made

Fluids & Electrolytes

Sixth Edition

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SixthEdition

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Fluids&electrolytesmadeincrediblyeasy!/clinicaleditor,LauraWillis.—Sixthedition.p.;cm.

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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

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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

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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