingleepisodeofbingedrinking.A
personsensitivetotheeffectsofalcoholmayhaveanattackofacutepancreatitisafewhourstoadayortwoafterdrinking;suchapersonmaynotneedtodrinkverymuchalcoholtoprecipitateanattack.Alcoholtypicallyresultsinamoreseveretypeofpancreatitisbecauseofthecellnecrosisthatoccurs.Withrepeatedattacks,pancreatitisbecomeschronic.
CauseandexocrineeffectAcutepancreatitiscanresultfromseveralother,lesscommon,causes.(SeeCausesofacutepancreatitis,page286.)Butnomatterwhatthecause,it’stheexocrinefunctionsthatfailduringacutepancreatitis.Theenzymesthatthepancreasnormallyexcretesintotheduodenumareinstead
activatedwithinthepancreasoritsductsandbegintodigestthepancreatictissueitself.Theinflammationthatresultscausesintensepain,third-spaceshiftoflargevolumesoffluids(whichresultsinhypovolemia),pancreaticfatnecrosis(withaccompanyingconsumptionofserumcalcium),and,occasionally,hemorrhage.
CausesofacutepancreatitisAlthoughgallstonesandalcoholconsumptionarethemostcommoncausesofacutepancreatitis,manyfactorscanleadtothedisorder.Here’salistofpossiblecauses.
Biliarytractdisease•
Gallstones•
SpasmorobstructionofthesphincterofOddi
Drugs•
Glucocorticoids•
Hormonalcontraceptives•
Immunosuppressantregimens•
Nonsteroidalanti-inflammatorydrugs•
Sulfonamides•
Tetracycline•
Thiazidediuretics
Infectiousagents•
Bacteria(suchasLegionella,Mycobacteriumtuberculosis,andMycoplasmapneumoniae)•
Parasites(suchasAscarisandClonorchis)•
Viruses(suchascytomegalovirus,hepatitisviruses,HIV[Fernandez&Kerman,2013],measles,mumps,andrubella)
Toxinsandmetabolicprocesses•
Cysticfibrosis•
Ethanol(alcohol)•
Hypercalcemia•
Hyperthyroidism•
Hypertriglyceridemia•
Methanol(Fernandez&Kerman,2013)•
Organophosphorusinsecticides(Fernandez&Kerman,2013)•
Renalfailure•
Scorpionvenom
Trauma•
Blunttrauma•
Injuryduringendoscopicretrogradecholangiopancreatography•
Injuryduringupperabdominal,renal,orcardiovascularsurgery•
Organtransplantation
Other•
Abnormalpancreaticstructure•
Atherosclerosis•
Autoimmunedisease•
Cystsortumors•
Emotionalorneurogenicfactors•
Heredity•
Hypothermia•
Inflammatoryboweldisease•
Penetratingpepticulcer•
Pregnancy(thirdtrimester)•
Shock
ImbalancescausedbyacutepancreatitisAcutepancreatitis—whethermildorsevere—cancausefluidandelectrolyteimbalances,includinghypovolemia,hyponatremia,hypocalcemia,hypomagnesemia,andhypokalemia.
Turnupthe(blood)volume!Hypovolemiaisamajorcauseofdeathinpatientswithacutepancreatitis.Severepancreaticdamagetriggersthereleaseofsystemicinflammatorymediatorsthatproduceincreasedcapillarypermeabilityandvasodilation.This,inturn,producesmassivefluidshiftsfromtheintravascularspacestotheinterstitialspacesandtheretroperitoneum,resultinginhypovolemia.Vomiting,diarrhea,excessivesweating,and,possibly,hemorrhagealsocontributetohypovolemia.
ThecaseofthelostelectrolytesAcutepancreatitiscanalsoresultinthelossofcalcium,magnesium,andpotassium.Vomitinganddiarrheacanresultinhyponatremia,hypokalemia,and(whensevere)hypomagnesemia.Hyponatremiacanalsoresultfromexcessivesweatingandincreasedantidiuretichormonesecretioncausedbyhypovolemia.Hypocalcemiainacutepancreatitisusuallyresultsfromconcomitanthypoalbuminemia.Fat
necrosis—causedbylipasenecrosingthefattissueinpancreaticinterstitiumandperipancreaticspaces—mayresultinthereleaseoffreefattyacidsandintraperitonealsaponification,furtherdecreasingserumcalciumlevels.Fatnecrosiscanalsoleadtohypomagnesemiabecausemagnesiumisdepositedinareasoffatnecrosis,whichreducesserumlevels.Becausehypomagnesemiacancontributetohypocalcemia,hypomagnesemiashouldbecorrectedfirst.
WhattolookforOften,theonlysymptomofmildpancreatitisissteadyepigastricpaincenterednearthenavel
that’sunrelievedbyvomiting.Inseverepancreatitis,thepatientwilllikelyreportsevere,persistent,piercingabdominalpain,usuallyinthemidepigastricregion,althoughthepainmaygeneralizeoroccurintheleftupperquadrantandradiatetothebackorotherareas.Thepatienttypicallydescribesthepainasboringorpenetratingandmayreportrecentconsumptionofalargemealoralcohol.Hispainmayeasewhenheleansforwardorwhenheliesonhissidewithhiskneesdrawntowardhischest.
SignlanguageOtherpossiblesignsandsymptomsincludenausea;vomiting;fever;mildjaundice;tachycardia;tachypnea;musclespasms;andfatty,foul-smellingstools.Dependingontheseverityoftheillnessanddegreeoffluidlossandhemorrhage,thepatientmayalsobehypotensive.AssessmentmayrevealGreyTurner’ssign(flankecchymosis);Cullen’ssign(periumbilicalecchymosis);Chvostek’sandTrousseau’ssigns(hypocalcemia);andabdominaldistention,rigidity,andtendernesswithhypoactivebowelsounds.Pancreatitiscanleadtosevere,life-threateningcomplications.Thepatientwillneedclose
monitoringforsignsandsymptomsthatmayindicatesuchcomplications.(SeeComplicationsofacutepancreatitis.)
ComplicationsofacutepancreatitisThepatientwithacutepancreatitiscanrapidlydevelopcomplications,especiallyifhehaspancreaticnecrosis.Monitorcloselyforsignsandsymptomsofthesecomplications:•
acuterenalfailure•
acuterespiratorydistresssyndrome•
acutetubularnecrosis•
atelectasis•
chronicpancreatitis•
diabetesmellitus•
disseminatedintravascularcoagulation•
duodenalorcommonbileductobstruction•
GIbleeding•
hemorrhagefromrupturednecroticpancreaticbloodvessels•
hypocalcemia•
hypotension•
infectiouspancreaticnecrosis•
intravascularfluidvolumedeficit•
multipleorgandysfunctionsyndrome•
pancreaticabscess•
pancreaticpseudocyst(andpossiblerupture)•
paralyticileus•
pleuraleffusion•
pneumonia•
pulmonaryedema•
reducedcardiaccontractility,output,andperfusionpressure•
respiratoryfailure
•shock•
splenicarterypseudoaneurysms•
systemicinflammatoryresponsesyndrome•
tetany•
thrombosisofthesplenicvein,superiormesentericvein,andportalveins.
WhattestsshowSeveraltypesofdiagnostictestscanhelpidentifyacutepancreatitis,includingimagingandbloodstudies.Severityscoringcanhelppredicttheseverityofthediseaseandthepatient’sprognosis.
Imagingstudies•ChestX-raysshowsuchpulmonarycomplicationsasatelectasis,pleuraleffusions(most
commonlyontheleftside),orinfiltratesthatsuggestadultrespiratorydistresssyndrome.•AbdominalX-raysexcludeothercausesofacuteabdominalpainandshowboweldilationand
ileus.
•Contrast-enhancedcomputedtomography(CT)scanningandultrasonographyshowanenlargedpancreaswithfluidcollection,gallstones,cysts,abscess,masses,andpseudocysts.CTscanningalsoshowsareasofnecrosis.Thisisthemostusefulofallimagingtechniquesfordiagnosis,detectionofapseudocyst,andrecognitionofpancreaticnecrosis(Fernandez&Kerman,2013).
•Endoscopicretrogradecholangiopancreatography(ERCP)showsswellingandductalsystemabnormalities.
•Magneticresonancecholangiopancreatographymayshowstonesinthecommonbileductandnecrosis;thetestdoesn’trequireanI.V.contrastmedium.
Bloodstudies•Elevatedserumamylaselevels(morethanthreetimesnormal)almostalwaysindicate
pancreatitis.Levelsnormallypeakin12to24hoursandreturntonormalwithin1week.•Serumlipaselevelsusuallyrisewithin4to8hoursoftheonsetofsymptomsandpeakinabout
24hours.Theytypicallyreturntonormalin8to14days.•Severalotherlevelsalsorise,includingglucose,triglyceride,bilirubin,aspartate
aminotransferase,alanineaminotransferase,lactatedehydrogenase,alkalinephosphatase,andbloodureanitrogen.Testsalsoshowaprolongedprothrombintimeandincreasedwhitebloodcellcount.
•Hematocrit;partialpressureofarterialoxygen;andcalcium,magnesium,potassium,andalbuminlevelsalldecrease.
SeverityscoringSeveraltoolshelppredicttheseverityofacutepancreatitisandthepatient’sprognosis.It’scrucialtousethesetoolsearlyonbecauseearlyrecognitionofseverepancreatitiscansignificantlyimprovetheoutcome.ToolsincludeRanson’scriteria,theacutephysiologicassessmentandchronichealthevaluation(APACHEII)score,themultiorgansystemfailure(MOSF)score,themodifiedGlasgowprognosticcriteria,andtheBalthazarscore.Ranson’scriterialookatseveralfactorsonadmission(thelocalinflammatoryeffectsof
pancreaticenzymes)andthenagain48hourslater(thesystemiceffects).Ifthepatientmeetsthreeormorecriteria,thecriteriapredictaseverecourseandanincreasedmortalityrisk.(SeeRanson’scriteria,page290.)
Ranson’scriteriaRanson’scriteriaallowearlydiagnosisofsevereacutepancreatitis.Themorecriteriathepatientmeets,themoreseveretheepisodeofpancreatitis—andthegreatertheriskofmortality.Thelistsbelowdetailthecriteriausedandtheprognosticimplications.Assign1pointforeachcriterionmet.
Criteriaonadmission•
Agegreaterthan55years•
Whitebloodcellcountgreaterthan16,000/mm3
•Serumglucosegreaterthan200mg/dl•
Lacticdehydrogenasegreaterthan350IU/L•
Aspartateaminotransferasegreaterthan250IU/L
Criteria48hoursafteradmission•
Greaterthan10%decreaseinhematocrit•
Bloodureanitrogenincreasegreaterthan5mg/dl•
Serumcalciumlessthan8mg/dl•
Partialpressureofarterialoxygenlessthan60mmHg•
Basedeficitgreaterthan4mEq/L•
Estimatedfluidsequestrationgreaterthan6L
Prognosticimplications•
Score0to2:2%mortality•
Score3to4:15%mortality•
Score5to6:40%mortality•
Score7to11:100%mortality
TheAPACHEIIscoreusesapointscorecalculatedfromroutinephysiologicmeasurementstoprovideastatisticalpredictionofmortality.However,thescoringsystemistime-consuming—aminusforassessingsevereacutepancreatitis.
ExtrasensitiveMoresensitivethanRanson’scriteriaandtheAPACHEII,theMOSFscorepredictstheseverityofthediseaseatadmissionandcanberecalculateddaily.It’stypicallyusedonintensivecareunits.Thescoringsystemevaluatessevenorgansystems,withahigherscoreindicatingmoreseveredisease.AllpatientswithaMOSFscoregreaterthanthreehaveseveredisease.SimilartoRanson’scriteriabutwithfewercriteria,themodifiedGlasgowcriteriaallowsfor
dailyscoring.TheBalthazarscoreusesCTscanresultstoarriveataprognosis.(SeeTheBalthazarscore:ACTscanseverityindex.)
TheBalthazarscore:ACTscanseverityindexTheBalthazarscoringsystemusesCTscanningtostagetheseverityofdisease.Patientswithsevereacutepancreatitisshouldundergoacontrast-enhancedCTscanafterthefirst3daystodistinguishinterstitialfromnecrotizingpancreatitis.Thefirsttableshowsgradesforacutepancreatitisandthedegreeofpancreaticnecrosis.The
secondtablegivestheriskformortalityandcomplicationsforeachscore.Thescoreitselfisacombinationofthepointsforthegradeofacutepancreatitiscombinedwiththepointsforthedegreeofpancreaticnecrosis
Howit’streatedTreatmentforacutepancreatitisaimstomaintaincirculationandfluidvolume,relievepain,decreasepancreaticsecretions,maintainnutrition,andpreventinfectionandcomplications,aswellascorrectingcontributingfactors,suchasremovalofgallstonesinacutepancreatitiscausedbygallstones(Fernandez&Kerman,2013).
KeepthosefluidsflowingPatientswithevidenceofsignificantthird-spacefluidshiftandthosewhohavealargeamountoffluidintheretroperitonealspaceneedaggressivefluidreplacement.Thesefluidshiftsdepleteintravascularvolumeandmayleadtotachycardia,hypotension,renalfailure,hemoconcentration,andgeneralizedcirculatorycollapse.Patientswhodevelophemoconcentrationarealsoatincreasedriskforpancreaticnecrosisandorganfailure.MostcasesofpancreatitisrespondwelltocolloidsorlactatedRinger’ssolutiontotreat
hypovolemiaandshock.Patientsrequireclosemonitoringforelectrolyteabnormalities,particularlyhypocalcemia,hypokalemia,andhypomagnesemia.Fluidreplacementaimstocorrecttheseimbalancesandreplacevolume.Ifapatientdevelopsnecrotizingpancreatitisorexperiencesasudden,severeattackwithhemorrhaging,hemayalsoneedpackedredbloodcellstomaintainhemodynamicstability.
PushingbackatpancreaticpainTheseverepainthattypicallyaccompaniespancreatitiscallsforpainrelief.MeperidinewaslongthoughttobethebestchoiceforpainmanagementbecauseitseemedtohavelessspasmodiceffectsonthesphincterofOddicomparedwithsuchopiatesasmorphineandfentanyl.However,morerecentstudiesshowthatopiatesmayprovidemorepainrelief,andpatientstoleratethemwell.Duetothedepressingeffectsontherespiratorysystemwithopioids,carefulobservationofpatientsmustbemaintainedwiththeadministrationofanyopioid(Fernandez&Kerman,2013).Positioningpatientsintheknee-to-chestpositionmayalsohelprelievepain.
Nofood,please—justrestPartoftreatmentincludeslettingthepancreasrest—andthatmeansgivingthepancreasabreakfromfood,whichstimulatesenzymesecretion.Initially,thepatientwithpancreatitisshould
receivenothingbymouth.Aspainsubsidesandthepatient’sconditionimproves,hecanbeginoralintake,withcarefulmonitoring.Thepatientshouldatfirstreceivesmallamountsofhigh-carbohydratefoodsbecausetheydon’tstimulatethepancreasasmuchasfatandprotein.
Ifneeded,antacidscanhelpneutralizegastricsecretions,andhistamineantagonistscandecreasehydrochloricacidproduction.Anticholinergicdrugscanreducevagalstimulation,decreaseGImotility,andinhibitpancreaticenzymesecretion.Ifthepatienthasseverepancreatitiswithsignificantpancreaticnecrosis,hemayneedinsulintocorrecthyperglycemia.Apatientwithrecurrentvomiting,gastricdistention,orintestinalileusmayneedanasogastric
(NG)tubeinserted.AnNGtubewithsuctioningalsosuppressespancreaticsecretionsbydecreasinggastricfluids.Althoughcontroversial,antibiotictherapyforacutepancreatitisisindicatedifsecondary
infectionornecrotizingpancreatitisispresent(Fernandez&Kerman,2013).
TheoralrouteisoutUntilapatientwithpancreatitiscantolerateoralintake,hemustreceivenutritionbyanalternatemethod.Inmildercases,foodshouldbewithheldfornomorethan7days.Apatientwithseverepancreatitisrequiresnutritionalsupportbecauseoftheinherentlyhighlevelofstressandhypercatabolism.Suchapatientmayreceivetotalparenteralnutrition(withoutlipidsiftriglyceridesareincreased)orentericfeedingstomaintainnutrition.
Memoryjogger
Toremembersomeofthekeytreatmentsforacutepancreatitis,justthinkofthewordPANCREAS:
Paincontrol
ArrestingshockwithI.V.fluids
Nasogastricintubation
Calciummonitoring
Renalevaluation
Ensuringpulmonaryfunction
Antibioticadministration
Surgeryorspecialproceduresasneeded.
EradicatinginfectionsAninactivebowelallowsintestinalfloratocrossthecolonicwallandinfectthepancreas,particularlynecroticareas,whicharethemostvulnerabletoinfection.Whennecroticpancreatictissuebecomesinfected,themortalityrateincreasesto40%to70%.Antibioticscanhelppreventinfectionortreatonethat’salreadypresent.Ifinfectedpancreatic
necrosisarises,thepatientmayneedsurgicaldebridementanddrainage.ThedoctormayalsouseaCTscantoguideaspirationofnecroticareas.Thisallowsidentificationoftheinfectingorganism,leadingtomoreeffectivetreatment.
CopingwithcomplicationsTopreventthediseasefromprogressing,thepatientmayneedsurgeryorERCPtoremovegallstonesorotherbiliarytractobstructions.Apatientwithapancreaticabscessorpseudocystmayneedsurgicaldrainage.Ifapatientdevelopscomplicationsinthecardiovascular,renal,pulmonary,GI,orneurologicsystem,he’llneedtreatmentforthespecificcomplication.
HowyouintervenePatientswithacutepancreatitisneedcarefulmonitoring,thoroughassessments,anddiligentnursingcare.Followtheseguidelines:•Teachthepatientandhisfamilyaboutacutepancreatitis,andincludethemwheneverpossible
incareplanning.(SeeTeachingaboutacutepancreatitis,page294.)
Teachingpoints
TeachingaboutacutepancreatitisWhenteachingapatientwithacutepancreatitis,besuretocoverthesetopicsandthenevaluateyourpatient’slearning:•
explanationaboutacutepancreatitis,includingitscauses,signsandsymptoms,treatment,possiblecomplications,andriskforrecurrence•
roleofalcoholinthedevelopmentofacutepancreatitis•
importanceofavoidingfactorsthatmayprecipitateanattack,especiallyalcoholandproductscontainingalcohol,suchascertaincoughandcoldmedications,andhigh-fatfoods•
dietarycounselingand,ifnecessary,theroleoflipid-loweringdrugsifpancreatitisresultedfromhightriglyceridelevels•
prescribedmedicationsandpossibleadverseeffects•
dietarymodificationsasindicated,includingtheneedforadiethighincarbohydratesandlowinfatsandproteinsaswellasrecommendationstoavoidcaffeineandirritatingfoods•
needtostopsmoking,ifapplicable•
signsandsymptomstoreporttothepractitioner•
importanceoffollow-upappointments•
referraltoanappropriatesupportgroupsuchasAlcoholicsAnonymous,ifindicated.
•Ensureapatentairway,andassessthepatient’srespiratorystatusatleasteveryhourorasordered.Assessforadventitiousordiminishedbreathsounds.Checkoxygensaturationlevelsandarterialbloodgasresultsasordered.
•Closelymonitorthepatient’scardiacandhemodynamicstatusatleasteveryhourorasordered.•Monitorthepatient’svitalsignsatleasteveryhourorasordered.•Placethepatientinacomfortablepositionthatminimizespainsuchassittingandleaning
forward,lyingonhissidewithhiskneesbent,orsittingwithhiskneesflexedtowardhischest.•Allowforperiodsofresttoreducemetabolicstress.•Ifthepatientdevelopsacuterespiratorysyndrome,anticipatetheneedforadditionaltherapies
suchaspronepositioning.•Providesupplementaloxygenasordered.•InitiateI.V.fluidreplacementtherapyasordered.Assessforsignsoffluidoverload,including
dyspnea,edema,andcrackles.•Monitorserumlaboratoryvalues(hematology,coagulation,andchemistry)forchanges.
Dangerousdrop-offs•Watchcloselyforsignsandsymptomsofhypokalemia(hypotension,muscleweakness,apathy,
confusion,andcardiacarrhythmias),hypomagnesemia(hypotension,tachycardia,confusion,tremors,twitching,hypoactivedeeptendonreflexes,andconfusion),andhypocalcemia(positiveChvostek’sandTrousseau’ssigns,tetany,seizures,andprolongedQTintervalsonanelectrocardiogram).Haveemergencyequipmentreadilyavailable.
•AssessforCullen’sandGreyTurner’ssigns,whichindicatehemorrhagicpancreatitis.•Monitorthepatient’sintakeandoutputclosely,andnotifythepractitionerifthepatienthasa
urineoutputoflessthan0.5ml/kg/hour.Weighthepatientdaily.•Monitorthepatient’sneurologicstatus,notingconfusionorlethargy.•Maintainthepatientinanormothermicstatetoreducethebody’sdemandforoxygen.•Assessthepatient’spainlevelandadministermedicationsasordered.•Administerantibioticsasordered,andmonitorserumpeakandtroughlevelsasappropriate.•Withholdalloralfluidsandfoodasorderedtopreventstimulationofpancreaticenzymes.
•InsertanNGtubeasordered.Checkplacementatleastevery4hours.Irrigatewithnormalsalinesolutiontomaintainpatency.Monitordrainageforfrankbleeding,andwatchforbleedinginvomitusandstool.
•Assessthepatient’sabdomenfordistentionandfordiminishedorabsentbowelsounds;
measurehisabdominalgirth.•Asordered,administerstoolsoftenerstorelieveconstipationcausedbyimmobilityandopioid
use.•Administerparenteralnutritiontherapyorenteralfeedingsasordered.Monitorbloodglucose
levels.Administerinsulinasordered.•Whenbowelsoundsbecomeactiveandthepatient’sconditionimproves,anticipateswitching
tohigh-carbohydrate,low-protein,low-fatoralfeedingsafter1or2daysonclearliquids.•Performrange-of-motionexercisestomaintainjointmobility.•Performmeticulousskincare.•Provideemotionalsupporttothepatientandhisfamily,andencouragethemtoexpresstheir
feelings.•Preparethepatientforsurgeryasindicated.•Documentyourassessmentsandinterventions.(SeeDocumentingacutepancreatitis,page
296.)
Chartsmart
DocumentingacutepancreatitisIfyourpatienthasacutepancreatitis,makesureyoudocumentthefollowinginformation:•
vitalsigns•
intakeandoutput•
laboratoryandimagingtestresults•
toleranceoftestingprocedures•
respiratorystatus•
dailyweight•
I.V.fluidtherapy•
patencyandappearanceofI.V.site•
nutritionsupplementation•
diet,whenapplicable•
medicationsadministered•
oxygenadministered,ifindicated•
painlevelandresponsetomedications•
positioningandresponse•
mentalstatus•
presenceandcharacteristicsofvomitusanddiarrhea•
correctplacementofNGtubeandcareprovided,ifpresent•
signsandsymptomsofimprovingorworseningcondition•
safetymeasures•
notificationofpractitioner•
allnursingassessments,observations,andinterventionsandthepatient’sresponse•
patientandfamilyteachingandtheirunderstanding.
That'sawrap!
Acutepancreatitisreview
Acutepancreatitisbasics•
Inflammationofthepancreas•
Twotypes:edematous,whichisusuallymild,accountsforabout85%ofcases,isself-limiting,andresolvesin5to7days;andnecrotizing,whichissevere,accountsforabout15%ofcases,isprogressive,andcausestissuedamageandcelldeath•
Mayprogresstochronicpancreatitiswithprogressiverecurrentepisodes
Causes•
Gallstonesmostcommoncause•
Alcoholconsumptionsecondmostcommoncause•
Otherbiliarytractdisease,drugs,infection,toxinsandmetabolicprocesses,trauma,andotherfactorslesscommoncauses
Effectsonpancreas•
Exocrinefunctionsfail•
Activatedenzymesinpancreasdigestpancreatictissue
ImbalancescausedbyacutepancreatitisHypovolemia•
Majorcauseofdeathinacutepancreatitis•
Occurswhenseverepancreaticdamagetriggersreleaseofsystemicinflammatorymediatorsthatproduceincreasedcapillarypermeabilityandvasodilation,leadingtomassivefluidshiftsfromintravasculartointerstitialspacesandretroperitoneum•
Canalsoresultfromvomiting,diarrhea,excessivesweating,and,possibly,hemorrhage
Hyponatremia•
Canresultfromvomiting,diarrhea,andexcessivesweating•
Alsooccurswhenhypovolemiacausesanincreaseinantidiuretichormonesecretion
Hypocalcemia•
Usuallyresultsfromconcomitanthypoalbuminemia•
Canbeworsenedbyfatnecrosis(causedbylipasenecrosingfattissueinpancreaticinterstitiumand
peripancreaticspaces)thatmayresultinthereleaseoffreefattyacidsandintraperitonealsaponification•
Canalsostemfromhypomagnesemia(hypomagnesemiashouldbeaddressedbeforehypocalcemia)
Hypomagnesemia•
Canresultfromvomitinganddiarrhea•
Canoccurwhenmagnesiumisdepositedinareasoffatnecrosis,decreasingserumlevels
Hypokalemia•
Maybecausedbyseverevomitinganddiarrhea
Signsandsymptoms•
Mildpancreatitis:steadyepigastricpaincenterednearthenavelandunrelievedbyvomiting•
Severepancreatitis:severe,persistent,piercingabdominalpain,usuallyinthemidepigastricregion;maygeneralizeoroccurinleftupperquadrantandradiatetothebackorotherareas;typicallyprecipitatedbyalargemealoralcoholconsumption;mayimprovewhenpatientleansforwardorliesonsidewithkneesdrawntowardchest•
Nausea•
Vomiting•
Fever•
Mildjaundice•
Tachycardia•
Tachypnea•
Musclespasms•
Fatty,foul-smellingstools•
Possiblehypotension•
GreyTurner’ssign(flankecchymosis)•
Cullen’ssign(periumbilicalecchymosis)•
Chvostek’sandTrousseau’ssigns(hypocalcemia)•
Abdominaldistention,rigidity,andtendernesswithhypoactivebowelsounds
Treatment•
Maintenanceofcirculationandfluidvolume(typicallyrequiresaggressivefluidreplacement)•
Painrelief(usingmedications,suchasmorphineandfentanyl,andpositioning)•
Reductionofpancreaticsecretionstoallowpancreastorest(nooralintake,medicationstorestpancreas,andpossiblyNGtubeinsertion)•
Maintenanceofnutrition(nutritionalsupport,suchastotalparenteralnutritionandentericfeedings)•
Preventionortreatmentofinfectionandcomplications(antibiotictherapyorsurgeryasneeded)
Quickquiz
1.Thepancreasfunctionsasbothanexocrineandendocrinegland.Whichoftheseisanexampleofitsexocrinefunction?
A.Thepancreasproduceshydrochloricacid.B.Amylaseisproducedintheacinarcells.C.InsulinisproducedintheisletsofLangerhans.D.Thepancreassecretesitsenzymesintothestomach.
Answer:B.Theproductionofamylaseintheacinarcellsisanexampleofexocrinefunction.
2.Themostcommoncauseofacutepancreatitisis:A.alcohol.B.eatinglow-fatfoods.C.gallstones.D.pregnancy.
Answer:C.Gallstonesarethemostcommoncauseofacutepancreatitis.
3.Whichoftheseimbalancestypicallyoccursinacutepancreatitis?A.HypovolemiaB.HypercalcemiaC.HypernatremiaD.Hypermagnesemia
Answer:A.Inacutepancreatitis,fluidshiftingfromtheintravascularspaceintotheinterstitialspacesandretroperitoneumcauseshypovolemia.
4.Thepatientwithacutepancreatitismayreportthathispaindecreases:A.whenheliesonhisstomach.B.aftervomiting.C.aftereatingalargemeal.D.whenheliesonhissidewithhiskneesdrawntowardhischest.
Answer:D.Paincausedbyacutepancreatitisiscommonlyrelievedwhenthepatientliesonhissidewithhiskneesdrawntowardhischest.
5.Patientsrecoveringfromacutepancreatitisshouldeatfoodsthatare:A.lowincarbohydratesandhighinfatsandproteins.B.lowincarbohydrates,proteins,andfats.C.highincarbohydratesandfatsandlowinproteins.D.highincarbohydratesandlowinfatsandproteins.
Answer:D.Thepatientrecoveringfromacutepancreatitisshouldeatfoodsthatarehighincarbohydratesandlowinfatsandproteins.
ScoringIfyouansweredallfivequestionscorrectly,bravo!You’renotonlyacute,you’repancreatitisproficient.Ifyouansweredfourquestionscorrectly,that’scool!You’reonyourwaytoglandularglory.Ifyouansweredfewerthanfourquestionscorrectly,that’sokay!Justreviewthechapteruntilyoucanfullydigesttheinformation.
ReferenceFernandez,H.,&Kerman,D.(2013).Pancreatitis.InR.Buttaro,J.Trybulski,P.Bailey,&J.Sandberg-
Cook(Eds.),Primarycare:Acollaborativepractice(4thed.).St.Louis,MO:ElsevierMosby.
Chapter17
Renalfailure
JustthefactsInthischapter,you’lllearn:
♦thedifferencebetweenacuteandchronicrenalfailure
♦fluid,electrolyte,andacid-baseimbalancesthatcanoccurwithrenalfailure
♦signsandsymptomsofrenalfailure
♦appropriatenursinginterventionsforpatientswithrenalfailure.
AlookatrenalfailureRenalfailureinvolvesadisruptionofnormalkidneyfunction.Thekidneysplayamajorroleinregulatingfluids,electrolytes,acids,andbases.Acuterenalfailureoccurssuddenlyandisusuallyreversible.Incontrast,chronicrenalfailureoccursslowlyandisirreversible.Bothacuteandchronicrenalfailureaffectthekidneys’functionalunit,thenephron,whichforms
urine.Imbalancesoccurasthekidneyslosetheabilitytoexcretewater,electrolytes,wastes,andacid-baseproductsthroughtheurine.Patientsmayalsodevelophypertension,anemia,anduremia,aswellasrenalosteodystrophy,whichincludesincreasedboneresorptionandareductionofbonemass.Let’slookathowacuteandchronicrenalfailuredevelop.
HowacuterenalfailurehappensAcuterenalfailurecanstemfromprerenalconditionssuchasheartfailure,whichcausesadiminishedbloodflowtothekidneys;fromintrarenalconditions,whichdamagethekidneysthemselves;orfromobstructivepostrenalconditionssuchasprostatitis,whichcancauseurinetobackupintothekidneys.(SeeCausesofacuterenalfailure.)
CausesofacuterenalfailureThecausesofacuterenalfailurecanbebrokendownintothreecategories:prerenal,intrarenal,andpostrenal.Prerenalcausesincludeconditionsthatdiminishbloodflowtothekidneys.Intrarenalcausesincludeconditionsthatdamagethekidneysthemselves.Postrenalcausesincludeconditionsthatobstructurineoutflow,whichcausesurinetobackupintothekidneys.Foreachtype,theaffectedstructuresarehighlightedintheillustrationsbelow.
Prerenalcauses•
Seriouscardiovasculardisorders•
Peripheralvasodilation•
Severevasoconstriction•
Renalvascularobstruction•
Intrarenalcauses•
Acutetubularnecrosis•
Nephrotoxins•
Exposuretoheavymetals•
Aminoglycosides,nonsteroidalanti-inflammatorydrugs,or
Postrenalcauses•
Bladderobstruction•
Ureteralorurethralobstruction•
Trauma
Trauma•
Shock(septic,hypovolemic,cardiogenic)
cephalosporins•
Ischemicdamagefrompoorlytreatedrenalfailure•
Eclampsia,postpartumrenalfailure,oruterinehemorrhage•
Myopathy,sepsis,ortransfusionreaction•
Trauma(crushinjury,etc.)
About5%ofhospitalizedpatientsdevelopacuterenalfailureatsomepointduringtheir
hospitalizations.Manyconditionsreducebloodfloworotherwisedamagethekidneys’nephrons.Acuterenalfailurenormallypassesthroughthreedistinctphases:oliguric-anuric,diuretic,andrecovery.
Phase1:Adangerousdrop-offAdecreaseinurineoutputisthefirstclinicalsignofacuterenalfailureduringthefirstphasecalledtheoliguric-anuricphase.Typically,astheglomerularfiltrationrate(GFR)decreases,thepatient’surineoutputdecreasestolessthan400mlduringa24-hourperiod.Whenthekidneysfail,nitrogenouswasteproductsaccumulateintheblood,whichcausesan
elevationinbloodureanitrogen(BUN)andserumcreatininelevels.Theresultisuremia.Electrolyteimbalances,metabolicacidosis,andothersymptomsfollowasthepatientbecomesincreasinglyuremicandrenaldysfunctiondisruptsotherbodysystems.Leftuntreated,theconditionisfatal.Theoliguric-anuricphasegenerallylasts1to2weeksbutmaylastforseveralmore.The
longerthepatientremainsinthisphase,thepoorertheprognosisforareturntonormalrenalfunction(Okusa&Rosner,2013).
Phase2:AbitbetterThesecondphase,ordiureticphase,startswithagradualincreaseindailyurineoutputfrom400ml/24hoursto1to2L/24hours.TheBUNlevelstopsrising.Althoughurineoutputbeginstoincreaseinthisphase,apotentialforfluidandelectrolyteimbalancesstillexistsasGFRincreasesanddehydrationmaydevelop.Thediureticphaselastsabout10days(Okusa&Rosner,2013).
Phase3:Ontheroadtorecovery
Thethirdphase,therecovery(orconvalescent)phase,beginswhenfluidandelectrolytevaluesstarttostabilize,indicatingareturntonormalkidneyfunction.Thepatientmayexperienceaslightreductioninkidneyfunctionfortherestofhislife,sohe’llstillbeatriskforfluidandelectrolyteimbalances.Therecoveryphasegenerallylastsfrom3to12months(Okusa&Rosner,2013).
HowchronicrenalfailurehappensChronicrenalfailure,whichhasamoreinsidiousonsetthanacuterenalfailure,mayresultfrom:•chronicglomerulardiseasesuchasglomerulonephritis•chronicinfections,suchaschronicpyelonephritisortuberculosis•congenitalanomaliessuchaspolycystickidneydisease•vasculardiseases,suchasrenalnephrosclerosisorhypertension•obstructionssuchasthosefromrenalcalculi•collagendiseasessuchassystemiclupuserythematosus•long-termtherapywithnephrotoxicdrugssuchasaminoglycosides•endocrinediseasessuchasdiabetesmellitus.
SettingthestageBecausechronicrenalfailurehasaslowonset,identifyingspecifictimeframesforitsstagesmaybedifficult.Therateatwhichkidneyfunctiondeterioratesdependsaswellonthespecificdiseasecausingthedeterioration.It’spossible,however,tostageprogressionofthediseasebythedegreeofkidneyfunction.Chronicrenalfailurecanbedividedintofourbasicstages:reducedrenalreserve(GFR40to70ml/minute)renalinsufficiency(GFR20to40ml/minute)renalfailure(GFR10to20ml/minute)end-stagerenaldisease(GFRlessthan10ml/minute).
RunningdownthereserveThekidneyshavegreatfunctionalreserve.Fewsymptomsdevelopuntilmorethan75%ofGFRislost.Theremainingfunctionalnephronsthendeteriorateprogressively;signsandsymptomsworsenasrenalfunctiondiminishes.Failingkidneyscan’tregulatefluidbalanceorfiltersolutesorparticipateeffectivelyinacid-basebalance.Ifchronicrenalfailurecontinuesunchecked,uremictoxinsaccumulateandproducepotentiallyfatalphysiologicchangesinallmajororgansystems.
ImbalancescausedbyrenalfailureRenalfailure—acuteorchronic—cancauseanumberoffluid,electrolyte,andacid-baseimbalances,including:•hypervolemiaorhypovolemia•hyponatremiaorhypernatremia•hypocalcemia•hyperkalemia•hypermagnesemia•hyperphosphatemia•metabolicacidosisormetabolicalkalosis.
Water,water,everywhere...ornotWhenurineoutputdecreases,especiallywiththemoresuddenonsetofacuterenalfailure,thebodyretainsfluid,whichcanleadtohypervolemia.Thatconditionmayalsooccuriffluidintakeexceedsurineoutput.Theresultingfluidretentioncanleadtohypertension,peripheraledema,heartfailure,orpulmonaryedema.
Hypovolemicwaterlossesusuallyoccurduringthediureticphaseofacuterenalfailureandcanresultinhypotensionorcirculatorycollapse.
PumpupthepotassiumAsthekidneys’abilitytoexcretepotassiumisimpaired,serumpotassiumlevelsincrease,resultinginhyperkalemia.Inchronicrenalfailure,apatienttendstotoleratehighpotassiumlevelsmorethanapatientwithacuterenalfailure,inwhichtheonsetismoresudden.Metabolicacidosis,whichoccurswithrenalfailure,causespotassiumtomovefrominsidethe
cellsintotheextracellularfluid.Thereleaseofpotassiumfromanynecroticorinjuredcellsworsenshyperkalemia.Additionalstressors—suchasinfection,gastrointestinal(GI)bleeding,trauma,andsurgery—canalsoleadtohighserumpotassiumlevels.
TippingthebalanceSerumcalciumandphosphorushaveaninverserelationship,sowhenonegoesoutofbalance,theotherfollowssuit.Secondaryimbalancescanoccurasaresult.Hyperphosphatemiadevelopswhenthekidneyslosetheabilitytoexcretephosphorus.
Consequently,highserumphosphoruslevelscauseadecreaseincalciumlevels.DecreasedactivationofvitaminDbythekidneysresultsindecreasedGIabsorptionofcalcium
—anothercauseforlowserumcalciumlevels.
ThesaltsituationSodiumlevelsmaybeeitherabnormallyhighorunusuallylowduringrenalfailure.HyponatremiacanoccurwithacuterenalfailurebecauseadecreasedGFRanddamaged
tubulesincreasewaterandsodiumretention.Thisdilutionalhyponatremicstatecanalsobe
causedbytheintracellular–extracellularexchangebetweensodiumandpotassiumduringmetabolicacidosis.Hypernatremiacanoccurwithdecreasedintravascularvolume.Aprogressioninthedegreeof
kidneyfailurecauseslesssodiumtobeexcreted,worseninghypernatremia.
MagnesiumtothemaxThepatientwithrenalfailuremayretainmagnesiumasaresultofadecreasedGFRanddestructionofthetubules.However,ahighserummagnesiumlevelusuallyisn’trecognizedunlessthepatientreceivesexternalsourcesofmagnesium,suchaslaxatives,antacids,I.V.solutions,orhyperalimentationsolutions.
Theacid-baseseesawMetabolicacidosisisthemostcommonacid-baseimbalanceoccurringwithrenalfailure.Itdevelopsasthekidneyslosetheabilitytosecretehydrogenions—anacid—intheurine.Theimbalanceisalsoexacerbatedasthekidneysfailtoholdontobicarbonate—abase.Patientswithchronicrenalfailurehavemoretimetocompensateforthisacid-baseimbalance
thanpatientswithacuterenalfailure.Thelungstrytocompensatefortheexcessacidbyincreasingthedepthandrateofrespirationsinanattempttoblowoffcarbondioxide.Metabolicalkalosisrarelyoccurswithrenalfailure.Whenitdoes,itusuallyresultsfrom
excessiveintakeofbicarbonate,giveninanefforttocorrectmetabolicacidosis.
WhattolookforThepatient’shistorymayrevealadisorderthatcancauserenalfailure;itmayalsoincludearecentepisodeoffever,chills,GIproblems(suchasanorexia,nausea,vomiting,diarrhea,orconstipation),andcentralnervoussystemproblemssuchasheadache.Signsandsymptomsvary,dependingonthelengthoftimeinwhichrenalfailuredevelops.(See
Laboratoryresultsassociatedwithacuterenalfailure.)Fewersignsmayappearinpatientswith
acuterenalfailurebecauseofthecondition’sshorterclinicalcourse.Inpatientswithchronicrenalfailure,however,almostallbodysystemsareaffected.Yourassessmentfindingswilllikelyinvolveseveralbodysystems.(SeeRecognizingrenalfailure,page306.)
LaboratoryresultsassociatedwithacuterenalfailureKeepalertfortheseearlysignsofacuterenalfailure:•
urineoutputbelow400mlover24hours•
increasedBUNlevel•
increasedserumcreatininelevel.
CAUTION!
RecognizingrenalfailureSignsandsymptomsassociatedwithrenalfailurearelistedherebybodysystem.Keepinmindthatyourpatientmaydevelopsomeorallofthem.
Neurologic•
Burning,itching,andpaininthelegsandfeet•
Coma•
Confusion•
Fatigue•
Headache•
Hiccups
•Irritability•
Listlessnessandsomnolence•
Muscleirritabilityandtwitching•
Seizures•
Shortenedattentionspanandmemory
Cardiovascular•
Anemia•
Arrhythmias•
Edema•
Heartfailure•
Hypertension•
Hypotension•
Irregularpulse•
Pericardialrub•
Tachycardia•
Weightgainwithfluidretention
Pulmonary•
Crackles•
Decreasedbreathsoundsifpneumoniaispresent•
Dyspnea•
Kussmaul’srespirations
GI•
Ammoniasmelltothebreath•
Anorexia•
Bleeding•
Constipationordiarrhea•
Drymouth•
InflammationandulcerationofGImucosa•
Metallictasteinthemouth•
Nauseaandvomiting•
Painonabdominalpalpationandpercussion
Integumentary•
Dry,brittlehairthatmaychangecolororfallouteasily•
Drymucousmembranes•
Dry,scalyskinwithecchymoses,petechiae,andpurpura•
Lossofskinturgor•
Severepruritus•
Thin,brittlefingernailswithlines•
Uremicfrost(inlaterstages)•
Yellow-bronzeskincolor
Genitourinary•
Amenorrheainwomen•
Anuriaoroliguria•
Changesinurinaryappearanceorpatterns•
Decreasedlibido•
Diluteurinewithcastsandcrystals•
Hematuria•
Impotenceinmen•
Infertility•
Proteinuria
Musculoskeletal•
Boneandmusclepain•
Gaitabnormalitiesorlossofambulation•
Inabilitytoambulate•
Musclecramps•
Muscleweakness•
Pathologicfractures
SaltshortageIncasesofrenalfailureinwhichthekidneyscan’tretainsalt,hyponatremiamayoccur.Thepatientmaycomplainofdrymouth,fatigue,andnausea.Youmaynotehypotension,lossofskinturgor,andlistlessnessthatprogressestosomnolenceandconfusion.Later,asthenumberoffunctioningnephronsdecreases,sodoesthekidney’scapacitytoexcrete
sodiumandpotassium.Urineoutputdecreases.Theurinemaybedilute,withcastsorcrystalspresent.Accumulationofpotassiumcausesmuscleirritabilityandthenmuscleweakness,irregularpulse,andlife-threateningcardiacarrhythmias.Sodiumretentioncausesfluidoverload,andedemabecomespalpable.Thepatientgainsweightfromfluidretention.Metabolicacidosiscanalsooccur.
HardontheheartWhenthecardiovascularsystemisinvolvedwithrenalfailure,you’llfindhypertensionandanirregularpulse.Tachycardiamayoccur.Youmaynotesignsofapericardialrubrelatedtopericarditis,especiallyinpatientswithchronicrenalfailure.Youmayalsohearcracklesatthebasesofthelungs,andyoumaypalpateperipheraledemaifheartfailureoccurs.
ThelungstakeaplungePulmonarychangesincludereducedpulmonarymacrophageactivitywithincreasedsusceptibilitytoinfection.Ifpneumoniaispresent,breathsoundsmaydecreaseoverareasofconsolidation.Cracklesatthelungbasesoccurwithpulmonaryedema.Kussmaul’srespirationsoccurwithmetabolicacidosis.
DowninthemouthWithinflammationandulcerationofGImucosa,inspectionofthemouthmayrevealgumulcerationandbleeding.Thepatientmaycomplainofhiccups,ametallictasteinthemouth,anorexia,nausea,andvomiting(causedbyesophageal,stomach,orbowelinvolvement).Youmaynoteanammoniasmelltothebreath.Abdominalpalpationandpercussionmaycausepain.
IntegumentaryindicatorsInspectionoftheskintypicallyrevealsayellow-bronzecolor.Theskinisdryandscalywithpurpura,ecchymoses,andpetechiaethatformasaresultofthrombocytopeniaandplateletdysfunctioncausedbyuremia.Inlaterstages,ifuntreated,thepatientmayexperienceuremicfrost(powderydepositsontheskinasaresultofureaanduricacidbeingexcretedinsweat)andthin,brittlefingernailswithcharacteristiclines.Mucousmembranesaredry.Hairisdryandbrittleandmaychangecolorandfallouteasily.Thepatientusuallycomplainsofsevereitching.
MusculoskeletalmaladiesThepatientmayhaveahistoryofpathologicfracturesandcomplainofboneandmusclepain,whichmaybecausedbyanimbalanceincalciumandphosphorusorintheamountofparathyroidhormone(PTH)produced.Youmaynotegaitabnormalitiesor,possibly,thatthepatientcannolongerambulate.
MoreproblemsWithchronicrenalfailure,thepatientmayhaveahistoryofinfertilityanddecreasedlibido.Womenmayhaveamenorrhea,andmenmaybeimpotent.Youmaynotechangesinthepatient’slevelofconsciousnessthatmayprogressfrommild
behaviorchanges,shortenedmemoryandattentionspan,apathy,drowsiness,andirritabilitytoconfusion,coma,andseizures.Thepatientmaycomplainofmusclecrampsandtwitchingcausedbymuscleirritability.Thepatientmayalsocomplainofpain,burning,anditchinginthelegsandfeetthatmayberelievedbyvoluntarilyshaking,moving,orrockingthem.Thosesymptomsmayeventuallyprogresstoparesthesiaandmotornervedysfunction.
WhattestsshowDiagnostictestresultstypicalofpatientswithrenalfailureinclude:•elevatedserumBUN,creatinine,potassium,andphosphoruslevels(SeeAge-relatedkidneychanges.)
Agesandstages
Age-relatedkidneychangesAspeopleage,nephronsarelostandthekidneysdecreaseinsize.ThesechangesdecreaserenalbloodflowandmayresultindoubledBUNlevelsinolderpatients.
•arterialbloodgas(ABG)resultsthatindicatemetabolicacidosis—specifically,alowpHandbicarbonatelevel
•lowhematocrit,lowhemoglobinlevel,andmildthrombocytopenia•urinalysisshowingcasts,cellulardebris,decreasedspecificgravity,proteinuria,andhematuria•electrocardiogram(ECG)showingtall,peakedTwaves;awidenedQRScomplex;and
disappearingPwavesifhyperkalemiaispresent.Otherstudies,suchaskidneybiopsy,kidney-ureter-bladderradiography,andkidney
ultrasonography,mayalsobeperformedtodeterminethecauseofrenalfailure.
Howit’streatedTreatmentofrenalfailureaimstocorrectspecificsymptomsandtoalterthediseaseprocess.
GolowproApatientwithrenalfailureneedstomakedietarychanges.Theyneedtofollowahigh-caloriediettomeetdailynutritionalrequirementsandtopreventbreakdownofbodyprotein.Theirdietalsoneedstorestrictphosphorus,sodium,andpotassium.Alow-proteindietwillreduceendproductsofproteinmetabolismthatthekidneysareunable
toexcrete.Theproteinapatientneedsshouldbeconsumedonlyinfoodsthatcontainallessentialaminoacidstopreventbreakdownofbodyprotein,suchaseggs,milk,poultry,andmeat.
Fine-tuningfluidsMaintainingfluidbalancerequirescarefulmonitoringofvitalsigns,weightchanges,andurineoutput.Fluidretentioncanbereduced,ifsomerenalfunctionremains,withtheuseofaloopdiureticsuchasfurosemide(Lasix)andwithrestrictionoffluid.Carefulmonitoringofserumpotassiumlevelsisnecessarytodetecthyperkalemia.Ifthepatient
developsthiscondition,emergencytreatmentshouldbeinitiated.(SeeEmergencytreatmentof
hyperkalemia.)Anon–aluminum-containing,phosphate-bindingagentmaybegiventolowerserumphosphoruslevels.
EmergencytreatmentofhyperkalemiaEmergencytreatmentofhyperkalemiaincludesadministrationofKayexalate,dialysis,administrationof50%hypertonicglucoseI.V.,regularinsulin,calciumgluconateI.V.,andsodiumbicarbonateI.V.
AkicktothemarrowInpatientswithchronicrenalfailure,kidneyproductionoferythropoietinisdiminished.Thishormonecontrolstherateofredbloodcell(RBC)productioninbonemarrowandfunctionsasagrowthfactoranddifferentiatingfactor.TreatmentincludesadministrationofsyntheticerythropoietintostimulatebonemarrowtoproduceRBCs.
Memoryjogger
Torememberdietarychangesneededtomanagerenalfailure,think“High,Lo,No.”
Highcalories
Lowprotein
Noaddedsalt(alsowatchthepotassium)
FillinginforthekidneysHemodialysisandperitonealdialysisareusedinbothacuteandchronicrenalfailure.Byassumingthefunctionofthekidneys,thesemeasureshelpcorrectfluidandelectrolytedisturbancesandrelievesomeofthesymptomsofrenalfailure.
HowyouinterveneCaringforapatientwithrenalfailurerequirescarefulmonitoring,administrationofvariousmedicinesandtherapeuticregimens,andempathicministeringtothepatientandfamily.(SeeTeachingaboutrenalfailure,page310.)Followtheseguidelines:
Teachingpoints
Teachingpoints
TeachingaboutrenalfailureWhenteachingapatientwithrenalfailure,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
basicsofrenalfailureanditstreatment•
prescribedmedications•
avoidanceofhigh-sodiumandhigh-potassiumfoods•
importanceofweighinghimselfdaily•
warningsignsandsymptomsandwhentoreportthem•
needforfrequentrestforapatientwithanemia•
referralstocounselingservices,ifindicated•
propermethodsofcaringforshunt,fistula,orvascularaccessdevice•
propermethodofperformingperitonealdialysisathome,ifappropriate.
•Assessthepatientcarefullytodeterminethetypeandseverityoffluid,electrolyte,andacid-baseimbalances.
•Maintainaccuratefluidintakeandoutputrecords.•Weighthepatientdaily,andcomparetheresultswiththe24-hourintakeandoutputrecord.•Monitorvitalsigns,includingbreathsoundsandcentralvenouspressurewhenavailable,to
detectchangesinfluidvolume.Reporthypertension,whichmayoccurasaresultoffluidandsodiumretention.
•Observethepatientforsignsandsymptomsoffluidoverload,suchasedema,boundingpulse,andshortnessofbreath.
•MonitorserumelectrolyteandABGlevelsforabnormalities.Reportsignificantchangestothepractitioner.
•Observethepatientforsignsandsymptomsthatmayindicateanelectrolyteoracid-baseimbalance—forexample,tetany,paresthesia,muscleweakness,tachypnea,orconfusion.
•MonitorECGreadingstodetectarrhythmiascausedbyelectrolyteimbalances.•Monitorhemoglobinlevelsandhematocrit.•Ifthepatientrequiresdialysis,checkthevascularaccesssiteevery2hoursforpatencyand
signsofclotting.Checkthesiteforbleedingafterdialysis.•Restrictfluidsasprescribed.•Administerprescribeddiureticstopatientswhosekidneyscanstillexcreteexcessfluid.•Administerotherprescribedmedications,suchasoralorI.V.electrolytereplacementtocorrect
electrolyteimbalancesandvitaminsupplementstocorrectnutritionaldeficiencies.•Knowtherouteofexcretionformedicationsbeinggiven.Drugsexcretedthroughthekidneysor
removedduringdialysismayrequiredosageadjustments.
•ExpecttoadministersodiumbicarbonateI.V.tocontrolacuteacidosisandorallytocontrolchronicacidosis.Rememberthatsodiumbicarbonatehasahighsodiumcontent.Multipledosesofthedrugmayresultinhypernatremia,whichcouldcontributetotheonsetofheartfailureandpulmonaryedema.
•Asnecessary,restrictelectrolyteintake,especiallypotassiumandphosphorus,topreventimbalances.Monitoranddocumentthepatient’sresponse.(SeeDocumentingrenalfailure.)
Chartsmart
DocumentingrenalfailureIfyourpatienthasrenalfailure,makesureyoudocumentthefollowinginformation:•
assessmentfindings,suchasthoserelatedtofluid,electrolyte,oracid-baseimbalances•
vitalsigns,includingbreathsoundsandcentralvenouspressurereadings(ifavailable)•
dailyweight•
laboratorytestresults•
intakeandoutput•
administrationofI.V.ororalelectrolytereplacementtherapy•
dialysisandcareofthevascularaccesssite•
notificationofthepractitioner•
patientandfamilyteachingandpatient’sresponse.
•Bepreparedtoinitiatedialysiswhenelectrolyteoracid-baseimbalancesdon’trespondtodrugtherapyorwhenfluidremovalisn’tpossible.
•Maintainnutritionalstatus.Provideadiethighincaloriesandlowinprotein,sodium,andpotassium.Initiateanutritionalconsultationasneeded.
•Ifagraftorfistulafordialysishasbeenplacedinthepatient’sarm,don’tusethatextremityformeasuringbloodpressure,drawingblood,orinsertingI.V.catheters.
•Provideemotionalsupporttothepatientandhisfamily.•Teachthepatientandhisfamilyaboutrenalfailureanditstreatment(NationalInstituteof
DiabetesandDigestiveandKidneyDiseases,2012;NationalKidneyFoundation,2013;Workeheh,2013).
That’sawrap!
That’sawrap!
Renalfailurereview
Renalfailurebasics•
Involvesdisruptionofnormalkidneyfunction•
Affectsthekidney’sfunctionalunit,thenephron,whichformsurine•
Resultsinkidneyslosingtheabilitytoexcretewater,electrolytes,wastes,andacid-baseproductsthroughtheurine,causingimbalances•
Mayleadtodevelopmentofhypertension,anemia,uremia,andrenalosteodystrophy•
Maybeacuteorchronic
Acuterenalfailure•
Occurssuddenly•
Usuallyreversible•
Maystemfromprerenal,intrarenal,orobstructivepostrenalconditions•
Dividedintothreephases:oliguric-anuric,diuretic,andrecovery
Chronicrenalfailure•
Occursslowly•
Irreversible•
Maystemfromchronicglomerulardisease,chronicinfections,congenitalanomalies,vasculardisease,long-termtherapywithnephrotoxicdrugs,andendocrinediseases•
Dividedintofourstages:reducedrenalreserve,renalinsufficiency,renalfailure,andend-stagerenaldisease
Imbalancescausedbyrenalfailure
Hypervolemia•
Occurswhenurineoutputdecreasesandthebodyretainsfluidorwhenfluidintakeexceedsurineoutput•
Mayleadtohypertension,peripheraledema,heartfailure,orpulmonaryedema
Hypovolemia•
Usuallyoccursduringthediureticphaseofacuterenalfailure•
Mayresultinhypotensionorcirculatorycollapse
Hyperkalemia•
Occursasthekidneys’abilitytoexcretepotassiumisimpaired•
Mayalsooccurbecausemetabolicacidosis,whichoccurswithrenalfailure,causespotassiumtomovefrominsidethecellsintotheextracellularfluid•
Maybeexacerbatedbyreleaseofpotassiumfromnecroticorinjuredcells•
Canalsobecausedbystressors,suchasinfection,GIbleeding,trauma,andsurgery
Hyperphosphatemia•
Developswhenthekidneyslosetheabilitytoexcretephosphorus
Hypocalcemia•
Occurswhenphosphoruslevelsincrease(calciumandphosphorushaveaninverserelationship)•
MayalsooccurbecausedecreasedactivationofvitaminDbythekidneysresultsindecreasedGIabsorptionofcalcium
Hyponatremia•
OccurswithacuterenalfailurebecausedecreasedGFRanddamagedtubulesincreasewaterandsodiumretention•
Canalsobecausedbytheintracellular–extracellularexchangebetweensodiumandpotassiumduringmetabolicacidosis
Hypernatremia•
Canoccurwithchronickidneydiseasebecauseprogressivekidneyfailureresultsintheexcretionoflesssodium
Hypermagnesemia•
MayresultfromdecreasedGFRanddestructionoftubules•
Isn’tusuallyapparentunlessthepatientisreceivingexternalsourcesofmagnesium,suchaslaxatives,antacids,I.V.solutions,orhyperalimentationsolutions
Metabolicacidosis•
Isthemostcommonacid-baseimbalanceoccurringwithrenalfailure•
Occurswhenthekidneyslosetheirabilitytosecretehydrogenions(acid)intheurine•
Alsooccurswhenthekidneysfailtostorebicarbonate(base)
Metabolicalkalosis•
Rarelyresultsfromexcessiveintakeofbicarbonate,whichmaybegiventocorrectmetabolicacidosis
Treatment•
Correctionofspecificsymptoms•
Treatmentoftheunderlyingdisease•
Low-protein,low-sodium,low-potassium,high-caloriediet•
Maintenanceoffluidandelectrolytebalance•
ErythropoietintostimulateproductionofRBCsinthebonemarrow•
Possiblyhemodialysisorperitonealdialysis•
Possiblyakidneytransplant
Quickquiz
1.ApatientwithhyperkalemiamayexperienceseveralECGchanges,including:A.flatTwaves,asmallQRScomplex,andnormalPwaves.B.tall,peakedTwaves;awidenedQRScomplex;anddisappearingPwaves.C.noTwaves,anormalQRScomplex,andflattenedormisshapedPwaves.D.tall,peakedTwaves;anormalQRScomplex;anddisappearingPwaves.
Answer:B.HighpotassiumlevelsmayresultindisappearingPwaves;awidenedQRScomplex;andtall,peakedTwavesbecauseoftheeffectoncardiaccells.
2.Whichofthefollowingistheoptimaldietforapatientwithrenalfailure?A.High-calorie,low-protein,low-sodium,low-potassiumB.High-calorie,high-protein,high-sodium,high-potassiumC.Low-calorie,high-protein,low-sodium,low-potassiumD.High-calorie,low-protein,low-sodium,high-potassium
Answer:A.Ahigh-calorie,low-protein,low-sodium,andlow-potassiumdietistheoptimaldietformeetingthemetabolicandnutritionalrequirementsofapatientwithrenalfailure.
3.Laboratoryresultsassociatedwithacuterenalfailureinclude:A.incsreasedBUNlevelanddecreasedserumcreatininelevel.B.decreasedBUNlevelandincreasedurineoutput.C.increasedBUNandserumcreatininelevels.D.increasedBUNlevelandincreasedurineoutput.
Answer:C.ThepatientwithacuterenalfailurehasincreasedBUNandserumcreatininelevelsanddecreasedurineoutput.
ScoringIfyouansweredallthreequestionscorrectly,greatjob!You’redominantintherenalarena!Ifyouansweredtwoquestionscorrectly,waytogo!Yourintelligenceisstillacuteandyourdiagnosisisoneofchronicsuccess!Ifyouansweredfewerthantwoquestionscorrectly,don’tlooksoglum.Shakeitoffandgoodluckwiththenextchapter.
ReferencesNationalInstituteofDiabetesandDigestiveandKidneyDiseases.(2012).Kidneydiseasestatisticsfor
theUnitedStates.Retrievedfromhttp://kidney.niddk.nih.gov/KUDiseases/pubs/kustats/index.aspx#9
NationalKidneyFoundation.(2013).Nephrologyessentials.Retrievedfromhttp://www.kidney.org/professionals/CAP/nephEssentials.cfm
Okusa,M.,&Rosner,M.(2013).Overviewofthemanagementofacutekidneyinjury(acuterenalfailure).Retrievedfromhttp://www.uptodate.com/contents/overview-of-the-management-of-acute-kidney-injury-acute-renal-failure
Workeheh,B.(2013).Acutekidneyinjury:Practiceessentials.Retrievedfromhttp://emedicine.medscape.com/article/243492-overview
Chapter18
Burns
JustthefactsInthischapter,you’lllearn:
♦thephysiologicchangesthatoccurwithsevereburninjuries
♦fluid,electrolyte,andacid-baseimbalancesthatoccurasaresultofsevereburninjuries
♦signsandsymptomsofburninjuries
♦treatmentsformanagingburninjuries
♦appropriatenursingcareforburnpatients.
AlookatburnsAmajorburnisahorrifyinginjury,requiringpainfultreatmentandalongperiodofrehabilitation.Destructionoftheepidermis,dermis,orsubcutaneouslayersoftheskincanaffecttheentirebodyand,inmanycases,islife-threatening.Ifnotfatal,aburncanbepermanentlydisfiguringandincapacitating,bothemotionallyandphysically.
DisruptingdutiesLikeanyinjurytotheskin,aburninterfereswiththeskin’sabilitytohelpkeepoutinfectiousorganisms,maintainfluidbalance,andregulatebodytemperature.Burninjuriescausemajorchangesinthebody’sfluidandelectrolytebalance.Manyofthoseimbalanceschangeovertimeastheinitialinjuryprogresses.Theextremeheatfromaburncanbesevereenoughtocompletelydestroycells.Evenwitha
lesserinjury,normalcellactivityisdisrupted.Withminimalinjury,thecellmayrecoveritsfunction.Theburnpatient’sprognosisdependsonthesizeandseverityoftheburn.Severalfactorsdeterminetheseverityofaburn,includingthecause,degree,andextentofthe
burnaswellasthepartofthebodyinvolved.Theoutcomeforaburnpatientisalsoaffectedbythepresenceofpreexistingmedicalconditionsandthepatient’sage.
TypesofburnsBurnscanresultfromthermalorelectricalinjuriesaswellasfromexposuretochemicalsandradiation.
ThermalburnsThemostcommontypeofburninjury,thermalburnsresultfromexposuretoeitherdry(flames)ormoist(steam,hotliquids)heat.Theycommonlyoccurwithresidentialfires,motorvehicleaccidents,childhoodaccidents,exposuretoimproperlystoredgasoline,exposuretospaceheaters,electricalmalfunctions,andarson.Othercausesmayincludetheimproperhandlingoffirecrackers,contactwithscaldingliquids,hottar,andkitchenaccidents.Becauseitseffectsaresimilartothoseofathermalburn,frostbiteisincludedinthiscategory.
Electricalburns
Electricalburnscommonlyoccuraftercontactwithfaultyelectricalwiring,high-voltagepowerlines,orimmersioninwaterthathasbeenelectrified.Thoseinjuriesmayalsobecausedbylightningstrikes.Anelectricalburnthatignitesthepatient’sclothingmaycausethermalburnsaswell.
HiddenhurtWhencaringforapatientwithanelectricalburn,keepinmindthattheremaybemoredamageinternallythanmeetstheeye.Checkthepatientforentranceandexitwoundsandbeawarethattheremaybecardiacdysrhythmias.Tissuedamagefromanelectricalburnisdifficulttoassessbecauseinternaldestructionalongtheconductionpathwayisusuallygreaterthanthesurfaceburnindicates.
ChemicalandradiationburnsChemicalburnsresultfromthedirectcontact,ingestion,inhalation,orinjectionofacids,alkalies,orvesicants.Thesechemicalsdestroyproteinintissues,leadingtonecrosis.Thetypeandextentofdamagecauseddependsonthepropertiesoftheparticularchemical.Radiationburnsaretypicallyassociatedwithsunburnorradiationtreatmentforcancer.These
burnstendtobesuperficial,involvingonlytheouterlayerofskin.
ClassificationofburnsBurnthicknessaffectscellfunction.Therefore,classifyingthedegreeofaburnhelpstodeterminethetypeofinterventionneeded.
First-degreeSuperficial(first-degree)burnsaffecttheepidermis.Theseburnsareusuallypinkorred,dry,andpainful.Noblisteringoccurswiththisburn;however,someedemamaybepresent.Theseburnsaren’tclassifiedasseverebecausetheepidermisremainsintactandcontinuestopreventwaterlossfromtheskin,sotheydon’taffectfluidandelectrolytebalance.Regrowthoftheepidermisoccurs,andhealingisgenerallyrapidwithoutscarring.
Second-degreeSuperficialpartial-thicknessanddeeppartial-thicknessburnsarethetwotypesofsecond-degreeburnsandaffectboththeepidermisanddermis.Theseburnsarecausedbybriefexposuretoflames,hotliquidsorsolids,dilutechemicals,orintenseradiation.Deeppartial-thicknessburnscanprogresstothird-degreeburnsoverthecourseofseveraldaysafterinjury.Toidentifyasuperficialpartial-thicknessburn,lookforpink,moist,andtenderskin
accompaniedbythin-walled,fluid-filledblisters.Deeppartial-thicknessburnscanbepainful,swollen,andred,withthick-walledblisterformation.Whenpressureisappliedtotheburn,itblanchesandrefills.Regenerationoftheepitheliallayermayoccur.Theamountofscarringvarieswiththistypeofburn.Second-degreeburnsthatcoversignificantareasofthebodymayleadtofluidandelectrolyteimbalances.
Third-degreeFull-thickness(third-degree)burnsdestroytheepidermisandthedermisandmayaffectsubcutaneoustissue.Theseburnslookdryandleathery,arepainless(becausenerveendingsaredestroyed),anddon’tblanchwhenpressureisapplied.Thecoloroftheburnedareavariesfromwhitetoblackorcharred.Full-thicknessburnsrequireskingraftingandcarrythegreatestriskoffluidandelectrolyte
imbalance.
Fourth-degreeDeepfull-thickness(fourth-degree)burnsextendbeyondthedermisandsubcutaneoustissuetothemusclelayerandcanincludetendonorbone.Fourth-degreeburnsarecharredandhard.Theburnedareasdonotblanch.Surgeryisrequired,
butevenso,theyhaveapoorprognosis.
BurnseverityTheseverityofaburncanbeestimatedbycorrelatingitsdepthandsize.Burnsarecategorizedasmajor,moderate,andminor.Assessmenttools,suchastheRuleofNinesortheLund-Browderclassification,areusedtoestimatethepercentageofbodysurfaceareainvolvedinaburn.(SeeEstimatingtheextentofaburn.)
EstimatingtheextentofaburnBecausebodysurfaceareavarieswithage,twodifferentmethodsareusedtoestimateburnsizeinadultandpediatricpatients.
RuleofNinesYoucanquicklyestimatetheextentofanadultpatient’sburnbyusingtheRuleofNines.Thismethodquantifiesbodysurfaceareainmultiplesof9,thusthename.Tousethismethod,mentallytransfertheburnsonyourpatienttothebodychartsbelow.Addthecorrespondingpercentagesforeachbodysectionburned.Usethetotal—aroughestimateofburnextent—tocalculateinitialfluidreplacementneeds.Iftheburndoesn’tcompletelycoverabodyarea,theburncanbeestimatedaboutthesizeofthepatient’spalmwhichequals1%ofthebody.
Lund-BrowderClassificationTheRuleofNinesisn’taccurateforinfantsorchildrenbecausetheirbodyshapes,andthereforeBSA,differfromthoseofadults.Forexample,aninfant’sheadaccountsforabout17%ofhistotalbodysurfacearea,comparedwith7%foranadult.Instead,usetheLund-Browderclassificationtodetermineburnsizeforinfantsandchildren.
MajorburnsMajorburns,whichrequiretreatmentinaspecializedburncarefacility,include:•second-degreeburnscoveringmorethan25%ofanadult’sbodysurfaceareaormorethan20%
ofachild’sbodysurfacearea
•third-degreeburnscoveringmorethan10%ofthebodysurfacearea•burnsonthehands,face,eyes,ears,feet,orgenitalia•allinhalationburns•allelectricalburns•burnscomplicatedbyfracturesorothermajortrauma•allburnsinpoor-riskpatients,suchaschildrenyoungerthanage5years,adultsolderthanage
60years,andpatientswhohavepreexistingmedicalconditionssuchasheartdisease.
ModerateburnsModerateburns,whichrequiretreatmentinaburncarefacilityorhospital,include:•third-degreeburnson2%to10%ofthebodysurfacearea,regardlessofbodysize•second-degreeburnson15%to25%ofanadult’sbodysurfaceareaand10%to20%ofa
child’s.
MinorburnsMinorburns,whichmaybehospitalizedbutnotnecessarilyataburncenterorcanbetreatedonanoutpatientbasis,include:•third-degreeburnsthatappearonlessthan2%ofthebodysurfacearea,regardlessofbodysize•second-degreeburnsonlessthan15%ofanadult’sbodysurfaceareaand10%ofachild’s
bodysurfacearea(mostchildrenaretransferredtoaburncenter).
PhasesofburnsBurnphasesdescribethephysiologicchangesthatoccurafteraburnandincludethefluidaccumulation,fluidremobilization,andconvalescentphasesinburns,whicharegreaterthan20%totalbodysurfacearea.Burnsaffectmanybodysystemsandcanleadtoseveralseriousfluidandelectrolyteimbalances,whichvarydependingonthephaseoftheburn.
FluidaccumulationphaseThefluidaccumulationphase,alsoknownastheburnshockphaseoremergentphase,occurswithinthefirst24to36hoursafteraburninjury,withitspeakoccurringbetween6and8hours.Duringthisphase,fluidshiftsfromthevascularcompartmenttotheinterstitialspace,aprocessknownasthird-spaceshift.Thisshiftoffluidscausesedema.Severeedemamaycompromisecirculationanddiminishpulsesintheextremities.
PermeabilityandplasmaBecauseoftheburninjury,capillarydamagealtersthepermeabilityofthevessels.Plasma—theliquidandproteinpartofblood—escapesfromthevascularcompartmentintotheinterstitium.Becauselessfluidisavailabletodilutetheblood,thebloodbecomeshemoconcentratedandthepatient’shemoglobinlevelandhematocritrise.Becauseofthethird-spaceshift(fluidsmovingoutofthevascularcompartment),hypovolemia
occurs.Hypovolemiacausesdecreasedcardiacoutput,tachycardia,andhypotension.Thepatientmaydevelopshockorarrhythmias,orhismentalstatusmaydecrease.Withtheburn’sdamagetotheskinsurface,theskin’sabilitytopreventwaterlossisalso
decreased.Asaresult,thepatientcanloseupto8Loffluidperdayor400ml/hour.
ThekidneystrytocopeDiminishedkidneyperfusioncausesdecreasedurineoutput.Inresponsetoaburn,thebodyproducesandreleasesstresshormones(aldosteroneandantidiuretichormone),whichcausethekidneystoretainsodiumandwater.
UneasybreathingDependingonthetypeofburn,apatientmayhaveacompromised,edematousairway.Lookforburnsoftheheadorneck,singednasalhairs,sootinthemouthornose,coughing,voicechanges,mucosalburns,andstridor.Youmayhearcracklesorwheezesoverthelungfields.Thepatientmaybreatherapidlyorpant.Circumferentialburnsandedemaoftheneckorchestcanrestrictrespirationsandcauseshortnessofbreath.
TissueturmoilInjuredtissuereleasesacidsthatcancauseadropinthepHlevelofbloodandsubsequentlyleadtometabolicacidosis.Damagetomuscletissueinfull-thicknessburnsandelectricalburnsresultsinreleaseofmyoglobin,whichcancauserenaldamageandacutetubularnecrosis.Myoglobingivesurineadarkenedappearance.
TheGItakesahitHypovolemiacanleadtodecreasedcirculationtotheGIsystem,resultinginparalyticileus.This
ismanifestedbydecreasedorabsentperistalsisandbowelsounds.Stressulcers,orCurling’sulcers,candevelopintheantrumofthestomachorintheduodenum
asaresultoftheintensephysiologicstressassociatedwithburntrauma.Theseulcerscanbeobservedbyendoscopyapproximately72hoursafterinjury.Curling’sulcersaremostlikelycausedduringthefluidaccumulationphaseasaresultof
decreasedbloodflowtothestomachalongwithrefluxofduodenalcontents.Largeamountsofpepsinarealsoreleased.Thecombinedischemia,pepsin,andacidleadstoulceration.SignsofCurling’sulcerincludebloodyorcoffee-groundemesisandoccultbloodinthestool.
Histamineblockersandantacidsareusedtoreducegastricacidityandulceration.Theselesionsusuallyhealoncethepatientrecoversfromtheacuteinjury.Thebody’smetabolicneedsalsoincreasebecauseoftheburninjury,usuallyinproportionto
thesizeoftheburnwound.Anegativenitrogenbalancecanoccuraswellasaresultoftissuedestruction,proteinloss,andthebody’sstressresponse.
Unbalanced!Manyelectrolyteimbalancescanoccurduringthefluidaccumulationphasebecauseofthehypermetabolicneedsandtheprioritythatfluidreplacementtakesovernutritionalneedsduringtheemergentphase:•Hyperkalemiacanresultfrommassivecellulartrauma,metabolicacidosis,orrenalfailure.
Theconditiondevelopsaspotassiumisreleasedintotheextracellularfluidintheinitialdaysfollowingtheinjury.
•Hypovolemiacanoccurasaresultoffluidlossesandfluidsmovingfromthevascularspacetotheinterstitialspace.Lostfluidresemblesintravascularfluidincompositionandcontainsproteinsandelectrolytes.
•Hyponatremiacanresultfromincreasedlossofsodiumandwaterfromthecells.Largeamountsofsodiumbecometrappedinedematousfluidduringthefluidaccumulationphase.Aqueoussilvernitratedressingsmayalsocontributetothiselectrolyteimbalance.
•Hypernatremiacanoccurasaresultoftheaggressiveuseofhypertonicsodiumsolutionsduringfluidreplacementtherapy.
•Hypocalcemiacanoccurbecausecalciumtravelstothedamagedtissueandbecomesimmobilizedattheburnsite.Thatmovementcanoccur12to24hoursaftertheburninjury.Itcanalsooccurbecauseofaninadequatedietaryintakeofcalciumorinadequatesupplementationduringtreatment.
•Metabolicacidosiscandevelopasaresultoftheaccumulationofacidsreleasedfromtheburnedtissue.Itcanalsooccurasaresultofdecreasedtissueperfusionfromhypovolemia.
•Respiratoryacidosiscanresultfrominadequateventilation,ashappensininhalationburns.
FluidremobilizationphaseThefluidremobilizationphase,alsoknownasthediuresisstageoracutestage,startsabout48hoursaftertheinitialburn.Duringthisphase,fluidshiftsbacktothevascularcompartment.Edemaattheburnsitedecreases,andbloodflowtothekidneysincreases,whichpromotesurineoutput.Sodiumislostthroughtheincreaseindiuresis,andpotassiumeithermovesbackintothecellsorislostthroughurine.
Memoryjogger
Torememberhowfluidsshiftfollowingaburninjury(theburnphases),thinkofanARC:
Accumulationphase—fluidsshiftfromthevascularcompartmentintotheinterstitialspaces.
Remobilizationphase—fluidmovesbacktothevascularcompartment.
Convalescentphase—majorfluidshiftshavebeenresolvedandhealingcanbegin.
ShiftybusinessFluidandelectrolyteimbalancespresentduringtheinitialphaseafteraburncanchangeduringthefluidremobilizationphase.Here’sarundownoftheseimbalances:•Hypokalemiacandevelopaspotassiumshiftsfromtheextracellularfluidbackintothecells.
Theconditionusuallyoccurs4to5daysafteramajorburn.•Hypervolemiacanoccurasfluidshiftsbacktothevascularcompartment.Excessive
administrationofI.V.fluidsmayexacerbatethecondition.•Hyponatremiamayoccurwhensodiumislostduringdiuresis.•Metabolicacidosiscanoccurwhenlossofsodiumresultsinthedepletionofbicarbonate.
ConvalescentphaseTheconvalescentphasebeginsafterthefluidaccumulationandremobilizationphaseshaveresolved.Duringthisphase,thefocusisonthehealingorreconstructionoftheburnwound.Althoughthemajorfluidshiftshavebeenresolved,furtherfluidandelectrolyteimbalancesmaycontinueasaresultofinadequatedietaryintake.Anemiacommonlydevelopsatthistimebecausesevereburnstypicallydestroyredbloodcells.
WhattestsshowDiagnostictestresultsyoumayseewhencaringforaburnpatientinclude:•increasedhemoglobinlevelsandhematocrit•increasedserumpotassiumlevels•decreasedserumsodiumlevels•decreasedserumcalciumlevels•increasedbloodureanitrogenandcreatininelevels,indicatingrenalfailure•lowpHandbicarbonatelevels,indicatingmetabolicacidosis•increasedcarboxyhemoglobinlevels,indicatingsmokeinhalation•electrocardiogram(ECG)changesreflectingelectrolyteimbalancesormyocardialdamage•myoglobinintheurine.
Edemaalert!Watchforsignsandsymptomsofpulmonaryedema,whichcanresultfromfluidreplacementtherapyandtheshiftoffluidbacktothevascularcompartment.Checkfordecreasedhemoglobinlevelsandhematocritduetohemodilutionfromthatfluidshift.
InspectforinfectionSkinimpairmentleadsnotonlytobodytemperaturealterationsandchillsbutalsotoinfection.Blisters,charring,andscarringmayappear,dependingonthetypeandageoftheburn.Withinfectedwounds,youmaynoteafoulodorandpurulentdrainage.
Howthey’retreatedPrioritiesintreatingaburnpatientreflecttheABCs—airway,breathing,andcirculation.Forapatientwithseverefacialburnsorsuspectedinhalationinjury,treatmenttopreventhypoxiaincludesendotracheal(ET)intubation,administrationofhighconcentrationsofoxygen,andpositive-pressureventilation.Beawarethatacuterespiratorydistresssyndromemaydevelop
fromboththebody’simmuneresponsetoinjuryandfluidleakageacrossthealveolocapillarymembrane.
Letitflow,letitflow,letitflowFluidresuscitationisavitalpartofburntreatment.Severalformulashavebeencreatedtoguideinitialtreatmentforburnpatients.TheParklandformulaisoneofthemorecommonlyusedformulas.(SeeFluidreplacementformula,page324.)
FluidreplacementformulaHere’sacommonlyusedformula,themodifiedParklandformula,forcalculatingfluidreplacementinburnpatients.Alwaysbasefluidreplacementonthepatient’sresponse,especiallyurineoutput.Urineoutputof30to50ml/hourisasignofadequaterenalperfusioninanadultand1ml/kg/hourinsmallchildren.
FormulaUse4mloflactatedRinger’ssolutionperkilogramofbodyweightperpercentageofbodysurfaceareaover24hours.Example:fora68-kg(150-lb)personwith27%bodysurfaceareaburns,4ml×68kg×27=
7,344mlover24hours.Giveone-halfofthetotaloverthefirst8hoursaftertheburnandtheremainderoverthenext16hours.
InitialtreatmentincludesadministrationoflactatedRinger’ssolutionthroughalarge-boreI.V.linetoexpandvascularvolume.Thisbalancedisotonicsolutionsupplieswater,sodium,andotherelectrolytes;itcanhelpcorrectmetabolicacidosisbecausethelactateinthesolutionisquicklymetabolizedintobicarbonate.
ColloidcontroversyHypertonicsolutionscalledcolloidsmaybeusedtoincreasebloodvolume.Colloidsdrawwaterfromtheinterstitialspaceintothevasculature.However,theuseofcolloidsintheimmediatepostburnperiodiscontroversialbecausetheyincreasecolloidosmoticpressureintheinterstitialspace,whichmayworsenedemaattheburnsite.Patientswhomaybenefitfromcolloidsolutionsarethoserequiringlowervolumeresuscitationsuchaspreexistingheartdisease,geriatricpatients,andinhalationinjuries.Examplesofcolloidsolutionsareplasma,albumin,anddextran.Asolutionofdextrose5%inlactatedRinger’sistypicallyreservedasamaintenancedosefor
childrentopreventlife-threateninghypoglycemia.Dextrose5%inwatermaybeusedtoreplacenormalinsensiblewaterlossaswellaswaterlossassociatedwithdamagetotheskinbarrierafterthefirst24hours.CentralandperipheralI.V.linesareinsertedasnecessary.PotassiummaybeaddedtoI.V.fluids48to72hoursaftertheburninjury.Anindwellingurinarycatheterpermitsaccuratemonitoringofurineoutput.Administrationof2
to4mgofmorphineI.V.alleviatespainandanxiety.Thepatientmayneedanasogastric(NG)tubetopreventgastricdistentionfromparalyticileus,alongwithhistamineblockersandantacidstopreventCurling’sulcers.Allburnpatientsneedaboosterof0.5mloftetanustoxoidgivenI.M.Burncarefacilitiesdon’t
recommendadministeringaprophylacticantibioticbecauseoveruseofantibioticsfostersthedevelopmentofresistantbacteria.
TreatmenttipsTreatmentoftheburnwoundincludes:•initialdebridementbywashingthesurfaceofthewoundareawithmildsoap•sharpdebridementofloosetissueandblistersbecauseblisterfluidcontainsvasospasticagents
thatcanworsentissueischemia•coverageofthewoundwithanantibacterialagent,suchassilversulfadiazine(Silvadene),and
anocclusivecottongauzedressing•removalofeschar(escharotomy)ifthepatientisatriskforvascular,circulatory,orrespiratory
compromise—forexample,ifthepatienthasacircumferentialburnthatcirclesaroundanextremity,thechestcavity,ortheabdomen,skingraftsmayalsoberequired.Ifthepatientisgoingtobetransferredtoaburncenter,defertotheirtreatmentcriteriapriortotransfer.Mostburncentersrequestthatnoantibacterialagentisappliedtotheburnbutrequiredrydressingsappliedtothewound.
HowyouinterveneForaburnpatient,properinterventionandgoodnursingcarecanmakethedifferencebetweenlifeanddeath.Duringtheemergentphase,immediate,aggressiveburntreatmenttoincreasethepatient’schanceforsurvivaltakesfirstpriority.Later,thepriorityshiftstoprovidingsupportivemeasuresandusingstrictaseptictechniquetominimizetheriskofinfection.(Fortipsonhowtohandleburnsoutsidethehealthcaresystem,seeEmergencyburncare,page326.)
EmergencyburncareHere’swhatyoushoulddoifyouencounterapersonwhohasjustbeenburned:•
Extinguishanyremainingflamesonthepatient’sclothing.•
Don’tdirectlytouchthepatientifhe’sstillconnectedtoliveelectricity.Unplugordisconnecttheelectricalsourceifpossible.•
AssesstheABCs(airway,breathing,circulation),andinitiatecardiopulmonaryresuscitationifnecessary.•
Assessthescopeoftheburnsandotherinjuries.•
Removethepatient’sclothing;cutaroundclothingthatstickstotheskin.•
Irrigateareasofchemicalburnswithcopiousamountsofwater.•
Removefromthepatientanyjewelryorothermetalobjectsthatcanretainheatandconstrictpatientmovement.•
Coverthepatientwithablanket.•
Sendforemergencymedicalassistance.
Herearesomegeneralburncareguidelines:•Maintainheadandspinalalignmentuntilheadandspinalcordinjurieshavebeenruledout.
Shockingsituation•Giveemergencytreatmentforelectricshockifneeded.Ifanelectricshockcausedventricular
fibrillationandsubsequentcardiacandrespiratoryarrest,begincardiopulmonaryresuscitationatonce.Trytoobtainanestimateofthevoltagethatcausedtheinjury.
•Makesurethepatienthasadequateairwayandeffectivebreathingandcirculation.Ifneeded,assistwithETintubation.ThepatientmayhaveatracheostomytubeinsertedifETintubationisn’tpossible.Administer100%oxygenasordered,andadjusttheflowtomaintainadequategasexchange.Drawbloodforarterialbloodgas(ABG)analysesasordered.
•Assessvitalsignsevery15minutes.Assessbreathsounds,andwatchforsignsofhypoxiaandpulmonaryedema.
•Takestepstocontrolbleeding,andremoveclothingthat’sstillsmoldering.Cutaroundclothingstucktothepatient’sskin.Removeringsandotherconstrictingitems.
•Assesstheskinforthelocation,depth,andextentoftheburn.•AssistwiththeinsertionofacentralvenouslineandadditionalarterialandI.V.lines.•StartI.V.therapyatoncetopreventhypovolemicshockandmaintaincardiacoutput.Followthe
Parklandformulaoranotherfluidresuscitationformula,asorderedbythedoctor.•Insertanindwellingurinarycatheterasordered,andmonitorintakeandoutputevery15to30
minutes.•Maintainadequatepulmonaryhygienebyturningthepatientandperformingposturaldrainage
regularly.•Watchforsignsofdecreasedtissueperfusion,increasedconfusion,andagitation.Assess
peripheralpulsesforadequacy.•Assessthepatient’sheartandhemodynamicstatusforchangesthatmightindicatefluid
imbalances,suchashypervolemiaorhypovolemia.
•Observethepatternofthird-spaceshifting(generalizededema,ascites,andpulmonaryorintracranialedema),anddocumentyourfindings.
•Monitorpotassiumlevels,andwatchforsignsandsymptomsofhyperkalemia,suchascardiacrhythmstripchanges;weakness;diarrhea;andaslowed,irregularheartrate.
•Monitorsodiumlevels,andwatchforsignsandsymptomsofhyponatremia,suchasincreasingconfusion,twitching,seizures,abdominalpain,nausea,andvomiting.
•Watchforsignsandsymptomsofmetabolicacidosis,suchasheadache;disorientation;drowsiness;nausea;vomiting;andrapid,shallowbreathing.
•MonitoroxygensaturationandABGresults.•Monitorotherlaboratoryresults.•MonitorECGresultsforarrhythmias.•AnticipatetheneedtoadministermaintenanceI.V.replacementfluidsbasedondaily
assessmentoffluid,electrolyte,acid-base,andnutritionalstatus.•Maintaincorebodytemperaturebycoveringthepatientwithasterileblanketandexposingonly
smallareasofhisbodyatatime.•InsertanNGtube,ifordered,todecompressthestomach.Avoidaspirationofstomachcontents
duringtheprocedure.•Obtainapreburnweightfromthepatientorfromafamilymemberorfriend.
•Ifbowelsoundsarepresent,provideadiethighinpotassium,protein,vitamins,fats,nitrogen,andcaloriestomaintainthepatient’spreburnweight.Ifnecessary,feedthepatiententerallyuntilhecantolerateoralfeedings.Ifhecan’ttolerateoralorenteralfeedings,administerhyperalimentationasordered.
•Weighthepatienteverydayatthesametimewiththesameamountoflinen,clothes,anddressings.
•Explainallprocedurestothepatientbeforeperformingthem.Speakcalmlyandclearlytohelpalleviateanxiety.Encouragethepatienttoparticipateinself-careasmuchaspossible.(SeeTeachingaboutburns.)
Teachingpoints
TeachingaboutburnsWhenteachingapatientaboutburns,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
burnbasicsandprevention•
thepatient’sparticularplanoftreatmentandwoundmanagement•
signsandsymptomstoreporttothepractitioner•
long-termcareissues,suchashomecarefollow-upandrehabilitation.
•Usestrictaseptictechniqueforallpatientcare,includingroutinelywashingyourhandsandusingprotectiveisolationclothing.
•Observethepatientforsignsofinfection,suchasfever,tachycardia,andpurulentwounddrainage.Burnpatientshaveanincreasedriskofinfectionfromdestructionoftheskinbarrierandthelossofnutrients.
•Administerananalgesic30minutesbeforewoundcare.•Culturewoundsbeforeapplyingatopicalantibioticforthefirsttime.•Coverburnswithadry,steriledressing.Nevercoverlargeburnswithsaline-soakeddressings
becausetheycandrasticallylowerbodytemperature.Atopicalointmentandanantibioticmaybeappliedasappropriate.Silvernitrateandmafenideacetate(Sulfamylon)cancauseelectrolyteimbalancesandmetabolicalterations.
•Maintainjointfunctionwithphysicaltherapyanduseofsupportgarmentsandsplints.•Notifythepractitionerofsignificantchangesinthepatient’sconditionandpertinentlaboratory
testresults.•Provideopportunitiesforthepatienttovoiceconcerns,especiallyaboutalteredbodyimage.If
appropriate,arrangeameetingwithanotherburnpatientwithsimilarinjuriesorreferthepatienttoaburnsupportgroup.Whenpossible,showthepatienthowbodilyfunctionsareimproving.Ifnecessary,referhimformentalhealthcounseling.
•Preparethepatientandfamilytogohome.•Documentallcaregiven,allteachingdone,andthepatient’sreactiontoeach.(SeeDocumentingburncare.)
Chartsmart
DocumentingburncareIfyourpatienthasburns,makesureyoudocumentthefollowinginformation:•
assessmentfindings•
depth,extent,andseverityofburninjury•
extentofedema•
pertinentlaboratoryresults•
I.V.therapy•
urinaryoutput•
otherinterventionssuchaswoundcare•
supportmadeavailabletothepatientandfamily•
patientandfamilyteachingalongwiththepatient’sresponse.
That’sawrap!
Burnbasics•
Usuallycausemajorchangesinthebody’sfluidandelectrolytebalance,whichmaychangeovertimeastheinitialinjuryprogresses•
Types:thermal,electrical,chemical,andradiation
Classificationofburns•
First-degree:superficialburnthataffectstheepidermis;fluidandelectrolytebalanceisn’taffected•
Second-degree:partial-thicknessburnthataffectstheepidermisanddermis;fluidandelectrolyteimbalancesoccurwithburnsthatcoversignificantareasofthebody•
Third-degree:full-thicknessburnthataffectstheepidermis,dermis,andtissuesbelowthedermis;carriesthegreatestriskoffluidandelectrolyteimbalances•
Fourth-degree:deepfull-thicknessburnsthatextendtothemuscle;prognosisispoor
Burnseverity•
Requirestheuseofassessmenttools,suchastheRuleofNinesortheLund-Browderclassification,toestimatethepercentageofbodysurfaceareainvolved•
Maybecategorizedasmajor,moderate,orminor
PhasesofburnsFluidaccumulationphase•
Occurswithinfirst24to36hoursafteraburn;alsoknownasburnshockphase•
Causesfluidtoshiftfromthevascularcompartmenttointerstitialspace(third-spaceshift),resultinginedema•
Producesstresshormonesthatcausethekidneystoretainsodiumandwater,leadingtodiminishedkidneyperfusionanddecreasedurineoutput•
Causessuchfluidandelectrolyteimbalancesas:–
Hyperkalemia—resultsfrommassivecellulartrauma,metabolicacidosis,orrenalfailure;developsaspotassiumisreleasedintoextracellularfluidduringinitialdaysfollowinginjury–
Hypovolemia—resultsfromfluidlossesandthird-spaceshift–
Hyponatremia—resultsfromincreasedcellularlossofsodiumandwater;causeslargeamountsofsodiumtobecometrappedinedematousfluid–
Hypernatremia—canresultfromaggressiveuseofhypertonicsodiumsolutionsduringfluidreplacementtherapy
–Hypocalcemia—canresultwhencalciumtravelstothedamagedtissueandbecomesimmobilizedatburnsite;mayalsoresultfrominadequatedietaryintakeofcalciumorinadequatesupplementationduringtreatment–
Metabolicacidosis—mayresultfromaccumulationofacidsreleasedbyburnedtissue;mayalsoresultfromdecreasedperfusionduetohypovolemia
Fluidremobilizationphase•
Beginsabout48hoursaftertheinitialburn•
Causesfluidtoshiftbackintothevascularcompartment•
Causessuchfluidandelectrolyteimbalancesas:–
Hypokalemia—candevelopaspotassiumshiftsfromextracellularfluidbackintothecells;usuallyoccurs4to5daysafteramajorburn–
Hypervolemia—canoccurasfluidshiftsbacktothevascularcompartment;mayresultfromgivingtoomuchI.V.fluid–
Hyponatremia—mayoccurwhensodiumislostduringdiuresis–
Metabolicacidosis—occurswhenlossofsodiumresultsinthedepletionofbicarbonate
Convalescentphase•
Beginsafterfirsttwophaseshavebeenresolved•
Maycausefurtherfluidandelectrolyteimbalancesasaresultofinadequatedietaryintake
Treatment•
Dependsontheseverityoftheburn•
Forsevereburns,airway,breathing,andcirculationarepriorities•
Involvesrehydrationwithfluidresuscitation•
Requiresmonitoringofurineoutputwithcatheter•
Mayrequirepainreliefmeasures•
Involveswoundcare
Quickquiz
1.Duringthefluidaccumulationphaseofamajorburninjury,fluidsshiftfromthe:A.intravascularspacetotheinterstitialspace.B.interstitialspacetotheintravascularspace.C.intracellularspacetotheinterstitialspace.D.intravascularspacetotheintracellularspace.
Answer:A.Duringthefluidaccumulationphase,fluidsshiftfromtheintravascularspacetotheinterstitialspace.
2.Hypovolemiausuallyoccursduringwhichmajorburnphase?A.FluidremobilizationB.FluidaccumulationC.ConvalescentD.Acute
Answer:B.Hypovolemiausuallyoccursduringthefluidaccumulationphaseasfluidmovesfromtheintravascularspacetotheinterstitialspace,aprocessknownasthird-spaceshift.
3.YouinsertanI.V.lineandbeginfluidresuscitation.ThedoctorwantsyoutousetheParklandformula.Thepatientisa155-lb(70-kg)maleandisestimatedathaving50%ofhistotalbodysurfaceareaburned.WhatamountoflactatedRinger’ssolutionshouldyouadministeroverthefirst8hours?
A.700mlB.7,000mlC.1,400mlD.6,000ml
Answer:B.TheParklandformulais4ml×thepercentageoftotalbodysurfaceareaburned×weightinkilograms.So,4ml×50%×70kg=14,000mlor14LoflactatedRinger’ssolutioninthefirst24hours.Therefore,youwouldgive7,000ml(orhalf)inthefirst8hours.
4.Duringthefluidremobilizationphaseofapatientwithburninjuries,thenursewouldexpecttoseesignsofwhichelectrolyteimbalance?
A.HypokalemiaB.HyperkalemiaC.HypernatremiaD.Hypovolemia
Answer:A.Hypokalemiaoccursinthefluidremobilization(diuresis)phaseaspotassiumshiftsfromtheextracellularfluidbackintothecells.
ScoringIfyouansweredallfourquestionscorrectly,outstanding!You’velearnedhowtobeattheheat!Ifyouansweredthreequestionscorrectly,waytogo!Youdon’thavemuchlefttolearnwhenitcomestoburns!Ifyouansweredfewerthanthreequestionscorrectly,don’tfeeltheheatjustyet.Therearestillacouplemorechapterstogo!
ReferencesBacomo,F.K.,&Chung,K.K.,(2011).Aprimeronburnresuscitation.JournalofEmergencies,
Trauma,andShock,4(1),109–113.Edlich,R.F.(2013).Thermalburns.Retrievedfromhttp://emedicine.medscape.com/article/1278244-
overviewHaberal,M.,Abali,A.E.,&Karakayali,H.(2010).Fluidmanagementinmajorburninjuries.Indian
JournalofPlasticSurgery,43(Suppl),S29–S36.Retrievedfromhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038406/
Jenkins,J.A.(2013).Emergentmanagementofthermalburns.Retrievedfromhttp://emedicine.medscape.com/article/769193-overview
Jeschke,M.G.,Pinto,R.,Herndon,D.N.,Finnerty,C.C.,&Kraft,R.(2014).Hypoglycemiaisassociatedwithincreasedpostburnmorbidityandmortalityinpediatricpatients.CriticalCareMedicine,42(5),1221–1331.doi:10.1097/CCM.0000000000000138
Jeschke,M.G.,Shahrokhi,S.,Finnerty,C.C.,Branski,L.K.,&Dibildox,M.(2013).Woundcoveragetechnologiesinburncare:Establishedtechniques.JournalofBurnCare&Research.Advanceonlinepublication.doi:10.1097/BCR.0b013e3182920d29
Kraft,R.,Herndon,D.N.,Finnerty,C.C.,Shahrokhi,S.,&Jeschke,M.G.(2013).Occurrenceofmultiorgandysfunctioninpediatricburnpatients:Incidenceandclinicaloutcome.AnnalsofSurgery,259(2),381–387.doi:10.1097/SLA.0b013e31828c4d04
Mitchell,K.B.,Khalil,E.,Brennan,A.,Shao,H.,Rabbitts,A.,Leahy,N.E.,...Gallagher,J.J.(2013).Newmanagementstrategyforfluidresuscitation:Quantifyingvolumeinthefirst48hoursafterburninjury.JournalofBurnCare&Research,34(1),196–202.doi;10.1097/BCR.0b013e3182700965
Namdar,T.,Stollwerck,P.L.,Stang,F.H.,Siemers,F.,Mailänder,P.,&Lange,T.(2010).Transdermalfluidlossinseverelyburnedpatients.GermanMedicalScience,8,Doc28.Retrievedfrom
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975262/Oliver,R.I.(2013).Burnresuscitationandearlymanagement.Retrievedfrom
http://emedicine.medscape.com/article/1277360-overviewSheridan,R.L.(2012).Burnrehabilitation.Retrievedfrom
http://emedicine.medscape.com/article/318436-overview#aw2aab6b5Sheridan,R.L.(2013).Initialevaluationandmanagementoftheburnpatient.Retrievedfrom
http://emedicine.medscape.com/article/435402-overview#a1
PartIV
Treatingimbalances
19 I.V.fluidreplacement
20 Totalparenteralnutrition
Chapter19
I.V.fluidreplacement
JustthefactsInthischapter,you’lllearn:
♦typesofI.V.fluidsandtheiruses
♦methodsusedtoadministerI.V.fluids
♦complicationsassociatedwithI.V.therapy
♦propercareforpatientsreceivingI.V.therapy.
AlookatI.V.therapyTomaintainhealth,thebalanceoffluidsandelectrolytesintheintracellularandextracellularspacesneedstoremainrelativelyconstant.Wheneverapersonexperiencesanillnessoraconditionthatpreventsnormalfluidintakeorcausesexcessivefluidloss,I.V.fluidreplacementmaybenecessary.
AlottoofferI.V.therapythatprovidesthepatientwithlife-sustainingfluids,electrolytes,andmedicationsofferstheadvantagesofimmediateandpredictabletherapeuticeffects.TheI.V.routeis,therefore,thepreferredroute,especiallyforadministeringfluids,bloodproducts,electrolytes,anddrugsinanemergency.ThisroutealsoallowsforfluidintakewhenapatienthasGImalabsorption.I.V.therapypermits
accuratedosagetitrationforanalgesicsandothermedications.PotentialdisadvantagesassociatedwithI.V.therapyincludedrugandsolutionincompatibility,adversereactionstovariousmedications,localizedinfection,sepsis,andothercomplications.
TypesofI.V.solutionsSolutionsusedforI.V.fluidreplacementfallintothebroadcategoriesofcrystalloids(whichmaybeisotonic,hypotonic,orhypertonic)andcolloids(whicharealwayshypertonic).
CrystalloidsCrystalloidsaresolutionswithsmallmoleculesthatfloweasilyfromthebloodstreamintocellsandtissues.Isotoniccrystalloidscontainaboutthesameconcentrationofosmoticallyactiveparticlesasextracellularfluid,sofluiddoesn’tshiftbetweentheextracellularandintracellularareas.
ConcentratingonconcentrationHypotoniccrystalloidsarelessconcentratedthanextracellularfluid,sotheymovefromthebloodstreamintocells,causingcellstoswell.Incontrast,hypertoniccrystalloidsaremorehighlyconcentratedthanextracellularfluid,sofluidispulledintothebloodstreamfromthecells,causingcellstoshrink.(SeeComparingfluidtonicity.)
ComparingfluidtonicityTheillustrationsbelowshowtheeffectsofdifferenttypesofI.V.fluidsonfluidmovementandcellsize.
IsotonicIsotonicfluids,suchasnormalsalinesolution,haveaconcentrationofdissolvedparticles,ortonicity,equaltothatoftheintracellularfluid.Osmoticpressureisthereforethesameinsideandoutsidethecells,sotheyneithershrinknorswellwithfluidmovement.
HypertonicHypertonicfluidhasatonicitygreaterthanthatofintracellularfluid,soosmoticpressureisunequalinsideandoutsidethecells.Dehydrationorrapidinfusionofhypertonicfluids,suchas3%salineor50%dextrose,drawswateroutofthecellsintothemorehighlyconcentratedextracellularfluid.
HypotonicHypotonicfluids,suchashalf-normalsalinesolution,haveatonicitylessthanthatofintracellularfluid,soosmoticpressuredrawswaterintothecellsfromtheextracellularfluid.SevereelectrolytelossesorinappropriateuseofI.V.fluidscanmakebodyfluidshypotonic.
IsotonicsolutionsIsotonicsolutionshaveanosmolality(concentration)between240and340mOsm/kg.Dextrose5%inwater(D5W),acommonlyadministeredisotonicfluid,hasanosmolalityof252mOsm/kg.Thedextrosemetabolizesquickly,however,actinglikeahypotonicsolutionandleavingwaterbehind.Infusinglargeamountsofthesolutionmaycausehyperglycemia.Normalsalinesolution,anotherisotonicsolution,containsonlytheelectrolytessodiumand
chloride.Otherisotonicfluidsaremoresimilartoextracellularfluid.Forinstance,Ringer’ssolutioncontainssodium,potassium,calcium,andchloride.
HypotonicsolutionsHypotonicsolutionsarefluidsthathaveanosmolalitylessthan240mOsm/kg.Anexampleofacommonlyusedhypotonicsolutionishalf-normalsalinesolution.
ItmakesacellswellHypotonicsolutionsshouldbegivencautiouslybecausefluidthenmovesfromtheextracellularspaceintocells,causingthemtoswell.Thatfluidshiftcancausecardiovascularcollapsefromvascularfluiddepletion.Itcanalsocauseincreasedintracranialpressure(ICP)fromfluidshiftingintobraincells.Hypotonicsolutionsshouldn’tbegiventopatientsatriskforincreasedICP—forexample,
thosewhohavehadastroke,headtrauma,orneurosurgery(Abunnaja,Cuviello,&Sanchez,2013).SignsofincreasedICPincludeachangeinthepatient’slevelofconsciousness;motororsensorydeficits;andchangesinthesize,shape,orresponsetolightinthepupils.Hypotonicsolutionsalsoshouldn’tbeusedforpatientswhosufferfromabnormalfluidshiftsintotheinterstitialspaceorthebodycavities—forexample,asaresultofliverdisease,aburn,ortrauma.
HypertonicsolutionsHypertonicsolutionsarethosethathaveanosmolalitygreaterthan340mOsm/kg.Examplesinclude:•dextrose5%inhalf-normalsalinesolution•3%sodiumchloridesolution•dextrose10%innormalsalinesolution.
TheincredibleshrinkingcellAhypertonicsolutiondrawsfluidsfromtheintracellularspace,causingcellstoshrinkandtheextracellularspacetoexpand.Patientswithcardiacorrenaldiseasemaybeunabletotolerateextrafluid.Watchforfluidoverloadandpulmonaryedema.Becausehypertonicsolutionsdrawfluidsfromcells,patientsatriskforcellulardehydration
(patientswithdiabeticketoacidosis[DKA],forexample)shouldn’treceivethem.(SeeAlookatI.V.solutions.)
AlookatI.V.solutionsThischartshowsexamplesofsomecommonlyusedI.V.fluidsandincludessomeoftheirclinicalusesandspecialconsiderations.
Colloids
Theuseofcolloidsovercrystalloidsiscontroversial.Still,thedoctormayprescribeacolloid—orplasmaexpander—ifyourpatient’sbloodvolumedoesn’timprovewithcrystalloids.Examplesofcolloidsthatmaybegiveninclude:•albumin(availablein5%solutions,whichareosmoticallyequaltoplasma,and25%solutions,
whichdrawaboutfourtimestheirvolumeininterstitialfluidintothecirculationwithin15minutesofadministration)
•plasmaproteinfraction•dextran•hetastarch.
FlowingintothestreamColloidspullfluidintothebloodstream.Theeffectsofcolloidslastseveraldaysiftheliningofthecapillariesisnormal.Thepatientneedstobecloselymonitoredduringacolloidinfusionforincreasedbloodpressure,dyspnea,andboundingpulse,whichareallsignsofhypervolemia.Ifneithercrystalloidsnorcolloidsareeffectiveintreatingtheimbalance,thepatientmay
requireabloodtransfusionorothertreatment.
DeliverymethodsThechoiceofI.V.deliveryisbasedonthepurposeofthetherapyanditsduration;thepatient’sdiagnosis,age,andhealthhistory;andtheconditionofthepatient’sveins.I.V.solutionscanbedeliveredthroughaperipheralorcentralvein.Cathetersandtubingarechosenbasedonthetherapyandsitetobeused.Here’salookathowtochooseasite—peripheralorcentral—andwhichequipmentyou’llneedforeach.
PeripherallinesPeripheralI.V.therapyisadministeredforshort-termorintermittenttherapythroughaveininthearmorhand.PotentialI.V.sitesincludethemetacarpal,cephalic,andbasilicveins.Inanadult,usingveinsinthelegorfootisunusualbecauseoftheriskofthrombophlebitisandshouldbeavoidedifatallpossible.Forneonatalandpediatricpatients,othersitesincludeveinsofthehead,neck,andlowerextremities.
GivethegreenlighttotherightsiteChooseasitethatmeetsthepatient’sneedforfluidswhilekeepingthepatientascomfortableaspossible.PlaceI.V.cathetersinthehandorlowerarmsositescanbemovedupwardasneeded.Usethepatient’snondominanthandifpossible.Forapatientwhohassufferedtraumaorcardiacarrest,usealargeveinintheantecubitalareatogainrapidaccess.Avoidtheantecubitalsiteina
mobilepatientbecausethecathetermaykinkwithmovementorcauseotherdiscomfort.Avoidusingveinsoverjoints.Cathetersinthoseveinsareuncomfortableandawkwardandcanbedisplacedeasily.Avoidusingveinsinthefeetofachildwhoisabletowalk.Alsoavoidusingveinsinthearm
ofapatientwhohasaninjury,lossofsensation,orarteriovenousfistulainthearm.Remember,don’tinsertanI.V.inthearmonthesamesideasamastectomywithaxillarynoderemovalorontheaffectedsideofapersonwhosufferedastroke.Ifthepatientisunabletospeakcoherently,performabasichead-to-toeassessmentpriortostartinganI.V.becausethepatientmayhaveacentralaccesssuchasanimplantedportorperipherallyinsertedcentralcatheterthatcanbeusedinstead.
Pickacath,notjustanycathThreemaintypesofcathetersareusedforinsertionintoaperipheralvein:•Steel-wingedinfusionneedlesareinsertedeasily,butinfiltrationiscommon.Thesecatheters
aresmall,nonflexible,andusedonlywhenaccesswithanotherdeviceprovesunsuccessful.Thecathetersarealsousedforshort-termtherapyinadults,especiallyforgivingmedicationsbyI.V.push(throughasyringeoverashortperiodoftime).
•Indwellingcathetersinsertedoverasteelneedleareeasytouseandlesslikelytoinfiltrate.Onceinplace,thesecathetersaremorecomfortableforthepatient.
•Plasticcathetersinsertedthroughahollowneedlearelongerandaremorecommonlyusedforcentralveininfusions.Thecathetermustbethreadedthroughtheveinforagreaterdistance,whichmakesthesecathetersmoredifficulttouse.
NeedlesizemattersChoosingtherightdiameter(orgauge)needleorcatheterisimportantforensuringadequateflowandpatientcomfort.Thehigherthegauge,thesmallerthediameteroftheneedle.
Ifyouwanttogivealotoffluidoverashortperiodoftime,orifyouwillbegivingmoreviscousfluids(suchasblood),useacatheterwithalowergauge(suchas14G,16G,or18G)andashorterlength,whichofferslessresistancetofluidflow.ForroutineI.V.fluidadministration,usehighergaugecatheters,suchasa20Gora22G.Frenchcathetersaretheexceptiontotheneedlegaugerule:Thehigherthenumber,thegreaterthediameter.
CentrallinesCentralvenoustherapyinvolvesadministeringsolutionsthroughacatheterplacedinacentralvein,typicallythesubclavianorinternaljugularvein,lesscommonlythefemoralvein.Centralvenoustherapyisusedforpatientswhohaveinadequateperipheralveins,needaccessforbloodsampling,requirealargevolumeoffluid,needahypertonicsolutiontobedilutedbyrapidbloodflowinalargervein,orneedahigh-calorienutritionalsupplement(Kuwaharaetal.2013).
Pickacath,part2Threemaintypesofcathetersareusedforshort-andlong-termcentralvenoustherapy:•Thetraditionalcentralvenouscatheterisamultilumencatheterusuallyusedforshort-term
therapy.Althoughthelumensizemayvary,amultilumencatheterprovidesmultipleI.V.accessusingoneinsertionsite.
•Aperipherallyinsertedcentralcatheterisnowcommonlyusedinhealthcarefacilitiesandinhomecare.Acertifiednursecaninsertthiscatheterthroughaveinintheantecubitalarea,cephalicorbasilicveins,atbedside.Fewer,lesssevereadverseeffectsoccurwiththesecathetersthanwithtraditionalcentralvenouscatheters.Also,thecatheterscanbeleftinplaceforseveralmonths,makingthemidealforlong-termtherapy(Seres,Valcarcel,&Guillaume,2013).
•Forextendedlong-termtherapy,thepatientmayreceiveavascularaccessportimplantedinapocketsurgicallyconstructedinthesubcutaneoustissueoratunneledcatheter,suchasaHickman,Broviac,andGroshong.Someofthesecathetershavemultiplelumensandareusedinthehealthcarefacilityandathome.
TubingsystemsThemechanicsofinfusingasolutionrequireatubingsystemthatcandeliveradrugatthecorrectinfusionrate.I.V.tubingisavailableprincipallyinmicrodripsets,whicharedesignedsothat60gttequal1ml.Microdripsetsareusefulforinfusionrateslowerthan100ml/hour—forinstance,whenusingasolutiontokeepaveinopen.Amacrodripset,ontheotherhand,isdesignedsothat10to15gttequal1ml,dependingonthe
manufacturer.Macrodripsetsarepreferredforinfusionratesgreaterthan100ml/hour—forinstance,whentreatingapatientwithshock.
GettingpumpedElectronicinfusionpumpsdeliverfluidsatpreciselycontrolledinfusionrates.Becauseeachmachinerequiresitsowntypeoftubing,checkthemanufacturer’sdirectionsbeforeuse.Mosttubingscontainanti–free-flowprotectiontopreventfluidoverloadandback-checkvalves
topreventdrugsfrommixinginsidepiggybacksystems(oneI.V.linepluggedintoanotheratapiggybackport).Filtersonsometubingeliminateparticulatematter,bacteria,andairbubbles.Othertypesoftubingareavailablespecificallyforadministeringindividualdrugsorforpiggybackingmultipledrugs.
ComplicationsofI.V.therapyCaringforapatientwithanI.V.linerequirescarefulmonitoringaswellasaclearunderstandingofwhatthepossiblecomplicationsare,whattodoiftheyarise,andhowtodealwithflowissues.Infiltration,infection,phlebitis,andthrombophlebitisarethemostcommoncomplicationsof
I.V.therapy.Othercomplicationsincludeextravasation,aseveredcatheter,anallergicreaction,anairembolism,speedshock,andfluidoverload.
Memoryjogger
Whenyou’retryingtothinkofthefourmostcommoncomplicationsofI.V.therapy,rememberthatgettinganycomplicationisaPITI:
Phlebitis
Infiltration
Thrombophlebitis
Infection.
InfiltrationDuringinfiltration,fluidmayleakfromtheveinintosurroundingtissue.Thisoccurswhentheaccessdevicedislodgesfromthevein.Lookforcoolnessatthesite,pain,swelling,leaking,andlackofbloodreturn.Also,lookforasluggishflowthatcontinuesevenifatourniquetisappliedabovethesite.Ifyouseeinfiltration,stoptheinfusion,removetheI.V.catheter,elevatetheextremity,andapplywarmsoaks.
GosmallTopreventinfiltration,usethesmallestcatheterthatwillaccomplishtheinfusion,avoidplacementinjointareas,andanchorthecatheterinplace.
InfectionI.V.therapyinvolvespuncturingtheskin,thebody’sbarriertoinfection.Asaresult,thepatientmaydevelopaninfection.Lookforpurulentdrainageatthesite,tenderness,erythema,warmth,orhardnessonpalpation.Signsandsymptomsthattheinfectionhasbecomesystemicincludefever,chills,andanelevatedwhitebloodcellcount.
InfectioninterventionsNursingactionsforaninfectedI.V.siteincludemonitoringvitalsignsandnotifyingthedoctor.Swabthesiteforculture,andremovethecatheterasordered.Topreventinfection,provideadequatedressingchangesandcontinuousassessmentofthesite,andalwaysmaintainaseptictechnique.
PhlebitisandthrombophlebitisPhlebitisisinflammationofthevein;thrombophlebitisisanirritationoftheveinwiththeformationofaclotandisusuallymorepainfulthanphlebitis.PoorinsertiontechniqueorthepH
orosmolalityofthesolutionormedicationcancausethesecomplications.Lookforpain,redness,swelling,orindurationatthesite;aredlinestreakingalongthevein;fever;orasluggishflowofthesolution.
FightingoffphlebitisWhenphlebitisorthrombophlebitisoccurs,removetheI.V.,monitorthepatient’svitalsigns,notifythedoctor,andapplywarmsoakstothesite.Topreventthesecomplications,chooselargeboreveinsandchangethecatheterevery72hourswheninfusingamedicationorsolutionwithhighosmolality.
ExtravasationSimilartoinfiltration,extravasationistheleakageoffluidintosurroundingtissues.Itresultswhenmedicationsseepthroughveinsandproduceblisteringand,eventually,necrosis.Initially,thepatientmayexperiencediscomfort,burning,orpainatthesite.Alsolookforskintightness,blanching,andlackofbloodreturn.Delayedreactionsincludeinflammationandpainwithin3to5daysandulcersornecrosiswithin2weeks.
EliminatingextravasationWhenadministeringmedicationsthatmayextravasate,knowyourfacility’spolicy.Whengivingcausticagents,suchaschemotherapy,checkforbloodreturnfrequentlyandstoptheinfusionifbloodreturnislost(Akbulut,2011).Nursingactionsincludenotifyingthepractitioner,infiltratingthesitewithanantidoteasordered,applyingiceearlyandwarmsoakslater,andelevatingtheextremity.Assessthecirculationandnervefunctionofthelimb.
SeveredcatheterAseveredcathetercanoccurwhenapieceofcatheterbecomesdislodgedandissetfreeinthe
vein.Lookforpainatthefragmentsite;decreasedbloodpressure;cyanosis;lossofconsciousness;andaweak,rapidpulse.Ifthisextremelyrarebutseriouscomplicationoccurs,applyatourniquetabovethesiteofpain,notifythedoctorimmediately,monitorthepatient,andprovidesupportasneeded.Toavoidtheproblemaltogether,don’treinsertaneedlethroughitsplasticcatheteroncetheneedlehasbeenwithdrawn.
AllergicreactionApatientmaysufferanallergicreactiontothefluid,medication,I.V.catheter,oreventhelatexportintheI.V.tubing.However,thesourceofthereactionmaynotbeknown.Lookforaredstreakextendingupthearm,rash,itching,wateryeyesandnose,shortnessofbreath,andwheezing.
OnthelookoutforanaphylaxisLeftuntreated,theconditionmayprogressrapidlytoanaphylaxis.NursingmeasuresforallergicreactionincludestoppingtheI.V.immediately,notifyingthedoctor,monitoringthepatient,andgivingoxygenandmedicationsasordered.
AirembolismAnairembolismoccurswhenairenterstheveinandcancauseadecreaseinbloodpressure,anincreaseinthepulserate,respiratorydistress,anincreaseinICP,andalossofconsciousness.
Whenairisapparent
Ifthepatientdevelopsanairembolism,notifythedoctorandclampofftheI.V.Placethepatientonhisleftside,andlowerhisheadtoallowtheairtoentertherightatrium,whereitcandispersemoresafelybywayofthepulmonaryartery.Monitorhim,andadministeroxygen.Toavoidthisseriouscomplication,primealltubingcompletely,tightenallconnectionssecurely,anduseanairdetectiondeviceonanI.V.pump.
SpeedshockSpeedshockoccurswhenI.V.solutionsormedicationsaregiventoorapidly.Almostimmediately,thepatientwillhavefacialflushing,anirregularpulse,asevereheadache,anddecreasedbloodpressure.Lossofconsciousnessandcardiacarrestmayalsooccur.Ifspeedshockoccurs,clampofftheI.V.,andnotifythepractitionerimmediately.Provide
oxygen,obtainvitalsignsfrequently,andadministermedicationsasordered.Also,keepinmindthattheuseofinfusioncontroldevicescanpreventthiscomplication.
FluidoverloadFluidoverloadcanhappengraduallyorsuddenly,dependingonhowwellthepatient’scirculatorysystemcanaccommodatethefluid.Lookforneckveindistention,puffyeyelids,edema,weightgain,increasedbloodpressure,increasedrespirations,shortnessofbreath,cough,andcracklesinthelungsonauscultation.
SlowtheflowIfthepatientdevelopsfluidoverload,slowtheI.V.rate,notifythepractitioner,andmonitorvitalsigns.Keepthepatientwarm,keeptheheadofthebedelevated,andgiveoxygenandothermedications(suchasadiuretic)asordered.
Howyouintervene
NursingcareforthepatientwithanI.V.includesthefollowingactions:•ChecktheI.V.orderforcompletenessandaccuracy.MostI.V.ordersexpireafter24hours.A
completeordershouldspecifytheamountandtypeofsolution,alladditivesandtheirconcentrations,andtherateanddurationoftheinfusion.Iftheorderisincompleteorconfusing,clarifytheorderbeforeproceeding.
•Monitordailyweightstodocumentfluidretentionorloss.A2%increaseordecreaseinbodyweightissignificant.A2.2-lb(1-kg)changecorrespondsto1qt(1L)offluidgainedorlost.
•Measureintakeandoutputcarefullyatscheduledintervals.Thekidneysattempttorestorefluidbalanceduringdehydrationbyreducingurineproduction.Aurineoutputoflessthan30ml/hoursignalsretentionofmetabolicwastes.Notifythepractitionerifyourpatient’surineoutputfallsbelow30ml/hour.
•Alwayscarefullymonitortheinfusionofsolutionsthatcontainmedicationbecauserapidinfusionandcirculationofthedrugcanbedangerous.
•Keepinmindthesize,age,andhistoryofyourpatientwhengivingI.V.fluidstopreventfluidoverload.Forpediatricpatients,useavolumecontrolI.V.deliverydevicetolimittheamountoffluidthepatientreceiveshourlyandtopreventtheaccidentaladministrationofexcessiveamountsoffluid.
•NotethepHoftheI.V.solution.ThepHcanaltertheeffectandstabilityofdrugsmixedintheI.V.bag.Consultmedicationliteratureorthepractitionerifyouhavequestions.
•Changethesite,dressing,andtubingasoftenasfacilitypolicyrequires.Solutionsshouldbechangedatleastevery24hours.(SeeDocumentinganI.V.infusion.)
Chartsmart
DocumentinganI.V.infusionIfyourpatienthasanI.V.infusion,makesureyoudocumentthefollowinginformation:•
thedate,time,andtypeofcatheterinserted•
thesiteofinsertionanditsappearance•
thetypeandamountoffluidinfused•
thepatient’stoleranceof,andresponseto,therapy•
patientandthepatient’sresponse(Altun,2010)
•WhenchangingI.V.tubing,don’tmoveordislodgetheI.V.device.Ifyouhavetroubledisconnectingthetubing,useahemostattoholdtheI.V.hubwhiletwistingthetubing.Don’tclampthehemostatshutbecausedoingsomaycrackthehub.
•Alwaysreportneedlestickinjuries.Exposuretoapatient’sbloodincreasestheriskofinfectionwithbloodbornevirusessuchasHIV,hepatitisBvirus,hepatitisCvirus,andcytomegalovirus.About1outof300peoplewithoccupationalneedlestickinjuriesbecomeHIV-seropositive.
Catchingclues•Alwayslistentoyourpatientcarefully.Subtlestatementssuchas“Ijustdon’tfeelright”maybe
yourcluetothebeginningofanallergicreaction.•KeepinmindthatacandidateforhomeI.V.therapymusthaveafamilymemberorfriendwho
cansafelyandcompetentlyadministertheI.V.fluidsaswellasabackupperson;asuitablehomeenvironment;atelephone;availabletransportation;adequatereadingskills;andtheabilitytoprepare,handle,store,anddisposeofequipmentproperly.ProceduresforcaringfortheI.V.arethesameathomeasinahealthcarefacility,exceptathome,thepatientusescleantechniqueinsteadofsteriletechnique.(SeeTeachingaboutI.V.therapy.)
Teachingpoints
Teachingpoints
TeachingaboutI.V.therapyWhenteachingapatientwhoisreceivingI.V.therapy,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
expectationsbefore,during,andaftertheI.V.procedure•
signsandsymptomsofcomplicationsandwhentoreportthem•
activityordietrestrictions•
careforanI.V.lineathome.
That’sawrap!
I.V.fluidreplacementreview
TypesofI.V.solutions•
Broadlyclassifiedascrystalloidsorcolloids
Crystalloids•
Solutionswithsmallmoleculesthatfloweasilyfromthebloodstreamintocellsandtissues•
Maybeisotonic,hypotonic,orhypertonic
Isotonicsolutions•
Containaboutthesameconcentrationofosmoticallyactiveparticlesasextracellularfluid,sofluiddoesn’tshiftbetweenextracellularandintracellularspaces•
Osmolality:240to340mOsm/kg•
Example:D5W,normalsalinesolution,anddextrose5%innormalsalinesolution
Hypotonicsolutions•
Arelessconcentratedthanextracellularfluid,whichallowsmovementfromthebloodstreamintothecells,causingcellstoexpand•
Osmolality:lessthan240mOsm/kg•
Example:half-normalsalinesolution•
CancausecardiovascularcollapsefromvascularfluiddepletionorincreasedICPfromfluidshiftingintobraincells•
AvoidusinginpatientsatriskforincreasedICP,suchasthosewhohavehadastroke,headtrauma,orneurosurgery(Abunnajaetal.,2013).•
Also,avoidusinginpatientswhosufferfromabnormalfluidshiftsintotheinterstitialspaceorbodycavities,suchasinliverdisease,burns,ortrauma
Hypertonicsolutions•
Aremoreconcentratedthanextracellularfluid,whichallowsmovementoffluidfromcellsintothebloodstream,causingcellstoshrink•
Osmolalitygreaterthan340mOsm/kg•
Examplesincludedextrose5%inhalf-normalsalinesolution,3%sodiumchloridesolution,anddextrose10%innormalsalinesolution•
Maynotbetoleratedbythosewithcardiacorrenaldisease•
Maycausefluidoverloadandpulmonaryedema•
Shouldnotbeusedinpatientsatriskforcellulardehydration,suchasthosewithDKA
Colloids•
Actasplasmaexpanders•
Arealwayshypertonic,pullingfluidfromcellsintothebloodstream•
Examples:albumin,plasmaproteinfraction,dextran,andhetastarch•
Requireclosemonitoringforsignsandsymptomsofhypervolemia,suchasincreasedbloodpressure,dyspnea,andboundingpulse
Deliverymethods•
MethodsincludeperipheralandcentralI.V.therapy•
Choicebasedonpurposeanddurationoftherapy;patient’sdiagnosis,age,andhealthhistory;conditionoftheveins•
Cathetersandtubingsareselectedaccordingtotypeoftherapyandsiteused
ComplicationsofI.V.therapy•
Infiltration:leakageoffluidfromveinintosurroundingtissuewhenaccessdevicedislodgesfromthevein•
Infection:mayoccurattheinsertionsite;requiresmonitoringforpurulentdrainage,tenderness,erythema,warmth,orhardnessatthesite•
Phlebitis:inflammationofthevein•
Thrombophlebitis:irritationoftheveinwithclotformation•
Extravasation:leakageoffluidintosurroundingtissues;resultswhenmedicationsseepthroughveins,producingblisteringandeventuallynecrosis•
Severedcatheter:dislodgmentofapieceofcatheterintothevein(rare)•
Allergicreaction:mayresultfromI.V.fluid,medication,catheter,orlatexportintheI.V.tubing•
Airembolism:entryofairintoavein;resultsindecreasedbloodpressure,increasedpulse,respiratorydistress,increasedICP,andlossofconsciousness•
Speedshock:toorapidinfusionofI.V.solutionsormedications;resultsinfacialflushing,irregularpulse,decreasedbloodpressure,andpossiblylossofconsciousnessandcardiacarrest•
Fluidoverload:gradualorsuddenoccurrence;producesneckveindistention,increasedbloodpressure,puffyeyelids,edema,weightgain,andrespiratorysymptoms
Quickquiz
1.Hypertonicsolutionscausefluidstomovefromthe:A.interstitialspacetotheintracellularspace.B.intracellularspacetotheextracellularspace.C.extracellularspacetotheintracellularspace.D.intracellularspacetotheinterstitialspace.
Answer:B.Hypertonicsolutions,becauseoftheirincreasedosmolality,drawfluidsoutofthecellsandintotheextracellularspace.
2.Hypotonicfluidsshouldn’tbeusedforapatientwith:A.increasedICP.B.DKAwhosebloodglucoselevelis200mg/dlormore.C.bloodlossasaresultoftrauma.D.waterreplacement.
Answer:A.HypotonicfluidscauseswellingofthecellsandcanfurtherincreaseICP.
3.WhichofthefollowingisasignofanallergytoI.V.tubing?A.ShortnessofbreathB.DrythroatC.Slow,boundingpulseD.Hypertension
Answer:A.Signsandsymptomsofanallergicreactionincludeshortnessofbreath,rash,anditching.
4.Yourpatientisa90-year-oldmalewithahistoryofheartfailure.Whenyoumakerounds,younoticethatanI.V.ofnormalsalinesolutionwasmistakenlygivenanhourbeforeandhasinfused600mlsincethen.Youshouldobservethispatientforsignsof:
A.septicshock.B.decreasedICP.C.circulatoryoverload.D.increasedICP.
Answer:C.Becauseofhisadvancedageandcardiaccondition,thetypeoffluidinfused,andtheinfusionrate,thepatientisatriskforcirculatoryoverload.
5.Whenahypotoniccrystalloidsolutionisinfusedintothebloodstream,itcausesthecellsto:
A.shrink.B.swell.
C.releasechloride.D.releasepotassium.
Answer:B.Hypotoniccrystalloidsarelessconcentratedthanextracellularfluids,sotheymovefromthebloodstreamintothecellandcausethecelltoexpandwithfluid.
6.Hypertonicsolutionsshouldbeusedcautiouslyinpatientswith:A.cancerorburns.B.cardiacorrenaldisease.C.respiratoryorGIdisease.D.hepaticorrenaldisease.
Answer:B.Ahypertonicsolutiondrawsfluidsfromtheintracellularspaceintothebloodstream.Patientswithcardiacorrenaldiseasemaybeunabletotoleratethatextrafluidvolume.
ScoringIfyouansweredallsixquestionscorrectly,bravo!You’veabsorbedtheinformationwell.Ifyouansweredfourorfivequestionscorrectly,excellent!Youinfusionhotshot,you!Ifyouansweredfewerthanfourquestionscorrectly,nobiggie.WithalittlemoreI.V.training,you’llbeinserting18gaugersinnotime!
ReferencesAbunnaja,S.,Cuviello,A.,&Sanchez,J.(2013).Enteralandnutritionintheperioperativeperiod:State
oftheart.Nutrients,5(2),608–623.doi:10.3390/nu5020608Akbulut,G.(2011).Newperspectivefornutritionalsupportofcancerpatients:Enteral/parenteral
nutrition.ExperimentalandTherapeuticMedicine,2(4),675–684.doi:10.3892/etm.2011.426Altun,I.(2010).Theefficacyofworkshoponbodyfluidsinhealthanddiseaseanditsimpactonnurses
training.PakistanJournalofMedicalSciences,26(2),426–429.Crawford,A.,&Harris,H.(2013).IVfluids:Whatnursesneedtoknow.Nursing2013,41(5),30–38.Earhart,A.,&McMahon,P.(2011).Vascularaccessandcontrastmedia.JournalofInfusionNursing,
34(2),97–105.Gonzales,E.(2008).Fluidresuscitationinthetraumapatient.JournalofTraumaNursing,15(3),149–
157.InfusionNursesSociety.(2011).Infusionnursingstandardsofpractice.JournalofInfusionNursing,
34(1S),S1–S110.Kuwahara,T.,Kaneda,S.,Shimono,K.,&Inoue,Y.(2013).Effectsoflipidemulsionandmultivitamins
onthegrowthofmicroorganismsinperipheralparenteralnutritionsolutions.InternationalJournalofMedicalSciences,10(9),1079–1084.doi:10.7150/ijms.6407
Lancaster,S.,Owens,A.Bryant,A.,Ramey,L.,Nicholson,J.,Gossett,K.,...Padgett,T.(2010).Emergency:Upperextremitydeepveinthrombosis.AmericanJournalofNursing,110(5),48–52.
Perlow,M.(2013).Perfusion,hypoperfusion,andischemiaprocesses:Theeffectonbodilyfunction.JournalofInfusionNursing,36(5),336–340.
Rosenthal,K.(2013).Intravenousfluids:Thewhysandwherefores.Nursing,36(7),26–27.Seres,D.,Valcarcel,M.,&Guillaume,A.(2013).Advantagesofenteralnutritionoverparenteral
nutrition.TherapeuticAdvancesinGastroenterology,6(2),157–167.doi:10.1177/1756283X12467564
Simmons,S.(2013).Takingthestingoutofanaphylaxis.NursingCriticalCare,5(3),10–16.Singh,A.,Carlin,B.,Shade,D.,&Kaplan,P.(2009).Theuseofhypertonicsalineforfluidresuscitation
insepsis:Areview.CriticalCareNursingQuarterly,32(1),10–13.
Chapter20
Totalparenteralnutrition
JustthefactsInthischapter,you’lllearn:
♦waystoidentifypatientswhocouldbenefitfromtotalparenteralnutrition(TPN)
♦thetypesofTPNcomponentsandtheirdeliverymethods
♦complicationsassociatedwithTPN
♦appropriatecareforpatientsreceivingTPN.
AlookatTPNTPNisahighlyconcentrated,hypertonicnutrientsolutionadministeredbywayofaninfusionpumpthroughalargecentralvein.Forpatientswithhighcaloricandnutritionalneedsduetoillnessorinjury,TPNprovidescrucialcalories;restoresnitrogenbalance;andreplacesessentialfluids,vitamins,electrolytes,minerals,andtraceelements(Mofidi&Kronn,2009).(SeeUnderstandingcommonTPNadditives.)
UnderstandingcommonTPNadditivesCommoncomponentsofTPNsolutions—suchasglucose,aminoacids,andotheradditives—areusedforspecificpurposes.Forinstance,glucoseprovidescaloriesformetabolism.Here’salistofothercommonadditivesandthepurposeseachserves.
Electrolytes•
Calciumpromotesdevelopmentandmaintenanceofbonesandteethandaidsinbloodclotting.•
Chlorideregulatesacid-basebalanceandmaintainsosmoticpressure.•
Magnesiumhelpsthebodyabsorbcarbohydratesandprotein.•
Phosphorusisessentialforcellenergyandcalciumbalance.•
Potassiumisneededforcellularactivityandcardiacfunction.•
Sodiumhelpscontrolwaterdistributionandmaintainsnormalfluidbalance.
Vitamins•
FolicacidisneededforDNAformationandpromotesgrowthanddevelopment.•
VitaminBcomplexhelpsthefinalabsorptionofcarbohydratesandprotein.•
VitaminChelpsinwoundhealing.•
VitaminDisessentialforbonemetabolismandmaintenanceofserumcalciumlevels.•
VitaminKhelpspreventbleedingdisorders.
Otheradditives•
Micronutrients(suchaszinc,copper,chromium,selenium,andmanganese)helpinwoundhealingandredbloodcellsynthesis.•
Aminoacidsprovidetheproteinsnecessaryfortissuerepairandimmunefunctions.•
Lipidssupporthormoneandprostaglandinsynthesisandpreventessentialfattyaciddeficiency.
TPNalsopromotestissueandwoundhealingandnormalmetabolicfunction;givesthebowelachancetoheal;reducesactivityinthegallbladder,pancreas,andsmallintestine;andisusedtoimproveapatient’sresponsetosurgery.
WhoneedsTPN?Patientswhocan’tmeettheirnutritionalneedsbyoralorenteralfeedingsmayrequireI.V.nutritionalsupplementationorTPN.Generally,thistreatmentisprescribedforanypatientwhocan’tabsorbnutrientsfromthegastrointestinal(GI)tractformorethan10days.Morespecificindicationsinclude:•debilitatingillnesseslastinglongerthan2weeks•lossof10%ormoreofpreillnessweight•serumalbuminlevelbelow3.5g/dl•excessivenitrogenlossfromawoundinfection,afistula,oranabscess•renalorhepaticfailure•nonfunctionoftheGItractlastingfor5to7days(AmericanSocietyofParenteralandEnteral
Nutrition,2014).(SeeKeyfactsaboutPPN,seepage354.)
KeyfactsaboutPPNPeripheralparenteralnutrition(PPN)isprescribedforpatientswhohaveamalfunctioningGItractandneedshort-termnutritionlastinglessthan2weeks.Itmaybeusedtoprovidepartialortotalnutritionalsupport.PPNisinfusedperipherallyinvariouscombinationsoflipid(fat)emulsionsandaminoacid–dextrosesolutions.Toensureadequatenutrition,PPNsolutionsinfinalconcentrationsoflessthanorequalto10%dextroseandlessthanorequalto5%proteinshouldn’tbeadministeredforlongerthan10daysunlessthey’resupplementedwithoralorenteralfeedings.
TPNtriggersCommonillnessesortreatmentsthatcantriggertheneedforTPNincludeinflammatoryboweldisease,ulcerativecolitis,bowelobstructionorresection,radiationenteritis,severediarrheaorvomiting,AIDS,chemotherapy,andseverepancreatitis,allofwhichhinderapatient’sabilitytoabsorbnutrients.Also,patientsmaybenefitfromTPNifthey’veundergonemajorsurgeryoriftheyhaveahighmetabolicrateresultingfromsepsis,trauma,orburnsofmorethan40%oftotalbodysurfacearea.InfantswithcongenitaloracquireddisordersmayneedTPNtopromotepropergrowthanddevelopment.TPNhaslimitedvalueforwell-nourishedpatientswithGItractsthatarehealthyorarelikelyto
resumenormalfunctionwithin10days.ThetreatmentalsomaybeinappropriateforapatientwithapoorprognosisorwhentherisksofTPNoutweighitsbenefits.
Today’sTPNtrendsThetrendoftoday’snutritionalsupplementationistotailorTPNformulastothepatient’sspecificneeds.Asaresult,standardTPNmixturesarebecominglesspopular.Nutritionalsupportteamsconsistingofnurses,doctors,pharmacists,anddietitiansassess,prescribefor,andmonitorpatientsreceivingTPN.Thesolutionsmayconsistof:•protein(essentialandnonessentialaminoacids),withvaryingtypesavailableforpatientswith
renalorliverfailure•dextrose(10%to35%concentration)•fatemulsions(20%to30%solution)•electrolytes•vitamins•traceelementmixtures.
LipidemulsionsLipidemulsionsarethickemulsionsthatsupplypatientswithbothessentialfattyacidsandcalories.Theseemulsionsassistinwoundhealing,redbloodcell(RBC)production,and
prostaglandinsynthesis.TheymaybepiggybackedwithTPN,givenalonethroughaseparateperipheralorcentralvenousline,ormixedwithaminoacidsanddextroseinonecontainer(totalnutrientadmixtures)andinfusedover24hours.
ThelimitsonlipidsLipidemulsionsshouldbegivencautiouslytopatientswithhepaticorpulmonarydisease,acutepancreatitis,anemia,oracoagulationdisorderandtopatientsatriskfordevelopingafatembolism.Theseemulsionsshouldn’tbegiventopatientswhohaveconditionsthatdisruptnormalfatmetabolism,suchaspathologichyperlipidemia,orlipidnephrosis.Also,makesureyoureportanyadversereactionstothepractitionersotheTPNregimencanbe
changedasneeded.(SeeAdversereactionstolipidemulsions.)
CAUTION!
AdversereactionstolipidemulsionsLipidemulsionscancauseimmediateadversereactionsaswellasdelayedcomplications.
Immediateorearlyadversereactionstolipidemulsions•
Backandchestpain•
Cyanosis•
Diaphoresisorflushing•
Dyspnea•
Headache•
Hypercoagulability•
Irritationatthesite•
Lethargyorsyncope
•Nauseaorvomiting•
Slightpressureovertheeyes•
Thrombocytopenia
Delayedcomplicationsassociatedwithprolongedadministration•
Blooddyscrasias•
Fattyliversyndrome•
Hepatomegaly•
Jaundice•
Splenomegaly
HowtoinfuseTPNTPNmustbeinfusedthroughacentralvein.Asahypertonicsolution,itmaybeuptosixtimestheconcentrationofbloodand,therefore,tooirritatingforaperipheralvein.TPNmaybeinfusedaroundtheclockorforpartoftheday—forinstance,asthepatientsleeps
atnight.Asterilecathetermadeofpolyurethaneorsiliconeisinsertedintothesubclavianorjugularvein.Apolyurethanecatheterisrigidduringinsertionbutsoftensatbodytemperature.It’sbiocompatible,sotissuesdon’treacttothematerialandit’slessthrombogenicthanearliertypesofmanufacturedcatheters.ASilasticcathetermaybeabetteralternativefortherapylastingmonthsoryearsbecauseit’smoreflexibleanddurableandit’scompatiblewithmanymedicationsandsolutions.
LookingtotheperipheralAperipherallyinsertedcentralcatheter,avariationofcentralvenoustherapy,canbeusedfortherapylasting3monthsormore.Thecatheterisinsertedthroughthebasilicorcephalicveinandthreadedsothatthetipliesinthesuperiorvenacava.Thepatientgenerallyexperienceslessdiscomfortwithaperipheralcatheter,especiallyifhe
canmovearoundeasily.Movementstimulatesbloodflowanddecreasestheriskofphlebitis.Peripherallyinsertedcentralcathetersareoftenusedforintermediate-termtherapy,bothathomeandinthehealthcarefacility.
WhattolookforSignsandsymptomsofelectrolyteimbalancescausedbyTPNadministrationincludeabdominalcramps,lethargy,confusion,malaise,muscleweakness,tetany,convulsions,andcardiacarrhythmias.Acid-baseimbalancescanalsooccurasaresultofthepatient’sconditionortheTPNcontent.Lookfortheseothercomplications:•heartfailureorpulmonaryedemafromfluidandelectrolyteadministration,conditionsthatcan
leadtotachycardia,lethargy,confusion,weakness,andlaboredbreathing•hyperglycemiafromdextroseinfusingtooquickly,aconditionthatmayrequireanadjustmentin
thepatient’sinsulindosage•adversereactionstomedicationsaddedtoTPN—forexample,addedinsulincancause
hypoglycemia,whichcanresultinconfusion,restlessness,lethargy,pallor,andtachycardia•catheter-relatedinfectionsandcatheterocclusion.
HowyouinterveneConstantassessmentandrapidinterventionarecriticalforpatientsreceivingTPN.WhencaringforapatientreceivingTPN,you’llwanttotaketheseactions:•CarefullymonitorpatientsreceivingTPNtodetectearlysignsofcomplications,suchas
infection,metabolicproblems,heartfailure,pulmonaryedema,orallergicreactions.AdjusttheTPNregimenasneeded.(SeeTeachingaboutTPN.)
Teachingpoints
Teachingpoints
TeachingaboutTPNWhenteachingapatientaboutTPN,besuretocoverthefollowingtopicsandthenevaluateyourpatient’slearning:•
basicsofTPNanditsspecificuse•
adversereactionsorcathetercomplicationsandwhentoreportthem•
basiccareofaTPNline•
maintenanceofequipment•
weight,caloriecount,intakeandoutput,andglucoselevelmonitoring.
•Assessthepatient’snutritionalstatus,andweighthepatientatthesametimeeachmorninginsimilarclothing,afterhevoids,andonthesamescale.Weightindicatesnutritionalprogressandalsodeterminesfluidoverload.Patientsideallyshouldgain1to2lb(0.5to1kg)/week.Weightgaingreaterthan1lb(0.5kg)/dayindicatesfluidretention.
•Assessthepatientforperipheralandpulmonaryedema.Edemaisasignoffluidoverload.
Thesugarsituation•Monitorserumglucoselevelsevery6hoursinitially,thenonceaday.Watchforthirstand
polyuria,whichareindicationsthatthepatientmayhavehyperglycemia.Periodically,confirmglucometerreadingswithlaboratorytestresults.Serumglucoselevelsshouldbelessthan200mg/dl.Thisindicatesthepatient’stoleranceoftheglucosesolution.
•Monitorforsignsandsymptomsofglucosemetabolismdisturbance,fluidandelectrolyteimbalances,andnutritionalproblems.SomepatientsmayrequireinsulinaddeddirectlytotheTPNforthedurationoftreatment.
•Monitorelectrolytelevelsdailyatfirstandthentwiceaweek.Keepinmindthatwhenapatientisseverelymalnourished,startingTPNmaysparkrefeedingsyndrome,whichincludesarapiddropinpotassium,magnesium,andphosphoruslevels.Toavoidcompromisingcardiacfunction,initiatefeedingslowlyandmonitorthepatient’selectrolytelevelscloselyuntiltheystabilize.
•Monitorproteinlevelstwiceaweek.Albuminlevelsmaydropinitiallyastreatmentrestoreshydration.
•Checkrenalfunctionbymonitoringbloodureanitrogen(BUN)andcreatininelevels;increasesmayindicateexcessaminoacidintake.
•Assessnitrogenbalancewith24-hoururinecollection.•Assessliverfunctionwithliverfunctiontests,bilirubin,triglyceride,andcholesterollevels.
Abnormalvaluesmayindicateintolerance.•Reviewthepatient’sserumchemistryandnutritionalstudies,andalertthepractitionerof
abnormalresults,whichmayindicatethattheTPNfluidconcentrationoringredientsmayneedtobeadjustedtomeetthepatient’sspecificneeds.
•AvoidanadversereactionbystartingTPNslowly—usually60to80ml/hourforthefirst24hours—andincreasinggradually.Continuallymonitorthepatient’scardiacandrespiratorystatus.
•Useaninfusionpumpforratecontrol.
Memoryjogger
TorememberhowtoavoidthecomplicationofrefeedingsyndromewhengivingTPNtoaseverelymalnourishedpatient,think“Startlowandgoslow.”
TPNtechnique•Usea1.2-micronfilterwhenadministeringTPNcontaininganI.V.fatemulsion(IVFE).Usea
0.2-micronfilterwhenadministeringaTPNsolutionthatdoesn’tcontainanIVFE.•RemovetheTPNsolutionfromtherefrigerator1hourbeforeadministeringitsothatitcan
warmtoroomtemperature.•ExaminetheTPNsolutionbeforeadministration.Itshouldbeclearorpaleyellowif
multivitaminsareaddedtothesolution.Ifyouseeparticulatematter,cloudiness,oranoilylayerinthebagwhenpreparingtohangaTPNsolution,returnthebagtothepharmacy.
•Flushcentrallinesaccordingtoprotocol.•Ifusingasingle-lumencentralvenousline,don’tusethelineforbloodorbloodproductsorto
giveabolusinjection,administersimultaneousI.V.solutions,measurethecentralvenouspressure,ordrawbloodforlaboratorytests.
•NeveraddmedicationstoaTPNsolutioncontaineronceit’sactivelyinfusing.•Don’tuseadd-ondevicessuchasathree-waystopcockunlessabsolutelynecessary;they
increasetheriskofinfection.•InfuseordiscardanyTPNsolutionwithin24hoursoncetheadministrationsetisattached.If
thenextTPNinfusionisnotavailablewhentheinfusioniscompleted,provide10%dextrosesolutionuntilthenextTPNinfusionisavailable.
•Performsitecareanddressingchangesatleastthreetimesaweek(onceaweekfortransparent
semipermeabledressings),orwheneverthedressingbecomeswet,soiled,ornonocclusive.Usestrictaseptictechnique.
•Monitorthepatientforsignsofinflammationandinfection,anddocumentanythingyoufind.TPNprovidestheperfectmediumformicrobialgrowth(bothlocalandsystemic).
•ChangetheI.V.administrationsetaccordingtofacilitypolicy,andalwaysuseaseptictechnique.ChangesofI.V.administrationsetsareusuallydoneevery24to72hours,dependingonthetypeofsolution.
TimingouttheTPN•Recordvitalsignsatleastevery4hours.Temperatureelevationisoneoftheearliestsignsof
catheter-relatedsepsis.•Provideemotionalsupport,especiallyifeatingisrestrictedbecauseofthepatient’scondition.•Providefrequentmouthcare.•WhileweaningthepatientfromTPN,documenthisdietaryintakeandtotalcalorieandprotein
intake.Usepercentageswhenrecordingfoodintake.Forinstance,chartthat,“Thepatientate50%ofabakedpotato,”ratherthan“Thepatienthadagoodappetite.”
•WhendiscontinuingTPN,decreasetheinfusionslowly,dependingoncurrentglucoseintake.Slowlydecreasingtheinfusionminimizestheriskofhyperinsulinemiaandresultinghypoglycemia.Weaningusuallytakesplaceover24to48hoursbutcanbecompletedin4to6hoursifthepatientreceivessufficientoralorI.V.carbohydrates.
•Promptlyreportanyadversereactionstothepractitioner.•Prepareyourpatientforhomecare.•Accuratelydocumentallaspectsofcare,accordingtofacilitypolicy.(SeeDocumentingTPN.)
Chartsmart
DocumentingTPNIfyourpatientisreceivingTPN,makesureyoudocumentthefollowinginformation:•
adversereactionsorcathetercomplications•
signsofinflammationorinfectionattheI.V.site•
nursinginterventions(includinginfusionrate)andthepatient’sresponse•
timeanddateofadministrationsetchanges•
specificdietaryintake•
patientteaching
That’sawrap!
Totalparenteralnutritionreview
Totalparenteralnutrition•
Highlyconcentrated,hypertonicnutrientsolutionusedforpatientswithhighcaloricandnutritionalneedsduetoillnessorinjury•
Providescrucialcalories;restoresnitrogenbalance;andreplacesessentialfluids,vitamins,electrolytes,minerals,andtraceelements•
Promotestissueandwoundhealingandnormalmetabolicfunction;givesthebowelachancetoheal;reducesactivityinthegallbladder,pancreas,andsmallintestine;andimprovesapatient’sresponsetosurgery
•Usedinpatientswhocan’tmeettheirnutritionalneedsbyoralorenteralfeedings,includingthosewithinflammatoryboweldisease,ulcerativecolitis,bowelobstructionorresection,radiationenteritis,severediarrheaorvomiting,AIDS,chemotherapy,andseverepancreatitis•
Typicallyhaslimitedvalueinwell-nourishedpatientswithGItractsthatarehealthyorarelikelytoresumenormalfunctionwithin10days•
Mustbeinfusedthroughacentralvein
CommonTPNadditivesElectrolytes•
Calcium:promotesdevelopmentandmaintenanceofbonesandteethandaidsinbloodclotting•
Chloride:regulatesacid-basebalanceandmaintainsosmoticpressure•
Magnesium:helpsthebodyabsorbcarbohydratesandprotein•
Phosphorus:essentialforcellenergyandcalciumbalance•
Sodium:helpscontrolwaterdistributionandmaintainsnormalfluidbalance(NationalInstitutesofHealth,2014)
Vitamins•
Folicacid:helpswithDNAformationandpromotesgrowthanddevelopment•
VitaminBcomplex:helpsthefinalabsorptionofcarbohydratesandprotein•
VitaminC:helpsinwoundhealing•
VitaminD:essentialforbonemetabolismandmaintenanceofserumcalciumlevels•
VitaminK:helpspreventbleedingdisorders(NationalInstitutesofHealth,2014)
Otheradditives•
Micronutrients(zinc,copper,chromium,selenium,manganese):helpinwoundhealingandRBCsynthesis•
Aminoacids:providetheproteinsnecessaryfortissuerepairandimmunefunctions
•Lipids:supporthormoneandprostaglandinsynthesis;preventessentialfattyaciddeficiency(NationalInstitutesofHealth,2014)
Lipidemulsions•
Thickpreparationsthatsupplypatientswithessentialfattyacidsandcalories•
Assistinwoundhealing,RBCproduction,andprostaglandinsynthesis•
MaybepiggybackedwithTPN•
Shouldbeusedcautiouslyinpatientswithhepaticorpulmonarydisease,acutepancreatitis,anemia,oracoagulationdisorderandinpatientsatriskfordevelopingafatembolism•
Shouldbeavoidedinpatientswithpathologichyperlipidemiaorlipidnephrosis(NationalInstitutesofHealth,2014)
TPNcomplications•
Electrolyteimbalances•
Acid-baseimbalances•
Heartfailureorpulmonaryedema•
Hyperglycemia•
Reboundhypoglycemia•
Refeedingsyndrome(inseverelymalnourishedpatients),whichincludesarapiddropinpotassium,magnesium,andphosphoruslevels
Monitoring•
Assessnutritionalstatusanddailyweight.•
Assessforedema,asignoffluidoverload.•
Monitorserumglucoselevelevery6hoursinitially,thenoncedaily.•
Monitorelectrolytelevelsdailyatfirst,thentwiceweekly.
•Monitorproteinlevelstwiceweekly.•
MonitorBUNandcreatininelevels,liverfunctiontests,andnitrogenbalance.
Quickquiz
1.WhenaseverelymalnourishedpatientstartsreceivingTPN,hislaboratorytestsshowarapiddropinpotassium,magnesium,andphosphoruslevels.Thefindingsindicatewhichofthefollowingconditions?
A.FluidshockB.HypervolemiaC.HypovolemiaD.Refeedingsyndrome
Answer:D.Thesefindingsaresignsofrefeedingsyndrome.
2.WhenpreparingtohangaTPNsolution,youseeanoilylayerinthebag.Youshould:A.gentlyagitatethesolutiontodispersethecontents.B.hangthesolution;theoilylayerwilldisperseintime.C.returnthesolutiontothepharmacy.D.squeezethebagtomixthesolution.
Answer:C.Thesolutionshouldbeclearorpaleyellow.Anoilylayerindicatesthatthefluidmayhavebeencontaminatedorimproperlypreparedanditshouldbereturnedtothepharmacy.
3.SitecareanddressingchangesforapatientwithTPNshouldbeperformedatleast:A.onceaweek.B.everyotherweek.C.everyday.D.threetimesaweek.
Answer:D.It’srecommendedthatsitecareanddressingchangesbeperformedthreetimesaweek;however,thepatient’sconditionorfacilitypolicymaydictatetheneedformorefrequentcare.
4.Infusionsoflipidemulsionsareusefulforpromoting:A.woundhealing.B.coagulationinbleedingdisorders.C.areductionininflammationfrompancreatitis.
D.decreasedhemoglobinlevelandhematocritinanemia.Answer:A.Lipidemulsionsassistinwoundhealing,intheproductionofRBCs,andinprostaglandinsynthesis.Theyshouldbeavoidedinpatientswithacutepancreatitisoracoagulationdisorderandusedcautiouslyinpatientswithacutepancreatitis.
ScoringIfyouansweredallfourquestionscorrectly,totallycool!Yourdailynutritionalintakemustincludeplentyofbrainfood!Ifyouansweredthreequestionscorrectly,youshouldstillbepumpedup!YourTPNknowledgeistop10!Ifyouansweredfewerthanthreequestionscorrectly,letmegiveyousome“parenteral”advice:Getyourenergyupandreviewthechapter!
ReferencesAmericanSocietyofParenteralandEnteralNutrition.(2014).Whatisparenteralnutrition?Retrieved
fromhttp://www.nutritioncare.org/wcontent.aspx?id=270Mofidi,S.,&Kronn,D.(2009).Emergencymanagementofinheritedmetabolicdisorders.Topicsin
ClinicalNutrition,24(4),374–384.NationalInstitutesofHealth.(2014).Totalparenteralnutrition.Retrievedfrom
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a601166.html
Appendicesandindex
Commonfluidandelectrolyteimbalancesinpediatricpatients
Commonfluidandelectrolyteimbalancesinelderlypatients
Transfusingbloodandselectedcomponents
Practicemakesperfect
Glossary
Selectedreferences
Index
Commonfluidandelectrolyteimbalancesinpediatricpatients
Commonfluidandelectrolyteimbalancesinelderlypatients
Transfusingbloodandselectedcomponents
Practicemakesperfect
1.Aconstructionworkerlaborsoutsidein90°F(32.2°C)temperatures.Whathormonewillhisbodyreleaseinlargerquantitiestohelphimretainwater?
A.InsulinB.AntidiuretichormoneC.ReninD.Cortisol
2.ApostoperativepatientisorderedanI.V.solutionofdextrose5%innormalsalinesolution.Whattypeoffluidisthissolution?
A.HypertonicB.HypotonicC.IsotonicD.Colloid
3.You’reteachingagroupofathleteshowtopreventexcessivefluidloss.Youshouldtellthemtoconsumefluidswhenthey:
A.experiencedrymouth.B.feellight-headedordizzy.C.arethirsty.D.sweat.
4.ApatientwithhyponatremiacausedbydiabetesinsipidusrequiresI.V.fluidreplacement.WhichI.V.fluidwouldprovidethegreatestconcentrationofsodiumreplacementifthepatientweretodevelopasubnormalserumsodiumlevel?
A.Dextrose5%inwaterB.Half-normalsalinesolutionC.Ringer’ssolutionD.Dextrose5%inlactatedRinger’ssolution
5.A29-year-oldpatientcomestotheemergencydepartmentafterbeinginvolvedinamotorvehicleaccident.Chestradiographyrevealsarightpneumothorax.Youexpecthisarterialbloodgasresultstoreflectwhichofthefollowing?
A.HispHislow,PaCO2ishigh,andbicarbonateisnormal.B.HispHislow,PaCO2islow,andbicarbonateislow.C.HispHislow,PaCO2ishigh,andbicarbonateislow.D.HispHishigh,PaCO2islow,andbicarbonateislow.
6.Apatientistransferredtotheintensivecareunitinsepticshock.Arterialbloodgasresultsshowthatthepatientisacidotic.Youexpecttheaniongaptobe:
A.0to4mEq/L.B.4to8mEq/L.C.8to14mEq/L.D.greaterthan14mEq/L.
7.Apatientwhosustainedmultipleabdominalinjuriesinamotorvehicleaccident2daysagobecomeshypotensive.Hisurineoutputforthepast4hourstotals45ml.Thedoctordecidestoinsertapulmonaryartery(PA)catheter.DuringmeasurementofPApressures,whatspecificinformationisbeingobtainedwhentheballooniswedgedinabranchofthePA?
A.Left-sidedheartfunctionB.CentralvenouspressureC.CardiacoutputD.Right-sidedheartfunction
8.ApatientwithAlzheimer’sdiseaseisadmittedwithsuspecteddehydrationafterherdaughterreportsthatthepatienthasrefusedtodrinkanythingforthepast3days.Thedoctorordersseverallaboratorytests.Whichlaboratorytestresultismostexpectedwithdehydration?
A.Urinespecificgravityof1.005B.Serumsodiumlevelof150mEq/LC.Hematocritof38%D.Serumcreatininelevelof0.8to1.5mg/dl
9.A53-year-oldhomelesspersonisadmittedwithdehydration.WhichtypeofI.V.fluidshouldbeavoidedwhentreatingthispatient?
A.IsotonicfluidB.ColloidfluidC.HypotonicfluidD.Hypertonicfluid
10.A78-year-oldpatientisadmittedwithpulmonaryedema.ThepatientisgivenI.V.morphine.Why?
A.TolowerhisbloodpressureB.TopromotediuresisC.ToslowhisbreathingD.Toremovefluidfromhislungs
11.Apatientdiagnosedwithlungcancerdevelopssyndromeofinappropriateantidiuretichormone,whichputshimatriskforhyponatremia.Whichserumsodiumlevelindicateshyponatremia?
A.128mEq/LB.135mEq/LC.142mEq/LD.150mEq/L
12.Whilebeingtreatedforhyponatremia,apatientdevelopsiatrogenichypernatremia.Whichtreatmentisappropriateforresolvingthisproblem?
A.FluidrestrictionB.HypotonicfluidadministrationC.HypertonicfluidadministrationD.Diuretictherapy
13.A35-year-oldmanwithahistoryoffoodpoisoningandsubsequentvomitingcomplainsofweakness,palpitations,abdominalpain,andcramping.Hisbodytemperatureis99.6°F(37.6°C).Electrocardiogramresultsshowirregularities.Whichimbalanceishemostlikelytohave?
A.HypervolemiaB.HypokalemiaC.AcidosisD.Hyperchloremia
14.A65-year-oldpatientreceivesdailydosesoffurosemide(Lasix)anddigoxin(Lanoxin)fortreatmentofheartfailure.Hisserumpotassiumlevelis3.1mEq/L.Whichassociatedelectrocardiogram(ECG)changeswouldyouexpect?
A.PeakedTwaveB.DepressedSTsegmentC.NarrowQRScomplexesD.AbsentPwaves
15.Aspartofapatient’streatmentforhypokalemia,thedoctorprescribesI.V.potassiumsupplementation.Atwhichrateshoulditbeadministered?
A.5mEq/hourB.10mEq/hourC.15mEq/hourD.20mEq/hour
16.Apatientwithahistoryofsystemiclupuserythematosusdevelopshyperkalemia.Thedoctorprescribessodiumpolystyrenesulfonate(Kayexalate)toreducethepatient’sserumpotassiumlevel.Thisdrugworksby:
A.forcingpotassiumintothecells.B.promotingrenalexcretionofpotassium.C.pullingpotassiumoutofthebowelforexcretion.D.pullingpotassiumintothebowelforexcretion.
17.A28-year-oldpatientisseenintheobstetricsclinicwithabloodpressureof220/130mmHgandabnormalreflexes.Thenurse-midwifecaringforhersuspectspreeclampsia.Aurinalysisforproteinisorderedimmediately,andproteinuriaisdetected.Thepatientistransportedtotheobstetricunitinthemedicalcenter.Onadmission,thenurseassessesthepatient’sdeeptendonreflexesas4+.Thisvaluemeansthereflexesare:
A.normalandactive.B.presentbutdiminished.C.slowtorespond.D.hyperactive.
18.Whichinterventionismostappropriateforthepatientreceivingacontinuousmagnesiumsulfateinfusion?
A.Insertanindwellingurinarycatheter.B.Attachthepatienttoacontinuouscardiacmonitor.C.Administercalciumgluconateevery4hours.D.Performneurologicchecksevery2hours.
19.Whichfindingsuggeststhatapatienthasreceivedtoomuchmagnesiumsulfate?A.MuscleweaknessB.TetanyC.TachycardiaD.Hyperreflexia
20.Apatientdevelopshypermagnesemia.Whichinterventionismosteffectiveinreducingserummagnesiumlevels?
A.Administeracation-exchangeresin.B.Infuseabolusofcalciumgluconate.C.IncreasethevolumeofI.V.andoralfluids.D.Administerantidiuretichormone.
21.A36-year-oldwomanwithahistoryofhyperthyroidismhasundergoneatotalthyroidectomy.Aftersurgery,sheexperienceshypotension,irritability,andcircumoralparesthesia.Hersurgicalwoundhaswell-approximatedborders,nobleeding,andminimalswelling.Herspeechandbreathingareunimpaired.Basedonthepatient’ssignsandsymptoms,herserumcalciumlevelislikelytobe:
A.greaterthan10.1mg/dl.B.10mg/dl.C.9mg/dl.D.8mg/dl.
22.A35-year-oldpatientwithahistoryofalcoholabuseisadmittedwithacutepancreatitis.Hiscalciumlevelonadmissionis7.6mg/dl.Whichfindingalsosuggests
hypocalcemia?A.ProlongedSTsegmentonanelectrocardiogram(ECG)B.ConstipationC.FlaccidreflexesD.Increasedcardiacoutput
23.Apatientwithacutehypocalcemiadevelopstorsadesdepointes.Whichdrugismostcommonlygiventotreatacutehypocalcemia?
A.CalciumcarbonateB.CalciumgluconateC.CalciumchlorideD.Calcitonin
24.Youneedtoprepareacalciuminfusionforapatientwithhypocalcemia.Youshouldmixthedruginwhichsolution?
A.NormalsalinesolutionB.Dextrose5%inwaterC.Half-normalsalinesolutionD.Dextrose5%inhalf-normalsalinesolution
25.Apublichealthnurseinahomelessshelterassessesa57-year-oldmanwithchronicalcoholism.Hehasaproductivecoughandalow-gradefever.He’s5′100(1.8m)andweighs135lb(61.2kg).Thenurse’snutritionalassessmentrevealshe’smalnourished.Thepatientisadmittedtoarespiratoryisolationroominacommunityhospitalbecausetuberculosisissuspected.Basedonhishistoryofalcoholabuse,youexpecthisserumphosphorousleveltobe:
A.belownormal.B.abovenormal.C.inthenormalrange.D.unaffected.
26.Apatient’sphosphorusleveliselevated.Whichofthefollowingelectrolytesshouldyouexpecttobedecreased?
A.CalciumB.PotassiumC.SodiumD.Magnesium
27.You’reteachingapatientwithhypophosphatemiaabouttheimportanceofconsumingphosphorus-richfoods.Youshouldrecommend:
A.pumpkin.B.cranberries.C.trout.
D.greenbeans.
28.A10-year-oldgirlwhorecentlyreturnedfromtravelingabroadcomplainsthatshe’sexperiencedfrequentepisodesofdiarrheaandweaknessforthelast3days.She’sdiagnosedwithgastroenteritis.Hertemperatureis102.4°F(39.1°C),herpulsesareweak,andherbloodpressureis76/40mmHg.Shehaspoorskinturgor,lowurineoutput,anddrymucousmembranes.Serumlaboratorystudiesrevealthechild’schlorideleveltobe88mEq/L.Thedirectcauseofthechild’shypochloremiaismostlikely:
A.fever.B.lowurineoutput.C.diarrhea.D.drymucousmembranes.
29.A39-year-oldpatientisadmittedwithseverevomitingandabdominalpain.Hisadmissionlaboratoryfindingsrevealhypochloremia.Whichotherelectrolytewouldyouexpecttobedeficient?
A.CalciumB.SodiumC.MagnesiumD.Phosphorus
30.A62-year-oldpatientwhounderwentapartialgastrectomy2daysagodevelopshypochloremia.Thisplacesthepatientatriskfor:
A.respiratoryacidosis.B.respiratoryalkalosis.C.metabolicacidosis.D.metabolicalkalosis.
31.A16-year-oldmalewitharecenthistoryofweightloss,increasedappetite,andurinaryfrequencyisseenintheclinic.Hecomplainsofweaknessandsyncope.Oninitialobservation,thenursenotesthathisskinandmucousmembranesaredryandthathiseyeballsappearsunken.Theteen’smotherreportsthathegetsupalotatnighttogotothebathroom.Hiscapillarybloodglucosemeasurementis480mg/dl.Whichacid-baseimbalanceshouldyoususpect?
A.MetabolicacidosisB.MetabolicalkalosisC.RespiratoryacidosisD.Respiratoryalkalosis
32.A23-year-oldpatientisadmittedwithdiabeticketoacidosis.Whichvaluefromthearterialbloodgasanalysissupportsthediagnosis?
A.pH:7.48
B.PaCO2:48mmHgC.Bicarbonate:28mEq/LD.Aniongap:17mEq/L
33.You’recaringfora33-year-oldpatientwhodevelopedGuillain-Barrésyndrome1weekaftercontractinganupperrespiratoryinfection.Thisplacesthepatientatriskforwhichacid-baseimbalance?
A.MetabolicacidosisB.MetabolicalkalosisC.RespiratoryacidosisD.Respiratoryalkalosis
34.Apatientwithahistoryofheartfailurecallsyoutoherroombecauseshe’sshortofbreath.Youassessherandfindthatherheartfailureisworsening.Whichtypeoffluidvolumeexcessisthepatientexperiencingbecauseofherheartfailure?
A.IntravascularB.ExtracellularC.IntracellularD.Interstitial
35.A27-year-oldwomaninher38thweekofpregnancyisadmittedtotheobstetricunitafterherbagofwaterbrokeathome.Youperformavaginalexaminationandnotethathercervixis6cmdilated.Youattachthefetalmonitorandfindthatthefetalheartrateisnormal.Asherlaborprogresses,shehyperventilates.Whichacid-baseimbalanceisshemostlikelytoexperienceifshecontinuestohyperventilate?
A.MetabolicacidosisB.MetabolicalkalosisC.RespiratoryacidosisD.Respiratoryalkalosis
36.A58-year-oldmancallsforemergencymedicalservicesfromhishomeafterheexperiencesexcruciatingsubsternalchestpain.He’srushedtotheemergencydepartmentwherehe’sgivennitroglycerinandmorphineforthepain.Electrocardiogramresultsshowchangesconsistentwithanacuteanteriorwallmyocardialinfarction(MI).AmaincomplicationofananteriorwallMIisheartfailure.Whichchamberoftheheartismostlikelytofailinthispatient?
A.RightatriumB.RightventricleC.LeftatriumD.Leftventricle
37.A74-year-oldmanwitha3-dayhistoryofworseningchronicobstructivepulmonarydiseaseishospitalized.Hisbreathingislabored,breathsoundsarecongestedwithrhonchithroughout,andhisSaO2(asmeasuredbypulseoximetry)is89%.He’splacedona35%aerosolmask,andbloodisdrawnforarterialbloodgasanalysis.TheresultsarepH,7.33;PaO2,68mmHg;PaCO2,53mmHg;andbicarbonate,18mEq/L.Whichacid-baseimbalancedoesthepatientmostlikelyhave?
A.MetabolicacidosisB.MetabolicalkalosisC.RespiratoryacidosisD.Respiratoryalkalosis
38.You’recaringfora54-year-oldpatientwhohassmokedtwopacksofcigarettesperdayforthepast35years.He’sbeenadmittedwithworseningchronicobstructivepulmonarydisease(COPD).Whyisitimportantforsupplementaloxygentobecarefullymonitoredinthispatient?
A.IncreasingthePaO2beyondwhat’sneededwillleadtooxygentoxicity.B.Highoxygenlevelswillpromotemicrobialgrowthinthepatient’slungs.C.IncreasedPaO2levelscandepressthedrivetobreatheinpatientswithCOPD.D.IncreasedPaO2levelscanelevatethedrivetobreatheinpatientswithCOPD.
39.Apatientreturnedfromthepostanesthesiacareunitwithanasogastric(NG)tubeinplace.Thedoctor’sorderstatesirrigateNGtubeq4h.Whichsolutionisthebestirrigant?
A.SalinesolutionB.DistilledwaterC.TapwaterD.Sterilewater
40.A66-year-oldwomanwhosurvivedacardiacarrestwasadmittedtotheintensivecareunit.Sheexperiencedaprolongedepisodeofhypotensionandisnowinacuterenalfailure.Frequentelectrolytelevelsareordered.Hemodialysisisscheduledtobeginwithin24hours.Whichtypeofrenalfailuredidthepatientexperience?
A.IntrarenalB.PrerenalC.PostrenalD.Renal
41.Apatientwithahistoryofhypertensiondevelopschronicrenalfailure.Whatshouldyouexpecttheglomerularfiltrationrate(GFR)tobe?
A.10to20ml/minuteB.20to40ml/minuteC.40to60ml/minuteD.Greaterthan60ml/minute
42.Apatientwhosustainedmassiveinternalinjuriesinamotorvehicleaccidentbecomeshypotensiveanddevelopsacuterenalfailure.Whichacid-baseimbalanceisthispatientmostlikelytoexperience?
A.RespiratoryacidosisB.RespiratoryalkalosisC.MetabolicacidosisD.Metabolicalkalosis
43.Apatientreceivedburninjuries48hoursago.He’senteringthesecondphaseofburninjury.Whatphysiologicchangescanbeexpected?
A.EdemadevelopmentB.IncreasedbloodvolumeC.DecreasedhemoglobinlevelD.Profuseurination
44.Afiremansustainsburnswhilefightinganapartmentfire.HereceivesfluidresuscitationusingtheParklandformula.Whichtypeoffluidisused?
A.NormalsalinesolutionB.Half-normalsalinesolutionC.LactatedRinger’ssolutionD.Dextrose5%inlactatedRinger’ssolution
45.A42-year-oldmanwithend-stageAIDShasfrequentepisodesofwaterystool.He’snauseatedandrefusestodrinkfluids.Hisbodytemperatureis102°F(38.9°C),hisbloodpressureis88/52mmHg,andhispulseis112beats/minute.Normalsalinesolutionisinfusingat150ml/hourthroughalarge-boreI.V.catheter.Whichtypeoffluidisnormalsalinesolution?
A.IsotonicB.HypotonicC.HypertonicD.Colloid
46.Apatient’sbloodvolumedoesn’timproveaftertheadministrationofcrystalloids.Thedoctorprescribesacolloidforthispatient.Whichofthefollowingsolutionsisacolloid?
A.Dextrose5%inhalf-normalsalinesolutionB.HetastarchC.Dextrose10%inwaterD.Dextrose5%inlactatedRinger’ssolution
47.An18-year-oldpatientwithCrohn’sdiseaseisunabletotolerateanelementaldiet.Totalparenteralnutrition(TPN)isindicatedwhenthepatient’sserumalbuminislessthan:
A.5g/dl.B.4.5g/dl.C.4g/dl.D.3.5g/dl.
48.Apatientreceivingtotalparenteralnutrition(TPN)requiresatransfusionofpackedredbloodcells.Beforeyoubeginthetransfusion,youshould:
A.infusetheblooddirectlyintotheTPNline.B.startaseparateI.V.lineforthebloodtransfusion.C.stoptheTPN,infusethebloodattheTPNsite,andthenrestarttheTPN.D.useaYconnectorandinfusethebloodsimultaneouslywiththeTPN.
49.Apatient’spostoperativehemoglobinlevelis7.9g/dl.Thedoctororders2unitsofpackedredbloodcells(RBCs)forthepatient.Bywhatpercentageshouldthisincreasethepatient’shematocrit?
A.3%B.6%C.9%D.12%
50.Apatientexperiencesatransfusionreaction15minutesafteryoubeginabloodtransfusion.Youcollecttheappropriatelaboratoryspecimens.Laboratoryresultsrevealhemoglobinuria.Whichtypeofreactionhasthepatientmostlikelyexperienced?
A.HemolyticB.FebrileC.AllergicD.Vasogenic
51.You’recaringforapatientwithadecreasedcalciumlevelof7.4mg/dl.Which
treatmentwouldyouexpecttoprovide?(Selectallthatapply.)A.I.V.calciumgluconateorI.V.calciumchlorideB.LoopdiureticsC.MagnesiumsupplementsD.VitaminDE.NormalsalinesolutionF.Hemodialysisorperitonealdialysis
52.You’recaringforapatientwithasuspectedoverdoseofmagnesium-containingantacidsandlaxatives.Onadmission,herlaboratoryvaluesformagnesiumweregreaterthan3mg/dl.Whichsignsandsymptomswouldyouexpecttosee?(Selectallthatapply.)
A.FlushingB.HypertensionC.HypotensionD.SeizuresE.NauseaandvomitingF.Bradycardia
53.Anewlyadmittedpatientisbeingtreatedforacutepancreatitis.Whichelectrolytedisordermaybenoted?
A.HypokalemiaB.HypercalcemiaC.HypermagnesemiaD.Hypophosphatemia
54.Themajorextracellularanionis:A.potassium.B.sodium.C.chloride.D.magnesium.
55.Watercomposeswhatpercentageoftotalbodyweight,dependingontheamountoffatpresent?
A.20%to30%B.20%to40%C.30%to50%D.45%to75%
56.Apatientarrivesattheemergencydepartmentwithgastroenteritiscausedbydehydration.Theadmittingnurserecordsthatthepatienthasbeenexperiencingvomitinganddiarrheaforthepast3days.ThedoctorordersacontinuousI.V.infusion.WhichI.V.solutionisbesttoadminister?
A.Dextrose5%in0.45%salinesolution
B.Dextrose5%inlactatedRinger’ssolutionC.0.45%salinesolutionD.LactatedRinger’ssolution
57.A65-year-oldwomanisadmittedtotheemergencydepartmentaftervomitingexcessivelyathome.Aftercheckingthepatient’sarterialbloodgas(ABG)levels,thedoctordiagnosesseveredehydration.UsingtheABGresultsasguide,whichacid-baseimbalancewouldyouexpectthepatienttohave?
A.RespiratoryacidosisB.MetabolicalkalosisC.RespiratoryalkalosisD.Metabolicacidosis
58.Amalnourished55-year-oldpatientwithahistoryofalcoholabusearrivesintheemergencydepartmentcomplainingofmuscleweaknessandcramps.Electrocardiogramtracingsshowevidenceofarrhythmias,andlaboratorytestsrevealhypomagnesemia.Whichelectrolytesaretypicallydepletedwithmagnesiumdeficiency?
A.CalciumandphosphorusB.PotassiumandphosphorusC.PotassiumandchlorideD.Chlorideandcalcium
59.Thedoctororderstapwaterenemasuntilclearforapatientscheduledforacolonoscopyinthemorning.Thenurseisawarethatafterthreesuchenemas,electrolyteimbalancesarelikelytooccur.Signsofwhichimbalanceshouldcausethemostconcern?
A.HypocalcemiaB.HypercalcemiaC.HypernatremiaD.Hypokalemia
60.Electrolytesaremadeupof:A.glucose,bases,andsalts.B.lipids,acids,andbases.C.bases,acids,andsalts.D.salts,glucose,andlipids.
Answers1.B.Onewaythebodyconserveswateristoreleasemoreantidiuretichormone,whichreducesdiuresis.
2.A.Asolutionofdextrose5%innormalsalineisconsideredhypertonicbecauseitsosmolalityis560mOsm/L.
3.C.Thesimplestmechanismformaintainingfluidbalanceisthethirstmechanism.Whenanindividualsensesthirst,heshoulddrinktoreplacelostfluid.
4.C.Ringer’ssolutioncontains147mEqofsodiumperliter.Half-normalsalinesolutioncontains77mEq/L.Dextrose5%inwatercontainsnosodium.Dextrose5%inlactatedRinger’ssolutioncontains130mEq/L.
5.A.Inpatientswithrespiratoryacidosis,pHislow,PaCO2ishigh,andbicarbonateisnormal.
6.D.Patientswhoareinanacidoticstatetypicallyhavehigherthannormalamountsoforganicacids,whichleadstoanelevatedaniongap(>14mEq/L).
7.A.WhenthetipofthePAcatheteriswedgedinabranchofthepulmonaryartery,itmeasurespressuresthatreflectleft-sidedheartfunction.
8.B.Becausesomeofthewaterpresentintheserumislost,causingdehydration,theserumsodiumlevelbecomeselevated.
9.D.Dehydrationisahypertonicstate;therefore,hypertonicfluidshouldbeavoidedbecauseitwouldworsenthepatient’scondition.Freewaterorisotonicorhypotonicfluidwouldbeasaferchoice.
10.C.Morphineisgiventothepatientwithpulmonaryedemabecauseitrelievesairhungeranddilatesbloodvessels,whichinturnreducespulmonarycongestionandtheamountofbloodthatreturnstotheheart.
11.A.Normalserumsodiumlevelis135to145mEq/L.Aserumsodiumlevellessthan135mEq/Lindicateshyponatremia.
12.D.Diureticsincreasesodiumlossintheurine,therebyloweringtheserumsodiumlevel.
13.B.Conditionssuchasvomitingthatleadtolossofgastricacidscancausehypokalemiaandalkalosis.
14.B.HypokalemiacausesvariousECGchanges,includingaflattenedorinvertedTwave,adepressedSTsegment,andacharacteristicUwave.
15.B.WhensupplementalpotassiumisgivenbyI.V.infusion,itshouldbeadministeredatarateof10mEq/hour.
16.D.Sodiumpolystyrenesulfonateisacation-exchangeresinthatcausespotassiumtomoveoutofthebloodintotheintestines.It’sthenexcretedinthestool.
17.D.Deeptendonreflexesaregradedona0to4+scale.0isabsent,1+ispresentbutdiminished,2+isnormal,3+isincreasedbutnotnecessarilyabnormal,and4+ishyperactive.
18.B.Magnesiumaffectscardiacfunctionandcancausearrhythmias.Therefore,anypatientreceivingamagnesiumsulfateinfusionshouldbeoncontinuouscardiacmonitoring.
19.A.Hypermagnesemiacausesmuscleweakness.Therefore,ifapatientdevelopsmuscleweaknesswhilereceivingmagnesium,mostlikelythedoseistoogreat.
20.C.Thebestmethodofreducingserummagnesiumlevelsistoincreaseurinaryexcretionofmagnesiumbyincreasingthepatient’sfluidintake.
21.D.Hypotension,irritability,andcircumoralparesthesiaaresignsandsymptomsofhypocalcemia.Because8.9to10.1mg/dlisthenormalrangefortotalserumcalciumlevels,8mg/dlistheonlyvalueherethatindicateshypocalcemia.
22.A.Thepatientwithhypocalcemiamayexperiencediarrhea,hyperactivedeeptendonreflexes,adiminishedresponsetodigoxin(Lanoxin),decreasedcardiacoutput,prolongedSTsegmentonanECG,andalengthenedQTinterval,whichplacesthepatientatriskfortorsadesdepointes(polymorphicventriculartachycardia).
23.B.Withacutecasesofhypocalcemia,I.V.calciumgluconateisusuallygiven.Calciumchlorideisalesscommonalternative.
24.B.Whenpreparingacalciuminfusion,addcalciumtoasolutioncontainingdextrose5%inwater.Solutionscontainingnormalsalinecauserenalcalciumloss.
25.A.Patientswhoabusealcoholtypicallyhaveserumphosphorouslevelsthatfallbelownormal.
26.A.Phosphorusandcalciumhaveaninverserelationship:Whenthelevelsofoneareincreased,thelevelsoftheotheraredecreased.Nosuchrelationshipexistsbetweenphosphorusandpotassium,sodium,ormagnesium.
27.C.Fishisafoodsourcethat’srichinphosphorus,sotroutwouldbehelpfultoapatientwithhypophosphatemia.
28.C.Thechild’slowserumchloridelevelisprobablycausedbyherdiarrhea.
29.B.Chlorideisanegativelychargedionthathasanelectricalattractiontosodium.Therefore,ifchloridelevelsbecomelow,sodoserumsodiumlevels.
30.D.Tocompensateforachlorideloss(hypochloremia),thekidneysretainbicarbonate.TheaccumulationofexcessbicarbonateinextracellularfluidcanraisethearterialpHabove7.45,causingmetabolicalkalosis.
31.A.Thepatienthassignsandsymptomsoftype1diabetesmellitus.Becauseofthe
accumulationofmetabolicwastes(e.g.,ketones),type1diabetesmellitusismostcommonlyassociatedwithmetabolicacidosis.
32.D.Metabolicacidosiscausestheaniongaptobegreaterthan14mEq/L.Withmetabolicacidosis,pHwillbelessthan7.35,bicarbonatewillbelessthan22mEq/L,andPaCO2willtypicallybeunaffected.
33.C.Incertainneuromusculardiseases,suchasGuillain-Barrésyndrome,therespiratorymusclesfailtorespondproperlytotherespiratorydrive,leadingtorespiratoryacidosis.
34.B.Becausetheheartdoesn’tpumpeffectivelyinapatientwithheartfailure,fluidimbalancesdevelop.Themostcommonfluidimbalanceassociatedwithheartfailureisextracellularvolumeexcess.Thisresultsfromtheheart’sfailuretopropelbloodforward,consequentvascularpooling,andthesodiumandwaterreabsorptiontriggeredbytherenin-angiotensin-aldosteronesystem.
35.D.Whenapatienthyperventilates,excesscarbondioxideisblownoff.ThisraisesthearterialpHabove7.45causingrespiratoryalkalosis.
36.D.WithananteriorwallMI,theleftventricleusuallyfails,causingheartfailure.
37.C.Whenapatient’sPaCO2iselevated,carbonicacidisretained,leadingtoacidosis.Becausetheacidosisisrespiratoryinorigin,thepatientmostlikelyhasrespiratoryacidosis.
38.C.IncreasedPaO2candepressthepatient’sdrivetobreathe,whichislargelydrivenbyhypoxemia.
39.A.Thebestsolutionforgastricirrigationisanisotonicsolutionsuchassalinesolution.
40.B.Thepatient’srenalfailurewasduetohypotension,whichisaprerenalcause.Prerenalcausesarethoseconditionsoutsideofthekidneysthatdiminishbloodflowtothekidneys.
41.A.RenalfailureoccurswhentheGFRis10to20ml/minute.Arateof40to70ml/minuteindicatesrenalreserve;20to40ml/minute,renalinsufficiency;andlessthan10ml/minute,end-stagerenaldisease.
42.C.Asthekidneyslosetheirabilitytoexcretehydrogenions,there’sabuildupofhydrogen,whichleadstometabolicacidosis.
43.D.Thesecondphaseoftheburninjury,knownastheremobilizationphase,startsabout48hoursaftertheinitialinjury.Duringthisphase,fluidshiftsbacktothevascularcompartment.Edemaattheburnsitedecreasesandbloodflowtokidneysincreases,whichincreasesdiuresis.
44.C.TheParklandformula,whichiswidelyusedforburnresuscitation,useslactated
Ringer’ssolution.
45.A.Normalsalinesolutionisanisotoniccrystalloidfluid.
46.B.Examplesofcolloidsincludealbumin,hetastarch,dextran,andplasmaproteinfraction.
47.D.TPNistypicallyindicatedwhentheserumalbuminlevelislessthan3.5g/dl.
48.B.Bloodtransfusionsshouldn’tbeinfusedwithTPN;therefore,aseparateI.V.lineshouldbesecuredforthebloodtransfusion.
49.B.OneunitofpackedRBCswillincreasehematocritby3%;2units,by6%.
50.A.Hemoglobinuriaisasignofahemolyticreactiontoabloodtransfusionandisn’trepresentativeofotherreactiontypes.
51.A,C,D.Treatmentofhypocalcemiafocusesoncorrectingtheimbalanceasquicklyaspossible.I.V.calciumgluconateorI.V.calciumchloridereplacescalciumlevels.Becausehypocalcemiamaynotbecorrectedbycalciumtherapyalone,expecttogivemagnesiumsupplementsaswell.Also,vitaminDsupplementsmaybeorderedtofacilitatecalcium’sabsorptioninthegastrointestinaltract.
52.A,C,E,F.Toomuchmagnesiumcausesvasodilationandirregularheartmusclecontractions,whichdecreasethebloodpressureandslowtheheartrate.Itmayalsocausenauseaandvomiting,facialflushing,andfeelingsofwarmth.
53.A.Hypokalemiamaybecausedbyseverevomitinganddiarrheainacutepancreatitisthatresultsinpotassiumloss.
54.C.Chlorideregulatesosmoticpressurebetweencompartmentsandformshydrochloricacidinthestomach.
55.D.Waterweightishighestduringinfancy,constitutingupto75%oftotalbodyweight.Itbeginsdecliningwithageduetotheamountofincreasedbodyfat.Inanolderadult,bodywatercontentis45%to55%ofbodyweight.
56.D.LactatedRinger’ssolutionistheinfusionofchoiceforacutevolumeexpansion.Itcontainsasmallamountofpotassiumalongwithlactate,aformoflacticacidthat’smetabolizedbythelivertoformbicarbonate,whichhelpsbufferthebloodagainsttheeffectsofacidosis.
57.B.Metabolicalkalosiscausesanincreaseinbicarbonatelevel,resultinginanonrespiratorylossofacid.
58.B.Malnutrition,diarrhea,anddiureticusecommonlycausehypomagnesemia.Lossofpotassiumandphosphorusfromskeletalmusclestypicallyresultsinmuscleweakness,cramps,andarrhythmias.
59.D.Tapwaterenemascancauseafluidvolumedeficit,whichconsequentlydecreasessodiumandpotassiumlevels.Thiscanleadtowaterintoxication,apotentiallylife-
threateningcondition.
60.C.Bases,acids,andsaltsdissociateintoionswheninawaterysolution.
Glossary
absorption:takingupofasubstancebycellsortissues
acid:substancethatdonateshydrogenions
acid-basebalance:mechanismbywhichthebody’sacidsandbasesarekeptinbalance
acidosis:conditionresultingfromtheaccumulationofacidorthelossofbase
adenosinetriphosphate(ATP):vitalphosphorus-containingcompoundthatrepresentsstoredenergyinthecells;neededtocarryoutthebody’sfunctions
aldosterone:adrenocorticalhormonethatregulatessodium,potassium,andfluidbalance
alkalosis:conditionresultingfromtheaccumulationofbaseorthelossofacid
anion:negativelychargedion,ofwhichproteins,chloride,bicarbonate,andphosphorusareamongthebody’smostplentiful
aniongap:measurementofthedifferencebetweentheamountofsodiumandtheamountofbicarbonateandchlorideintheblood
antidiuretichormone(ADH):hormonemadebythehypothalamusandreleasedbythepituitaryglandthatdecreasestheproductionofurinebyincreasingthereabsorptionofwaterbytherenaltubules
anuria:absenceofurineformationoroutputoflessthan100mlofurinein24hours
base:substancethatacceptshydrogenions
buffer:substancethat,whencombinedwithacidsorbases,minimizeschangesinpH
calcification:depositofcalciumphosphateinsofttissuesthatcanoccurwithprolongedhighserumphosphoruslevels;canleadtoorgandysfunction
calcium:positivelychargedioninvolvedinthestructureandfunctionofbones,impulsetransmission,thebloodclottingprocess,andthenormalfunctionofheartandskeletalmuscles
carboxyhemoglobin:moleculeofcarbonmonoxideandhemoglobinthatpreventsthenormaltransferofoxygenandcarbondioxide;canresultinasphyxiationordeath
cation:positivelychargedion,ofwhichsodium,potassium,calcium,magnesium,andhydrogenarethebody’smostplentiful
cation-exchangeresin:medicationusedtolowerserumpotassiumlevelsbyexchangingsodiumionsforpotassiumionsinthegastrointestinaltract
chloride:mostabundantanioninextracellularfluid;maintainsserumosmolalityandfluid,electrolyte,andacid-basebalance
Chvostek’ssign:abnormalspasmoffacialmusclesthatmayindicatehypocalcemiaortetany;testedbylightlytappingthefacialnerve(uppercheek,belowthezygomaticbone)
colloid:largemolecule,suchasalbumin,thatnormallydoesn’tcrossthecapillarymembrane
colloidosmoticpressure:pressureexertedbycolloidsinthevasculature
compensation:processbywhichonesystem(renalorrespiratory)attemptstocorrectanacid-basedisturbanceintheothersystem
crystalloid:solute,suchassodiumorglucose,thatcrossesthecapillarymembraneinsolution
diuretics:classofmedicationsactingatvariouspointsalongthenephrontoincreaseurineoutput,resultinginthelossofwaterandelectrolytes
electrolyte:solutethatseparatesinasolventintoelectricallychargedparticlescalledions
factorVIII(cryoprecipitate):antihemophilicfactorrecoveredfromfreshfrozenplasma;instrumentalinbloodclotting
glomerularfiltrationrate(GFR):rateatwhichtheglomeruliinthekidneysfilterblood;normallyoccursatarateof125ml/minute
hydrostaticpressure:pressureexertedbyfluidinthebloodvessels
hypercapnia:partialpressureofcarbondioxideinarterialbloodthat’sgreaterthan45mmHg
hyperchloremicmetabolicacidosis:conditionresultingfromadeficitinbicarbonateionsandanincreaseinchlorideions,whichcausesadecreaseinpH
hypervolemia:excessoffluidandsolutesinextracellularfluid;canbecausedbyincreasedfluidintake,fluidshiftsinthebody,orrenalfailure
hypocapnia:partialpressureofcarbondioxideinarterialbloodthat’slessthan35mmHg
hypochloremicmetabolicalkalosis:conditioncausedbyadeficitinchlorideandasubsequentincreaseinbicarbonatethatultimatelycausesanincreaseinpH
hypotonic:solutionthathasfewersolutesthananothersolution
hypovolemia:conditionmarkedbythelossoffluidandsolutesfromextracellularfluidthat,ifleftuntreated,canprogresstohypovolemicshock
hypovolemicshock:potentiallylife-threateningconditioninwhichadecreasedbloodvolumeleadstolowcardiacoutputandpoortissueperfusion
hypoxemia:oxygendeficitinarterialblood(lowerthan80mmHg)
hypoxia:oxygendeficitinthetissues
interstitialfluid:fluidsurroundingcellsthat,withplasma,makesupextracellularfluid
isotonicsolution:solutionthathasthesameconcentrationofsolutesasanothersolution
magnesium:cationlocatedprimarilyinintracellularfluidthatpromotesefficientenergyuse,aidsproteinsynthesis,regulatesnerveandmuscleimpulses,andpromotescardiovascularfunction
metabolicacidosis:conditioninwhichexcessacidorreducedbicarbonateintheblooddropsthearterialbloodpHbelow7.35
metabolicalkalosis:conditioninwhichexcessbicarbonateorreducedacidinthebloodincreasesthearterialbloodpHabove7.45
oliguria:lowurineoutput;lessthan400ml/24hours
osmolality:concentrationofasolution;expressedinmilliosmolsperkilogramofsolution
osmolarity:concentrationofasolution;expressedinmilliosmolsperliterofsolution
osmoticpressure:pressureexertedbyasoluteinsolutiononasemipermeablemembrane
osmoreceptors:specialsensingcellsinthehypothalamusthatrespondtochangesintheosmolalityofblood
osteodystrophy:defectivebonedevelopment;canoccurwithinthefaceofprolongedelevatedserumphosphoruslevels
osteomalacia:softeningofbonetissuesduetodemineralization;commonlyaccompanieschronichypocalcemia
pH:measurementofthepercentageofhydrogenionsinasolution;normalpHis7.35to7.45ofarterialblood
phosphorus:anionlocatedprimarilyinintracellularfluid;involvedinmaintainingboneandcellstructure,maintainingstorageofenergyincells,andaidingoxygendeliverytotissue
potassium:majorintracellularcationinvolvedinskeletalmusclecontraction,fluiddistribution,osmoticpressure,andacid-basebalanceaswellasheartbeatregulation
pulmonaryedema:abnormalfluidaccumulationinthelungs;life-threateningcondition
reabsorption:takingin,orabsorbing,asubstanceagain
renin:enzymethat’sreleasedbythekidneysintotheblood;ittriggersaseriesofreactionsthatproduceangiotensin,apotentvasoconstrictor
resorption:lossofasubstancethroughphysiologicorpathologicmeanssuchaslossofcalciumfrombone
respiratoryacidosis:acid-basedisturbancecausedbyfailureofthelungstoeliminatesufficientcarbondioxide;partialpressureofarterialcarbondioxideabove45mmHgandpHbelow7.35
respiratoryalkalosis:acid-baseimbalancethatoccurswhenthelungseliminatemorecarbondioxidethannormal;partialpressureofarterialcarbondioxidebelow35mmHgandpHabove7.45
rhabdomyolysis:disorderinwhichskeletalmuscleisdestroyed;causesintracellularcontentstospillintoextracellularfluid
sodium:majorcationofextracellularfluidinvolvedinregulatingextracellularfluidvolume,transmittingnerveimpulses,andmaintainingacid-basebalance
tetany:conditioncausedbyabnormalcalciummetabolism;characterizedbypainfulmusclespasms,cramps,andsharpflexionofthewristandanklejoints
third-spacefluidshift:movementoffluidoutoftheintravascularspaceintoanotherbodyspacesuchastheabdominalcavity
Trousseau’ssign:carpal(wrist)spasmelicitedbyapplyingabloodpressurecufftotheupperarmandinflatingittoapressure20mmHgabovethepatient’ssystolicbloodpressure;indicatesthepresenceofhypocalcemia
uremia:excessofureaandothernitrogenouswastesintheblood
uremicfrost:powderydepositsofureaanduricacidsaltsontheskin,especiallytheface;causedbytheexcretionofnitrogenouscompoundsinsweat
waterintoxication:conditioninwhichexcesswaterinthecellsresultsincellularswelling
SelectedReferences
Dudek,S.G.(2013).Nutritionessentialsfornursingpractice(7thed.).Philadelphia,PA:LippincottWilliams&Wilkins.
Gahart,B.L.,&Nazareno,A.R.(2014).Intravenousmedications:Ahandbookfornursesandhealthprofessionals(30thed.).St.Louis,MO:Elsevier.
Hogan,M.A.(2012).Pearsonreviews&rationales:Fluids,electrolytes,&acid-basebalancewithnursingreviewsandrationale(3rded.).SaddleRiver,NJ:PearsonEducation.
Ignatavicius,D.D.,&Workman,L.(2012).Medical-surgicalnursing:Patient-centeredcollaborativecare(7thed.).Philadelphia,PA:Saunders.
I.V.therapymadeincrediblyeasy(5thed.).(2012).Philadelphia,PA:LippincottWilliams&Wilkins.
Longo,D.,Fauci,A.,Kasper,D.,Hauser,S.,Jameson,J.,&Loscalzo,J.(2012).Harrison’sprinciplesofinternalmedicine(18thed.).NewYork,NY:McGraw-Hill.
Portablefluidsandelectrolytes.(2008).Philadelphia,PA:LippincottWilliams&Wilkins.
Smeltzer,S.,&Bare,B.(2014).Brunner&Suddarth’stextbookofmedical-surgicalnursing(13thed.).Philadelphia,PA:LippincottWilliams&Wilkins.
Weinstein,S.(2014).Plumer’sprinciples&practiceofintravenoustherapy(9thed.).Philadelphia,PA:LippincottWilliams&Wilkins.
Weisberg,L.(2008).ManagementofseverehyperkalemiaCriticalCareMedicine,36(12),3246–3251.
Index
AAcid-basebalanceacrossthelifespan,42chlorideregulationand,187diagnosingimbalances,44–49imbalances,201–232infants,205potassiumrolein,106i
Acidosis,38,39i,106imetabolic,214–221respiratory,202–209
Acids,37–39regulation,39–44
Activetransport,fluids,9iAdenosinetriphosphate(ATP),9i,86,167Adolescents.seePediatricpatientsAfterload(pressure),248increased,253
Aging.seealsoElderlypatients;Pediatricpatientsacid-basebalanceand,42calciumlevelsand,148dehydrationand,63fluidbalanceand,6heat-relatedhealthalterations,241hyperkalemia,115hypernatremia,96hypokalemia,108kidneysandelectrolyteimbalance,28kidneysandfluidbalance,12magnesiumlevelsand,126renalfailureand,308respiratoryacidosisand,205
Airembolism,inI.V.therapy,345Albumin,calculatingcalciumlevelsand,149tAlbuminmagnesium,11iAlcoholabuse,pancreatitisand,285Alcoholism,hypomagnesemiaand,129
Aldosterone,production,14iAlkalosis,40i,106imetabolic,222–227respiratory,209–214
Allergicreaction,inI.V.therapy,345Alveolarhypoventilation,263iAminoacids,componentofTPNsolutions,353Anaphylaxis,inI.V.therapy,345Aniongap,46–47,47ihyperchloremicmetabolicacidosis,195i
Anions,22,22iAntidiuretichormone(ADH),64,95fluidbalanceand,12–13,13isodiumand,85–86,86i
APACHEII,inacutepancreatitis,289Arterialbloodgas(ABG)analysis,44,44i,201–202inaccurateresults,46interpretingresults,45–46metabolicacidosis,218tmetabolicalkalosis,226trespiratoryacidosis,207trespiratoryalkalosis,213trespiratoryfailure,266
Arteriallines(A-lines),forbloodpressuremeasurement,59Arterialoxygensaturation,44Atrialnatriureticpeptide(ANP),27fluidbalanceand,15–16,16i
BBalthazarscore,acutepancreatitis,291tBases,37–39regulation,39–44
Bicarbonateinarterialbloodgasanalysis,45chlorideand,188ifunctions,23,25
Bicarbonatebuffersystem,41Bloodpressureautomatedmeasurement,58cuffmeasurement,55–58,56idirectmeasurements,59
Dopplermeasurement,58measurementproblems,57imultiplemeasurements,61palpablepressures,58
Bowelmovements,excessiveGIfluidloss,274Burnshockphaseofburns,320Burns,315–331chemicalandradiation,316classification,317diagnosis,323documentation,328electrical,316emergencycare,326testimatingextentof,319ifluidreplacementformula,324nursingintervention,325–328phasesof,318–322severity,318teachingpatients,327thermal,316treatment,323–325types,316–317
CCalcification,hyperphosphatemiaand,177,178iCalcitonin,calciumlevelsand,148Calcium,147–166balance,150icalculatingalbuminlevels,149tdietarysources,149functions,23,25I.V.administration,156iintakeissues,151levelsbyage,148malabsorptionmaladies,151regulation,148–150
Calciumchloride,hyperkalemiaand,118Calciumgluconate,hyperkalemiaand,118Capillaryfiltration,10Carbondioxide,hyperventilationand,42iCardiacdilation,252
Cardiachypertrophy,252Cardiacoutput,248Cations,22Centralvenouspressure(CVP),55,61–62,62iCentralvenoustherapy,341–342Chemicalandradiationburns,316Chemicalbuffers,40–41Chloride,186–200acid-basebalanceand,187bicarbonateand,188idietarysources,187functions,23,25regulation,187
Chvostek’ssign,hypocalcemia,154iColloidsI.V.solutions,338useinburnpatients,324
Compensation,arterialblood,46Conduction,235Continuousrenalreplacementtherapy(CRRT),75,75iContractility(squeeze),248Convalescentphaseofburns,322Convection,235CRRT.seeContinuousrenalreplacementtherapy(CRRT)Crystalloids,I.V.solutions,336Cushing’sdisease,metabolicalkalosisand,224
DDehydration,62–65dangersigns,64diagnosis,64documentation,66excessiveGIfluidloss,273mentalstatuschanges,64monitoringandintervention,65olderadults,17signsandsymptoms,240teachingpatients,65treatment,64–65
Dextrose,electrolytecontent,32tDiabetesinsipidus,hypernatremiaand,96
Diabeticketoacidosis(DKA),113hypophosphatemiaand,171
Diffusion,8,8iDiureticphase,renalfailure,302Diureticsfluidandelectrolytebalance,30,31iheartfailureand,253hyperchloremiaand,194metabolicalkalosisand,222
Dopamine,levelsinmetabolicacidosis,220Dopplerbloodpressure,58,58i
EEdemainburnpatients,320inhypervolemia,72–73pitting,73ipulmonary,74i
Edematouspancreatitis,284Elderlypatientsdehydration,17excessiveGIfluidloss,278hyperkalemia,115hypernatremiaand,96hypocalcemia,151hypokalemia,108hypophosphatemia,170
Electricalburns,316Electrolytes.seealsoFluidandelectrolytebalancebalancing,31–36componentofTPNsolutions,353documentingimbalances,27levels,24movement,24
Electroneutrality,22Emergentphaseofburns,320Enemas,excessiveGIfluidlossand,274Evaporation,236Extracellularfluids(ECF),4,5iExtravasation,inI.V.therapy,344
FFirst-degreeburns,317Fluidaccumulationphaseofburns,320–322Fluidandelectrolytebalancediureticsand,30,31idrugeffects,31iI.V.fluideffects,30kidneyregulation,28,29iorganandglandinvolvement,27
Fluidbalance,3–20measurement,61mechanismtomaintain,11–18
Fluidcompartments,5iFluidoverload,inI.V.therapy,345Fluidremobilizationphaseofburns,322Fluidreplacementformula,burnpatients,324Fluidvolume,55–62cuffmeasurement,55–58,56i
Fluids.seealsoFluidandelectrolytebalanceagingeffects,6,12balancing,3–20insensiblelosses,3movement
withinthecells,8throughcapillaries,10iwithinthevascularsystem,10
reabsorption,10sensiblelosses,4sitesinvolvedinloss,4isolutemovementand,27types,6–8
Fourth-degreeburns,317
GGallstones,acutepancreatitisand,284–285,286tGIfluidloss,272–281adolescents,275causes,272diagnosis,276documentation,278
imbalancescausedby,273nursingintervention,277–278signsandsymptoms,276teachingpatients,277treatment,277
Glomerularfiltrationrate(GFR),12,302–303
HHeart,roleinfluidandelectrolytebalance,27Heartfailure,248–261advanced,255causes,249,253–254compensatoryresponses,250–251diagnosis,255documentation,257drugsusedin,256–257imbalancescausedby,252–253left-sided,250i,254nursingintervention,257–258right-sided,251i,254–255signsandsymptoms,254surgery,257teachingpatients,258treatment,255–256
Heartrate,248Heatcramps,237,241Heatexhaustion,237,242Heatrash,237,241Heat-relatedhealthalterations,235–247age-relatedrisks,240,241diagnosis,240documentation,244drugsthatcause,237nursingintervention,243prevention,244risks,238–239signsandsymptoms,238,239tteachingpatients,244treatment,241–242types,237–238
Heatstroke,238,242
Heatsyncope,238,242Hydrostaticpressure,10Hyperactivedeeptendonreflexes(DTRs)grading,132ihypomagnesemiaand,128,131
Hypercalcemia,157–162causes,157–159dangersigns,160diagnosis,160documentation,162drugsassociatedwith,159nursingintervention,161–162signsandsymptoms,159–160teachingpatients,162treatment,160–161whentreatmentdoesn’twork,161
Hyperchloremia,193–197causes,193diagnosis,194diuretics,194drugsassociatedwith,193nursingintervention,196signsandsymptoms,194teachingpatients,196treatment,194–195
Hyperchloremicmetabolicacidosis,aniongapand,195iHyperglycemia,hypophosphatemiaand,170Hyperkalemia,114–120inburnpatients,321calciumchlorideorcalciumgluconate,118causes,114–115diagnosis,116–117,116idiet,120documentation,120drugsassociatedwith,115elderlypatients,115emergencytreatment,309heartfailureand,253intervention,118–119prematureinfants,115renalfailureand,303–304,309
respiratoryfailureand,263signsandsymptoms,116teachingpatients,120treatment,117
Hypermagnesemia,136–143causes,136–138diagnosis,139documentation,142drugsandsupplementsassociatedwith,138nursinginterventions,140–142renalfailureand,303–305signsandsymptoms,138–139,139tteachingpatients,141treatment,139–140
Hypernatremia,94–99inburnpatients,322causes,94–95diagnosis,98documentation,99drugsassociatedwith,97telderlypatients,96excessivesodiumintake,96–97fluidmovementin,95nursinginterventions,98–99renalfailureand,303–304signsandsymptoms,97–98teachingpatients,99treatment,98waterdeficit,96
Hyperphosphatemia,175–181calcification,177,178icauses,176–177cow’smilkand,177diagnosis,178documentation,181drugsassociatedwith,177nursingintervention,180renalfailureand,303–304signsandsymptoms,177teachingpatients,180treatment,178–179
Hyperthermia,239tHypertonicdehydration,62Hypertonicfluids,7,7iHypertonicsolutions,336,337i,339–340tHyperventilationcarbondioxideand,42ihypophosphatemiaand,170respiratoryalkalosisand,210
Hypervolemia,71–77inburnpatients,322CRRT,75,75idiagnosis,73documentation,77edema,72–73heartfailureand,252nursingcare,76renalfailureand,303–304respiratoryfailureand,263signsandsymptoms,72–73teachingpatients,76treatment,74–75
Hypervolemichyponatremia,89Hypoalbuminemia,acutepancreatitisand,287Hypocalcemia,150–157acutepancreatitisand,287inburnpatients,322causes,150–152diagnosis,153–154,154idocumentation,157drugsassociatedwith,152elderlypatients,151I.V.administrationofcalcium,156isignsandsymptoms,153teachingpatients,157treatmentandinterventions,154–155
Hypochloremia,188–192causes,188–190,189idiagnosis,191documentation,192drugsassociatedwith,189excessiveGIfluidloss,273
nursingintervention,191–192signsandsymptoms,190teachingpatients,192treatment,191
Hypochloremicalkalosis,189,189iinfants,190
Hypokalemia,108–114acutepancreatitisand,287inburnpatients,322commoncauses,108–109dangersigns,110diagnosis,110,110idiet,120disordersassociatedwith,109documentation,120drugsassociatedwith,109elderlypatients,108excessiveGIfluidloss,273heartfailureand,253monitoringandintervention,111–112renalfailureand,303–304respiratoryfailureand,263signsandsymptoms,109–110,240teachingpatients,120whentreatmentdoesn’twork,112
Hypomagnesemia,128–137acutepancreatitisand,287alcoholismand,129causes,128–130diagnosis,134documentation,137drugsassociatedwith,130excessiveGIfluidloss,273heartfailureand,253identificationof,131signsandsymptoms,130–134teachingpatients,136treatmentandintervention,134–135
Hyponatremia,87–94acutepancreatitisand,287inburnpatients,321,322
causes,88criticalsteps,93diagnosis,92documenting,99drugsassociatedwith,89texcessiveGIfluidloss,273fluidmovementin,88iheartfailureand,252–253hypervolemic,89hypovolemic,89isovolemic(dilutional),90nursinginterventions,93renalfailureand,303–305signsandsymptoms,91–92,240teachingpatients,99treatment,92–93
Hypophosphatemia,169–175causes,170diagnosis,173documentation,175drugsassociatedwith,171elderlypatients,170malabsorptionsyndromesand,170–171nursingintervention,173–174signsandsymptoms,171–172teachingpatients,174treatment,173
Hypotonicdehydration,62Hypotonicfluids,7,7iHypotonicsolutions,337,337i,339tHypoventilation,207Hypovolemia,65–71acutepancreatitisand,286–287inburnpatients,320,321causes,66dangersigns,68tdiagnosis,68documentation,71excessiveGIfluidloss,273heartfailureand,252nursingresponsibilities,69–70
renalfailureand,303–304respiratoryfailureand,263signsandsymptoms,67teachingpatients,70treatment,68–69
Hypovolemichyponatremia,89Hypovolemicshock,67–68hemodynamicvaluesin,70
Hypoxia,respiratoryalkalosisand,210
IInfants.seealsoPediatricpatients;Prematureinfantsrespiratoryacidosis,205
Infection,inI.V.therapy,343Infiltration,inI.V.therapy,343Insensiblefluidlosses,3Intracellularfluids(ICF),4,5iIntrapulmonaryshunting,263iIntravenousfluids(I.V.)comparingfluidtoxicity,337icomplications,343–346components,32tdeliverymethods,338–343documentation,347effectsonfluidandelectrolytebalance,30nursingintervention,346–347replacement,335–351severedcatheter,344teachingpatients,347tubingsystems,342–343typesofsolutions,336–338(seealsospecifictype)
Ions,21,22iIsotonicdehydration,62Isotonicfluid,6,6iIsotonicsolutions,336,337i,339tIsovolemichyponatremia(dilutional),90I.V.seeIntravenousfluids
JJuxtaglomerularcells,13
KKidneys.seealsoRenalfailureacid-baseregulationand,40,42–44hyperphosphatemiaand,176hypophosphatemiaand,171roleinfluidandelectrolytebalance,28,29iroleinfluidbalance,11–12
Kussmaul’srespirations,metabolicacidosisand,217
LLactatedRinger’ssolution,electrolytecontent,32tLacticacidosis,219iheartfailureand,253
Laxatives,excessiveGIfluidlossand,274Lipidemulsionsadversereactionsto,355tinTPN,355
Lipids,componentofTPNsolutions,353Lund-Browderclassification,inestimatingextentofburns,319i
MMagnesium,125–146absorptionproblems,129dangersignsoflowlevels,128dietarysources,127ifunctions,23,25gaugingstatuswithpatellarreflex,141iGIproblems,129levels,126levelsatdifferentages,126regulation,127urinaryproblems,129
Magnesiumsulfateinfusion,136injection,134preventingmedicationerrors,136
Majorburns,318Metabolicacidosis,214–221inburnpatients,322causes,215,216–217i
diagnosis,218documentation,221dopamineand,220excessiveGIfluidloss,273nursinginterventions,220–221renalfailureand,303–305respiratoryfailureand,265signsandsymptoms,217–218teachingpatients,221treatment,219–220
Metabolicalkalosis,222–227causes,222–223,223–224idiagnosis,225documentation,227drugsassociatedwith,224excessiveGIfluidloss,273nursingintervention,226–227renalfailureand,303–305signsandsymptoms,225teachingpatients,227treatment,226
Micronutrients,componentofTPNsolutions,353Minorburns,318Moderateburns,318ModifiedParklandformula,324Multiorgansystemfailure(MOSF),inacutepancreatitis,289–290Myoglobin,inburnpatients,321
NNecrotizingpancreatitis,284
OOliguric-anuricphase,renalfailure,302Osmosis,9i
PPancreas,functions,283Pancreatitisacute,282–299
causes,284–285,286t
complications,288tdiagnosis,288–289documentation,296edematousvs.necrotizing,284imbalancescausedby,286–287nursingintervention,293–295painrelief,292severityscoring,289signsandsymptoms,287teachingpatients,294treatment,290–293
chronic,285Parathyroidhormone(PTH)calciumlevelsand,148hyperphosphatemiaand,176hypophosphatemiaand,171phosphorusand,168,169i
Partialpressureofcarbondioxideinarterialblood,44Partialpressureofoxygeninarterialblood,44Patellarreflex,testsformagnesiumlevels,141iPediatricpatientsdehydrationand,63estimatingextentofburns,319iexcessiveGIfluidlossand,275hyperkalemia,115hypernatremia,96hypochloremicalkalosisininfants,190hypokalemia,108
PeripheralI.V.therapy,340–341Peripheralparenteralnutrition(PPN),354pHarterialblood,45normal,38iunderstandingof,37–39
Phlebitis,inI.V.therapy,344Phosphate.seePhosphorusPhosphatebuffersystem,41Phosphorus,167–185calciumlevelsand,149dietarysources,168functions,23,25
parathyroidhormoneand,168,169iregulation,168–169
Plasmacolloidosmoticpressure,11Potassium,105–124dietarysources,107drugsassociatedwithdepletion,109functions,23,25guidelinesforadministration,113regulation,107roleinacid-basebalance,106i
Preload(volume),248increased,251,253
Prematureinfants,hyperkalemia,115Proteinbuffers,41Pulmonaryarterycatheterbloodpressuremeasurement,59–61,60iports,60i
Pulmonaryarterypressure(PAP),55Pulmonaryedema,74iinburnpatients,323
RRadiation,235Ranson’scriteria,inacutepancreatitis,289,290tReabsorption,fluids,10Refeedingsyndrome,170Renalfailure,300–314acuteorchronic,300agingeffects,308cardiovascularsigns,306t,307causes,300,301i,302–303diagnosis,308diureticphase,302documentation,311genitourinarysigns,306tGIsigns,306t,307imbalancescausedby,303–304integumentarysigns,306t,307laboratoryresults,305musculoskeletalsigns,306t,307neurologicsigns,306t
nursingintervention,309–311phase1(oliguric-anuricphase),302pulmonarysigns,306t,307recoveryphase,302signsandsymptoms,305–306teachingpatients,310treatment,308–309
Renin-angiotensin-aldosteronesystem,27fluidbalanceand,13–15,14–15i
Respiratoryacidosis,202–209inburnpatients,322causes,202–206,203–204idiagnosis,206–207documentation,209drugsassociatedwith,204nursingintervention,207–208respiratoryfailureand,264signsandsymptoms,206teachingpatients,208treatment,207–208
Respiratoryalkalosis,209–214causes,210diagnosis,212–213documentation,214drugsassociatedwith,210nursingintervention,214respiratoryfailureand,264signsandsymptoms,210–213,211–212iteachingpatients,214treatment,213
Respiratorychanges,inburnpatients,320Respiratoryfailure,262–271causes,262–263,264tdiagnosis,266nursingintervention,267–268signsandsymptoms,265teachingpatients,268treatment,266–267worsening,266
Respiratorysystem,acid-baseregulationand,40,41–42,42iRinger’ssolution,electrolytecontent,32t
RuleofNines,inestimatingextentofburns,319i
SSecond-degreeburns,317Sensiblefluidlosses,4Serumelectrolytetestresults,26tSerumpH,calciumlevelsand,149Severedcatheter,inI.V.therapy,344Sodium,84–104dietarysources,85excessiveintake,96–97functions,23,25regulation,85–87,86i
Sodiumchloride,electrolytecontent,32tSodium-potassiumpump,85–87,87i,107Speedshock,inI.V.therapy,345Stressulcers(Curling’sulcers),inburnpatients,321Suctioningofstomachcontents,excessiveGIfluidloss,273Sympatheticnervoussystem,heartfailureand,250Syndromeofinappropriateantidiuretichormone(SIADH)secretion,77–78,90,91i
TThermalburns,316Third-degreeburns,317Third-spacefluidshifts,67Thirst,fluidbalanceand,16–17Thrombophlebitis,inI.V.therapy,344Totalparenteralnutrition(TPN),352–362commonadditives,353documentation,359infusionfacts,356nursingintervention,356–358signsandsymptomsofproblems,357teachingpatients,356technique,358timingout,358–359uses,352–353
Trousseau’ssign,hypocalcemia,154i
V
V/Qmismatch,263iVasopressin.seeAntidiuretichormone(ADH)VitaminD,calciumlevelsand,149Vitamins,componentofTPNsolutions,353Vomitingcharacteristicsandcauses,274excessiveGIfluidloss,273
WWaterintoxication,77–79causes,77diagnosis,78documentation,79nursingcare,79signsandsymptoms,78teachingpatients,79treatment,78