外科学教学课件：水电解质－英

FLUIDANDELECTROLYTEMANAGEMENT

OFTHESURGICALPATIENTObjectiveDistributionofwaterandelectrolytesinthebodyMechanismofmodulationforwaterandelectrolytesandacid-basebalanceDisorderofwaterandelectrolytesandacid-basebalanceMechanismClinicalsymptomsandsignsDiagnosisTreatmentsWaterisimportantforlivinglifeTransportationofelectrolytes,oxygen,nutrients,etcMetabolismWasteeliminationetcMultiplewatercompartmentsMultiplewatercompartmentsseparatedbymembranesSubstantialdifferencesinsolutecompositionwithinthecompartmentsBalanceismaintainedacrossthemembranesThisbalance(homeostasis)issustainedbytheconsumptionofenergy

Intracellularfluid(ICF)Extracellularfluid(ECF)InterstitialfluidPlasmaMultiplewatercompartmentsBodywaterandsolutecompositionTotalbodywater(TBW)constitutesbetween50%and60%ofthetotalbodyweightinmostadultsTBWconstitutesupto70%ofthetotalbodyweightinchildrenPercentageofTBWtothebodyweight40%15%5%15%5%35%MALEFEMALEICFECFINTERSTITIIAL

FLUIDPLASMAPrincipalcations&anionsinICF&ECFECFWaterandsolutesintheplasmaFilteracrossthemicrovascularmembraneinterstitialfluidflowthroughthelymphaticsReturnbacktotheplasmaECFWaterinboneandindenseconnectivetissue(cartilageandtendons)FixedDoesnotreadilyflowintheinterstitiumandlymphaticsWaterandsolutesincirculationDrinkingandeatingWaterintheGItractisincreasedWaterandnutrientsconsumedDistributedinECFandICFcompartmentsNutrientssupportmetabolismWasteproductsreleasedfromcellstransportedfromtheICFtotheECFtransportedthroughthelymphaticstotheplasmaWasteexcretedprimarilythroughrenalfunctionCO2exhaledinrespiratorygasesWaterandsolutescanbeeliminatedWaterandelectrolytesinevacuatedstoolWaterinrespiratorygasesWaterandelectrolytesinsweatThesethreetypesofexcretionarenottightlyregulatedRenalfunctionIscriticaltothehomeostasisofECFandICFModulatedbyacomplexinteractionLocalregulatoryfactorsTo

keep

the

volumeofplasmaSystemichormones

(ADHfromthehypothalamusandpituitary

)To

keep

the

normal

osmolality

inICF&ECFOsmolalityAmeasureofthetotalnumberofsolutespermassofwaterIsclinicallymeasuredinunitsofmillimolesperkilogramofwater(mmol/kgH2O)Normalosmolality:300mmol/kgH2O(280—310)PrincipalosmolesinICFandECFWaterandsolutesmovementTokeepthebodyfluidhomeostasisTBWmovesacrosscellmembranesDistributesbetweenICFandECFTokeepthesameosmolalityinICFandECFCellmembranesarereadilypermeabletowaterWatershiftsrapidlybetweenECFandICFtoachievebalanceinosmolalityThemajorityofsolutesDetermineosmolalityinthetwofluidcompartmentsCrossthecellmembraneonlythroughregulatedtransportmechanismsPassivetransport:concentrationgradientActivetransportmechanismsConsumebiochemicalenergyMoveelectrolytesacrossthecellmembraneWaterandsolutesmovementToregulatesthesizeoftheICFandECFbycontroloftheexcretionofsolutesinurinebycontroloftheosmolalityofurineRenalfunctioninwatercontrolRenalfunctioninwatercontrolRenalcontrolof[Na+]excretion(with[Cl-])DeterminesthesizeoftheECFcompartmentIf[Na+]isretainedtotalbody[Na+]massExpandsthesizeoftheECFcompartmentRenalfunctioncontrolsthevolumeofTBWbyproducingurinewitharangeofosmolalityfrom100to1200mmol/kgH2OTransportenzymesoncellmembraneSustainthedifferenceinelectrolytecompositionbetweenICFandECFActivelytransport[Na+]fromICWtoECWinexchangefor[K+]TheenzymeNa+,K+-ATPaseplaysakeyroleintheactivetransportBinds3[Na+]inICFBinds2[K+]inECFUsestheenergyprovidedbyhydrolysisofATPtoADP3[Na+]outofthecell2[K+]inECFenterthecellNa+,K+-ATPaseactivityisanetnegativeintracellularchargeDueto3cationsoutand2cationsintothecellNa+,K+-ATPaseinactivetransportTheNa+,K+-ATPasepumpisconstantlyactiveContinuouslyconsumestheenergyinATPtoADPSustaintherestingmembranepotentialInsufficientoxygenisavailabletosustainaerobicmetabolismConsequently,cellularATPlevelsfallThesodiumpumpfunctionisimpairedLeadtocelldysfunctionanddeathTheintracellularsodiumconcentrationincreasesTherestingmembranepotentialdeclinesNa+,K+-ATPaseClassificationofBodyFluidChangesDisordersinfluidbalanceinthreecategories:DisturbancesofvolumeDisturbancesofconcentrationDisturbancesofcompositionVolumeChangesVolumeDeficitVolumeExcessVolumeDeficitECFdeficitisthemostcommoninsurgicalpatientsThelossoffluid:waterandelectrolytesInthesameproportionasthatinnormalECFCauseofvolumedeficitLossofgastrointestinalfluidVomitingNasogastricsuctionDiarrheaFistuladrainageSofttissueinjuresInfectionsIntra-abdominalandretroperitonealinflammatoryprocessesPeritonitisIntestinalobstructionBurnsSignsandsymptomsModerateSevereCNSSleepinessApathySlowresponsesAnorexiaCessationusualactivityDecreasedtendonreflexesAnesthesiaofdistalextremitiesStuporComaGastrointestinalProgressivedecreaseinfoodconsumptionNausea,vomitingRefusaltoeatSilentileusanddistentionCardiovascularOrthostatichypotensionTachycardiaCollapsingpulseCutaneouslividityHypotensionDistantheartsoundsColdextremitiesAbsentperipheralpulsesManagementofVolumeDeficitFluidadministrationEvaluatethedegreeofdehydrationMild:lossof1-2%ofbodyweightModerate:lossof3-5%ofbodyweightSevere:lossof6-7%ofbodyweightForexample:Moderate:lossof3-5%ofbodyweight(60Kg)Waterloss:5%×60=3L=3000mlLossof25%ofECFD1:½ofthevolumeinfusedD2:¼ofthevolumeinfusedD3:¼ofthevolumeinfusedManagementofVolumeDeficitVolumeexcessECFexcessisiatrogenicorsecondarytorenalinsufficiencyBothplasmaandinterstitialfluidareincreasedEdema:allorgansandtissuesFortheyoung:circulatoryoverloadFortheelder:congestiveheartfailurewithpulmonaryedemadevelopsECFexcessModerateSevereSubcutaneousedemaGastrointestinalAtSurgery:Edemaofstomach,colon,lesserandgreateromenta,andsmallbowelmesenteryCardiovacularElevatedvenouspressureDistentionofperipheralveinsIncreasedcardiacoutputLoudheartsoundsFunctionalmurmursBoundingpulseHighpulsepressureIncreasedpulmonarysecondsoundgallopPulmonaryedemaManagementofvolumeexcessTreattheprimarydiseasesControlthewaterintakeIncreasethewaterexcretionTheserum[Na+]:142mEq/L(138to145)Theserum[Na+]isresponsibleforthetonicityofbodyfluidConcentrationchangesHyponatremiaSodiumlossinECF:Mild:[Na+]130---138mEq/LModerate:[Na+]120---130mEq/LSevere:[Na+]<120mEq/L.PatientswithmildhyponatremiararelyhavesignsorsymptomsTheclinicalindicationsofhyponatremiaDecreasedresponsivenessSeizuresCatastrophicrespiratoryarrestSeverehyponatremiaSeverehyponatremia:[Na+]<120mEq/L.[Na+]osmolality

inECFandICFCellsareswellingIntracranialcellswellingCausingheadachesandlethargyRapidlyprogresstocomaorhaveseizuresHyponatremia

SymptomsandsignsModerateSevereCNSMuscletwitchingConvulsionsHyperactivetendonreflexesLossofreflexesIncreasedintracranialpressure(compensated)Increasedintracranialpressure(decompensated)CardiovascularChangesinbloodpressureandpulsesecondarytoincreasedintracranialpressureTissueSignsSalivation,lacrimationWaterydiarrheaFingerprintingofskinRenalOliguriaprogressingtoanuriaOliguriaCauseofhyponatremiaLossofGIfluidsVomitingDiarrheaNasogastricsuctionFistuladrainageLoopdiureticsandIVinfusionofmannitol

ExcessiveinfusionofhypotonicsolutionsSevereinjuryorburnsLowsodiumin

enteralnutritionRenallossofsodiumduetothebraindiseaseCauseofacutehyponatremiaECFisreplacedwitheitheranenterallyorIVinfusedhypotonicfluidIVinfusionof5%dextroseinwaterrapidlyproduceshyponatremiaInthepatientswithHemorrhageAnacutediarrheaPancreatitisBurnwoundInflammatoryedemahasdevelopedHyponatremiaexacerbatedifbloodvolumecontractedTreatmentofacutehyponatremiaIVinfuseisotonicsalineAddhypertonicsaline(10%NaCl)toexpandacontractedECFvolumeTherateofinfusionofsodium-containingsolutions:increasingserum[Na+]<0.25mEq/L/hrNaCl(g)=½(142mmol/L-serum[Na+])×Kg×0.6÷170.5(female)ChronicHyponatremiaThesyndromeofinappropriatereleaseofantidiuretichormone(SIADH)

ChronicrenaldiseasemayhaveanimpairedcapacitytoretainsodiumManagementforchronichyponatremiaRapidcorrectionof[Na+]inpatientswithchronichyponatremiacanleadasevere,permanentneurologicdisorderTherateofsodiuminfusion<0.25mEq/L/hrTherateofincreaseinserum[Na+]<8mEq/kg/dayRestrictingintakeofwaterinmildandmoderatehyponatremiaHypernatremiaandSyndromesofHypertonicityAnacuteonsetofhypernatremiaincreasesECFosmolalityContractsthesizeoftheICFcompartmentModeratehypernatremia：serum[Na+]146--159mEq/LSeverhypernatremia:serum[Na+]>160mEq/LCommoncause:waterlossForexample:1.Thewaterlostafterexcessivesweatinginahotenvironment2.Unregulatedlossofhypo-osmoticgastrointestinalfluidsNeurologicdamageduetocontractionofbraincellvolumeSeverhypernatremia[Na+]>160mEq/LAnalteredlevelofconsciousnessandseizuresComaandintracerebralhemorrhageTreatmentofHypernatremiaIVororaladministrationofwaterforhypernatremiasecondarytodehydrationIVinfusionofisotonicsalinesolutionsduetoreducedbloodvolumesuntilthecontractedECFhasbeenrestoredSerum[Na+]shouldbeloweredatarate<8mEq/dayArapiddeclineinECFosmolalityleadstocerebralinjury(swelling)FormulaH2O(ml)=([Na+]–142mmol/L)×Kg×4D1:Infusionof½volumeofH2O(ml)D2:¼volumeD3:¼volumeTreatmentofHypernatremiaPotassiumThenormal[K+]concentrationinECFis4.5mmol/LMostofpotassium(98%)islocatedintheICFInthedailyintakeofadiet,anindividualconsumes50to100mmolofpotassium(3-4g)Theexcess[K+]consumedinthedietisclearedinurineTherenin-angiotensin-aldosteronehormoneaxisplaysakeyroleinrenalcontrolof[K+]clearanceHormonealdosteroneincreasesinplasma,theconcentrationofpotassiuminurineincreasesHyperkalemia

[K+]>5.0mmol/L[K+]>6mmol/LIimpairnormaldepolarizationandrepolarizationCardiacarrhythmiasoftenprovelethalElectrocardiographicchanges[K+]:6--7mmol/L:TallTwavesSymmetricallypeakedTwavesindicatedangeroushyperkalemia[K+]>7mmol/LP-waveamplitudesontheelectrocardiogramdecreasePRsegmentsincreaseTheQRScomplexwidens.[K+]>8mmol/L:suddenlylethalarrhythmiasensueAsystoleVentricularfibrillationAwidepulselessidioventricularrhythmECGchangesindicatinghyperkalemiaCauseofhyperkalemiaAnacuterenaldysfunctionorrenalfailureSuddenreleaseofpotassiumfromICFcancausehyperkalemiaReperfusionofischemicskeletalmuscleisaclinicalsyndromeandreleaseofK+.ReperfusioninjuryoccursatthecompletionofarterialinjuryrepairTreatmentofAcuteHyperkalemiaStopallinfusionofpotassiumIVinfusionof10%CaCl2or10%calciumgluconateIVinfusionofNaHCO3GlucoseandinsulininfusionImmediatehemodialysisPotassium-bindingresinsintotheGItractwith20%sorbitolPromotionofrenalkaliuresisbyloopdiureticHypokalemia[K+]<3.5mmol/LSymptoms:fatigue,weakness,andileus[K+]<2.5mmol/L:Rhabdomyolysismayoccur[K+]<2mmol/L:FlaccidparalysiswithrespiratorycompromisecanoccurCauseofHypokalemiaPersistentvomitingDrainlargevolumesvianasogastrictubesDiarrheaHigh-outputentericPancreaticfistulasPatientswithcongestiveheartfailuremanagedwithmultipledrugsPatientstreatedwithdiureticsthatexcreteurinewithanelevated[K+]Long-termdiuretictherapyTreatmentofAcuteHypokalemiaRequirepotassiumreplacementPotassiuminfusion<arateof0.3mmol/kg/hrHighconcentrationsofpotassiuminIVfluidscanbeirritatingtoperipheralsmallveinsInfusionsmayrequireacentralvenouscatheterPatientsrarelyrequiremorethan200mmolofpotassiumin1dayDailyintake:KCl3—4gPotassiumreplacement:oralorIVAstateofanadequateurine(>30-40ml/H)KCl≤3gperLitersolutionSlowinfusionIVMaximaladay:KCl8gTreatmentofAcuteHypokalemiaCalciumAcriticalcomponentofreactionsinICFandECFAnessentialcofactorinthecoagulationcascadeParticipatesintheregulationofneuronal,myocardial,andrenalcellularfunctionCalciuminECFispresentinthreemolecularformsprotein-boundcalciumdiffusiblecalciumcomplextoanions(bicarbonate,phosphate,andacetate)ionizedcalcium(iCa2+)ThebiochemicallyactivespeciesisiCa2+MagnesiumMagnesiumisanessentialcationinICFSerum[Mg2+]concentration:1.4and2.0mEq/LSeveraldiseasesthatdepletemagnesiumhaveparalleleffectsoncalciumHypercalcemiaserumcalcium>2.75mmol/LCauseofhypercalcemiaPatientswithhyperparathyroidismsecondarytoaparathyroidadenomaPatientswithmalignancy-relatedseverehypercalcemiaArenalconcentratingdefectandleadstopolyuriaWeakness,stupor,andCNSdysfunctionArenalconcentratingdefectLeadstopolyuriaandlossofsodiumandwaterDehydrationRenallithiasisHypercalcemiaManagementofHypercalcemiaCorrectionoftheprimaryproblemExcisionofthediseasedparathyroidtissueSalineinfusiontoexpandECWAloopdiuretictocleartheurinarycalciumIsotonicsalineinfusionisessentialHypercalcemicwithrenalfailurecanbemanagedbyhemodialysisBisphosphonates

canbemanagedthoserelatedtoreleaseofcalciumfrombonebytumorHypocalcemiaSerumcalcium<2mmol/LAcutehypocalcemiacanbealife-threateningeventImpairstransmembranedepolarizationLeadtocentralnervoussystemdysfunctionMusclespasms(includingtetany),andseizuresPainfulmusclespasmsInducearespiratoryalkalosisCardiacdysfunctionECG:aprolongedQTintervalleadingtoheartblockorventricularfibrillationVitaminDmetabolicdeficitHypoparathyroidismAcuteseverepancreatitisRenalfailureTumorCauseofhypocalcemiaManagementofHypocalcemiaInfusionof10mLofa10%CaCl2solution272mgofcalcium=13.6mmolofCa2+Infusionof10mLofa10%calciumgluconate90mgofcalcium=4.5mmolofCa2+Hypermagnesemiamostoftenseeninpatientswithrenalfailureexacerbatedbytheingestionofmagnesium-containingdrugs,particularlyantacidsMagnesiumblockstheshiftofcalciumintomyocardialcellsseverehypermagnesemiashowevidenceofheartfailure.HypomagnesemiaDevelopinpatientswithchronicdiarrheasyndromeprolongedaggressivediuretictherapywithheavyethanolintakediabeticpatientswithpersistentosmoticdiuresisThemagnitudeofmagnesiumdeficiencyparallelsthemagnitudeofhypocalcemiaCorrectionofhypomagnesemiaIVinfusionofmagnesiumsulfate(MgSO4)Severehypomagnesemia(<1.0mEq/L)requiressustainedtherapyCorrectionofhypomagnesemiacanalsoreducetheriskforcardiacarrhythmiasACID-BASEBALANCEpH:thenegativelogoftheH+concentrationMaintainedinanarrowlimitspH:7.35—7.45Acid:thebyproductofmetabolismNeutralizedbybuffersystemsExcretedbylungandkidneyBuffersystemsRenalfunctionRespiratoryfunctionPlaythecriticalroleinacid-basebalanceACID-BASEBALANCEBuffersystemsBuffersystems:consistingofWeakacidorbaseSaltofthatacidorbaseBuffersinICFandECFHCO3-/H2CO3H2PO42-IMIDAZOLEONPROTEINSECW95%4%1%ICW42%6%52%ThebicarbonatebuffersystemAdominantbuffersysteminbiologicsystemsIsimportantinbothICFandECFIskeytoenablingprotontransportacrosscellmembranes

H++HCO3-=H2O+CO2Renal

functionTherenaltubulecellsconsumebiochemicalenergyandpumpprotonsintourineEnablingnetexcretionofprotons(asNH4+)TherenaltubulecellscannotrecoverthebicarbonatefilteredattheglomerulusSoallowinglossofbicarbonateinanalkalineurine.ThepulmonarysystemIncreasethelossofCO2inrespiratorygasesbyincreasingalveolarventilationDecreasethelossofCO2inrespiratorygasesbydecreasingalveolarventilationCanconsequentlyreducethePaco2inECFTimelinessisacriticaldistinctionTime

to

correcttheprotonconcentrationinECFTherenalsysteminhoursthepulmonarysysteminminutes

AfrequentandpotentiallylethalproblemforpatientsPatientsareacidoticiftheyhaveanexcessnumberofprotonsintheirbodyfluidsPatientsarealkaloticiftheyhaveasignificantdeficitinprotonsintheirbodyfluidsAcidemiameansthattheprotonconcentrationinECFexceeds40nmol/LAlkalemiameanstheprotonconcentrationinECFislessthan40nmol/LAcid-BaseDisorderspHandMeasurementofProtonConcentrationArterialbloodgasanalysisisusedtoassesstotalbodyacid-basebalanceBloodgastestsreport:pHPaco2HCO3-(mEq/L)pHAmeasureoftheprotonconcentrationIscalculatedasthelogtothebase10of1dividedbytheprotonconcentrationPaco2

isinfluencedbytherateofCO2productioninaerobicenergymetabolismisinfluencedbytherateofclearanceofCO2duringpulmonaryalveolarventilationHenderson-HasselbalchEquationBicarbonatePaco2patient'sacid-basestatuspH=6.1+log[(HCO3-)/(H2CO3)]pH=6.1+log[(HCO3-)/(0.03×Paco2)]pH=6.1+log(24/1.33)=7.4(HCO3-)/(H2CO3)=20/1

7.35≤pH≤7.45Acidemia:pH<7.35Alkalemia:pH>7.45Acid-BaseDisordersAcid-BaseDisordersAcidemia(ECFpH<7.35)metabolic(meaningadeficiencyofHCO3-)respiratory(anelevationinPaco2)Alkalemia(ECFpH>7.45)metabolic(meaningexcessHCO3-)respiratory(adecreaseinPaco2)Six-StepSequentialApproachtotheInterpretationofArterialBloodGas

OBSERVATIONINTERPRETATIONINTERVENTIONIsthepHotherthan7.40Acidosisif<7.35Alkalosisif>7.45ClinicalevaluationforthecausaldiseaseIsthepH<7.20or>7.55SeveredisorderPromptcorrectionrequiredIsthePaCO2otherthan40mmHg?VentilationcompensatesorcontributestothedisorderChangetheventilationsothatPaCO2compensatesIsthebasedeficitotherthanzero?Bicarbonateloss/gaincompensatesorcontributestothedisorderInfuseNaHCO3orHCltocorrecttotheprotonconcentrationDoestheurinepHreflectacidosis/alkalosis?Acid/alkalineurineindicatesthatrenalfunctioncompensatedorcontributesRenal-activedrugsorelectrolytereplacementsothatthenephroncontributesIstheaniongap<12mmol/L?Valuesabove12mmol/LsuggestlacticorketoacidosisCorrecttheprimarymetabolicProblemAniongap=[Na+]+[K+]-[Cl-]

AcidosisandAlkalosisDefectCommonCauseBHCO320H2CO31CompensationRespiratoryacidosisRetentionofCO2(decreasedalveolarventilation)DepressionofrespiratorycenterbymorphineCNSinjuryPulmonarydiseaseDenominatorRatiolessthan20:1RenalRetentionofbicarbonate,increasedammoniaformationChlorideshiftintoredcellsRespiratoryalkalosisExcessivelossofCO2(increasedalveolarventilation)Hyperventilation:emotional,severepain,assistedventilation,encephaitisDenominatorRatiogreaterthan20:1RenalExcretionofbicarbonate,retentionofacidsalts,decreasedammonia

formationMetabolicacidosisRetentionoffixedacidsorlossofbasebicarbonateDiabetes,azotemia,lacticacidaccumulation,

starvationDiarrhea,smallbowelfistulaeNumerator

Ratiolessthan20:1Pulmonary(rapid):increasedrateanddepthofbreathingRenal(slow)AsinrespiratoryacidosisMetabolicalkalosisLossoffixedacidsGainofbasebicarbonatePotassiumdepletionVomitingorgastricsuctionwithpyloricobstructionExcessiveintakeofbicarbonateDiureticsNumeratorRatiogreaterthan20:1Pulmonary(rapid):DecreasedrateanddepthofbreathingRenal(slow):AsinrespiratoryalkalosisRespiratoryandMetabolicComponentsofAcid-BaseDisordersAcute(uncompensated)Chronic(partiallycompensated)pHPco2(respiratorycomponent)PlasmaHCO3-(metaboliccomponent)pHPco2(respiratorycomponent)PlasmaHCO3-(metaboliccomponent)RespiratoryacidosisNRespiratoryalkalosisNMetabolicacidosisNMetabolicalkalosisN?

DefectCommonCauseManagementRespiratoryacidosisRetentionofCO2(decreasedalveolarventilation)DepressionofrespiratorycenterbymorphineCNSinjuryPulmonarydiseaseCorrectthepulmonarydefectEndotrachealintubationandmechanicalventilationEncouragedeepbreathing,coughing,humidifiedair,avoidingoversedationRespiratoryalkalosisExcessivelossofCO2(increasedalveolarventilation)Hyperventilation:emotional,severepain,assistedventilation,encephalitisAdjustproperventilatoryrateandvolumeDangerous:1.Complicatewithhypokalemialeadingtoventriculararrhythmias2.AShiftoftheoxygendissociationcurvetotheleft–limitingtheHBtounloadO2attissueMetabolicacidosisRetentionoffixedacidsLossofbase