最新英文班水电解质授课幻灯片.ppt

伴有水、电和酸、碱紊乱的程度1存在严重的脱水,如何补液？2第三间隙的液体急剧积聚，何为第三间隙？3Na+155mmol/l,Cl-115mmol/l,K+6.5mmol/l,Ca1.0mmmol/l，如何纠正？4伴有代谢性酸中毒、呼吸性碱中毒，如何处理？ Fluid&ElectrolyteandAcid-basedisturbancesEnqiangMaoPh.D.DepartmentofSurgery,RuijinHospital,Shanghai Fig15％BodyWeight40％BodyWeight（Female35％）PO4-Na+Na+Na+CI-CI-HCO3-HCO3-K+K+K+protein5%BodyWeightNa+K+ATPaseInterstitialFluid(ISF)PlasmaIntracellularFluid(ICF)ExtracellularFluidIntracellularFluid（ECF）（ICF）AnatomyofBodyFluidsCompartmentsMg2+Protein Howtodifferentiatefunctionandnon-functioninterstitialfluidsFunction:Takingpartinmodulatingthebalanceofbodyfluids. Non-function:Fluidsincavityinnormalstatus.Includingcerebrospinal,joint,pericardiumandabdominalcavityfluids. ThirdSpaceDefinition:Pathophysiologicly,relativelynonfunctionalextracellularfluid.MainlyforthechangeofquantityofnonfunctionalECF. Distribution:exudatesinburns;ascites;softtissueinjuries.bowelwall;peritoneum;infectedlesions.Attention:notconfusedwiththenonfunctioningcomponentsfrominterstitialfluid. TheConceptofOsmoticPressure Pressureleadingtotheshiftofwaterthroughsemi-permeablemembranewaterwaterSemi-permeablemembraneAnionandCationaswellasnon-electrolyteparticles Definitionthenumberofosmoticallyactiveparticlesorionsperunitvolume.Unit:milliosmolesperliter（mOsm/L） PlasmaOsmoticPressureNormalRange=290~310mOsm/L RelationbetweenOsmoticpressureanddistributionofbodyfluidOsmoticPressure：CrystalOPandColloidOPPlasmaCrystalOP:[Na+]contributesamajorportionofOP PlasmaticColloidOP：PlasmaproteincontributesaforceleadingtodistributionofECFInterstitialCrystalOP：Contributestotheshiftofextracellularandintracellularwater PlasmaInterstitialFluidICFECFNa+ColloidOPPlasmaticproteinCrystalOPSemi-permeablemembraneCrystalOPColloidOPCrystalOP TheRegulationofBodyFluidBalanceMaintainingnormalosmoticpressureMaintainingnormalconcentration&IntegraldoseofnatriumMaintainingnormalVolume(Blood-volume) MaintainingosmoticpressureposteriorhypophysisADHDistalrenaltubules&collectingtubuleshypothalamusosmoticpressurereceptorSensitivity：ECFOsmoticpressure±1～2％（6mOsm）ReleaseofADH Maintainingtheconcentration&Integraldoseofnatrium:DistalrenaltublemaculardensaadrenalcortexreninangiotoninaldosteroneIncreasedNa＋reabsorption&eliminatingK＋、DecreasedremovingHCO3-、acidurine Volumeregulation(Blood-volume)Glomerulusparacell+AssayingCVP、AP&PAWPreninangiotoninadrenalcortexaldosterone Classificationofbodyfluidchange(FourTypes)VolumeChanges(ECF)VolumeDeficitVolumeExcessConcentrationChangesHyponatremiaHypernatremia MixedvolumeandConcentrationAbnormalitiesECFDeficitandExcesswithHyponatremiaECFDeficitandExcesswithHypernatremia CompositionChangesAcid-basedisturbancesPotassium,Calcium,Magnesiumabnormalities VolumeChanges IsotonicECFdeficit Etiologies(Acute)External-losses:gastrointestinalfluidsduetovomiting,nasogasticsuction,diarrhea,anddigestivetractfistula Internal-losses:sequestration(ThirdSpace）Softtissueinjuriesandinfection,burnsIntra-abdominalandretroperitonealinflammationintestinalobstruction,bowelwall,peritonitis ClinicalmanifestationsSeeingTablebelow ModerateSevereCNSSleepinessDecreasedtendonreflexesApathyAnesthesiaofdistalextremitiesSlowresponsesStuporAnorexiaComaCessationofusualactivityGIProgressivedecreaseinNausea,VomitingfoodconsumptionRefusaltoeatSilentileusanddistention ModerateSevereCVOrthostatichypotensionCutaneouslividityTachycardiaHypotensionCollapsedveinsDistantheartsoundsCollapsingpulseColdextremitiesTissuesignsSoft,smalltongueAtonicmuscleslongitudinalwrinklingSunkeneyesDecreasedskinturgor(充盈)MetablismTemperatureTemperature IsotonicECFdeficitDiagnosisEtiologyClinicalmanifestation:SeeingTablementionedabove. LaboratoryIncreasedRBC,WBC,PLTandplasmaproteinIncreasedHCTNormalserumsodium&chloridehyperbaricurine IsotonicECFdeficitFluid&electrolytetherapyToeliminateetiologiesQualityofSolution-Isotonicsodiumsolution-LactatedRinger’ssolution Quantityhydropenicquantity＋continuouslossesquantityRateandGoalTomoderateBP&PulserateUrinaryOutput30～50ml/hr IsotonicECFexcessEtiologyIatrogenicSecondarytorenalinsufficiencymajoroperationSeveretraumaInfectionRenalvascularconstrictionIncreasedADH&AldosteroneRetentionofsodium&water IsotonicECFexcessClinicalmanifestationsCirculatoryoverloadBasilarralesHeartfailureTissuesignsSubcutaneouspittingedema IsotonicECFexcessFluid&electrolytetherapyRestrictionofwater&sodiumColloid+DiureticsHypertonicdiuresis:relievecerebro-edema20%mannitol MixedVolumeandConcentrationAbnormalities HypotonicECFdeficit Continuestodrinkwaterwhilelosinglargevolumesofgastrointestinalfluids.Thelossofalargeamountofsalt,suchasviasweat,andkidney.Etiologies(Secondary) Inthepostoperativeperiodwhengastrointestinallossesarereplacedwithonly5%dextroneinwaterorhypotonicsodiumsolution. HypotonicECFdeficitClinicalmanifestationsCNSsigns─increasedintracranialpressure&secondaryhypertensionTissuesigns─excessiveintracellularwaterDigestivesystem:Vomiting,Nausea HyponatremicstatesClinicalmanifestationsShock:ProgressingtooliguricrenalfailurepromptlyAsymptomatic─Untilltheserumsodiumfallsbelow120mmol/L Oneimportantexception─Closedheadinjury,inwhichmildhyponatremiamaybeextremelydeleterious HypotonicECFdeficit-DiagnosisEtiologyLaboratorySerumsodiumconcentration<135mmol/LDecreasedurinarysodiumandHypobaricurine（<1.010）IncreasedHCTandserumBUN&NPN ClinicalManifestation MildormoderatehyponatremiaFluid&electrolytetherapyEliminatingetiologiesQualityofsolution:NS、5%GNSandor10%Nacl SeverehyponatremiaFluid&electrolytetherapyTBW(liters)=Bodyweight(kg)×0.6(female0.5)Sodiumdeficit(mmol)=Serumsodium(standard－actual)×TBWTotalAmount:Halfofsodiumdeficit+Requisiteamountperday Quality:5%sodiumchloridesolution(2/3)+Isotonicsodiumchloride(1/3)Shockcolloid:crystalloid=1:2~3Convulsionsorcoma5%NaCl100~250ml Rateofincrementofsodiumis0.5~1mmol/L/h;andnomorethan12mmol/Lwithin24hs.Complication:OsmoticDemyelinationSyndrome(ODS).Pontinedemyelination(桥脑脱髓鞘样变) Managementofsevereacuteandchronichyponatremia EFW:electrolyte–freewater TherapyforSevereAcutehyponatremiaAim:ShrinkthesizeofbraincellswithhypertonicsalineNa+<120mmol/L,havingseizures.Toraisetheplasma[Na+]by5mmol/Lduringthenexthour. Raising[Na+]to130mmol/Lat1~2mmol/h;and<12mmol/Lwithin24h.Howtocalculatetheamountof10％NaClperhourRaising[Na+/h]×Kg×0.6(女0.5)=theamountofmmolofNaCl TherapyforSevereChronichyponatremiaConvulsionorComa:PNarise<5mmol/Lin2-3hoursNoconvulsion:PNarise<8mmol/L/dayRestrictwaterThinkICFK+ HypertonicECFdeficit Etiology(Primary)Restrictedwaterintakeincircumstances:SweatBurnDiabeticcoma HypertonicECFdeficitClinicalmanifestationsCentralnervesystemrestless,weakness,delirium,maniacalbehevior,comatissuesigns-dryandthirsty,stickymucousmembranes DehydrationfeverTachycardiaOliguria HypertonicECFdeficitDiagnosisEtiologyLaboratoryIncreasedsodium(>150mmol/L)&HCTHyperbaricurine ClinicalManifestationExtremelythirstyHighfeverOliguria HypertonicECFdeficitFluid&electrolytetherapyPrinciples-Adopting5％GS,0.45%NaCl,waterviaintestine-Halfofvolumedeficit＋Requisiteamountperday MeasuresWithloss1%bodyweight，infusing400～500mlsupplementalquantities(ml)=[actualserumsodium－normalserumsodium(mmol/L)]×bodyweight(kg)×4 ClassificationofECFchanges CompositionChanges Hypokelamia(<3.5mmol/L)CommoncauseExcessiveexcretion:Kidney;Digestivetract(Vomiting,Diarrhea,Gastricsuction,Intestinalfistula) Lessin-take:Lessdietaryintake;potassium-freeparenteralfluidsRedistributionThetransferofextracellularpotassiumintocells（Alkalosis） 2K+1H+3Na+CellH++HCO3-=H2O+CO22K+1H+3Na+ General:Anorexia,Nausea,VomitingSkeletalmuscles(Diminishedtoabsenttendonreflexes,respiratoryhypoventilation)Smoothmuscles(Paralyticileus)Cardiacmuscles(Hypotension)HypokelamiaClinicalmanifestations Muscularweakness→Flaccidparalysis(k+<2.5mmol/L）CNS（Serumpotassium＜2.0mmol/L）Morbus→Obnubilation(神志不清)、disorientationHypokelamiaClinicalmanifestations CardiovascularECG:STsegmentdepression,decreasedTwave,IncreasedUwave,T5.5mmol/L)Commoncauses RenalexcretiondecreasedAbnormaldistributionAcidosisAcutetumorlysis,burn,Acuteintravascularhemolysis gastrointestinalNausea&vomitingIntermittentcolic&diarrheaParesthesia(感觉异常)&WeaknessHyperkelamiaClinicalmanifestations CardiovascularBradycardiaMicrocirculatorydysfunction(Becold,cyanosis,paleandhypotension) EKGShorteningofQTintervalandhighpeakedTwave→WidenedQRS,PRintervalprolongation→disappearanceofPwave→degenerationoftheQRStoasinewavepattern→Ventricularasystole(心搏停止)orfibrilationHyperkelamiaClinicalmanifestations AnyinexplicablesymptomsECGSerumpotassiumion>5.5mmol/LHyperkelamiaDiagnosis WithholdingofexogenouslyadministeredpotassiumcorrectionoftheunderlyingcauseAnti-arrhythmia-10%CalciumgluconateinfusedHyperkelamiaTreatment Loweringofserumpotassium-Transferpotassiumintocells（5%NaHCO3;11.2%Sodiumlactate,GI-diuretics-Cation-exchangeresins(oral;maintainingclysis)-peritonealdialysis,orhemodialysis,hemofiltration 高钾血症EKG变化？10分钟内起效？静脉推注葡酸钙去除病因转移到细胞内：胰岛素NaHCO3泌尿系统测尿钾胃肠道减少口服离子交换树脂口服或灌肠尿钾低血液透析增加尿钾排出：盐皮质激素NaHCO3乙酰唑胺是不 DisturbancesofCalciumHypocalcemia(<2.0mmol/L)Causes:acutepancreatitis;renalfailure;intestinalfistula;InfusionofavastreserveofbloodManifestation－Symptoms:numbness;tingling(麻刺感);Apnea;Tetany－Signs:Hyperactivetendonreflexes;Chvostek’sSigns Treatments:10%calciumgluconate;5%CalciumChloride DisturbancesofCalciumHypercalcemia(>4.0mmol/L)Causes:hyperparathyroidism;BonyMetastasisManifestations:Fatigue;VomitingTreatment:EDTA;Na2SO4 Acid-baseimbalanceBuffersystemAweakacidorbase&thesaltofthatacidorbaseIntracellularExtracellularRedcellB.Protein/H.ProteinB.HCO3/H2CO3B.Hb/HHbB2HPO4/BH2PO4B.HbO2/HHbO2AnionGap=[Na+]－[Cl-+HCO3-] Assumption:pre-existingpotassiumdepletionOutcome:Intracellular(3K＋)andextracellular(2Na+、1H+)exchangeIntheregulationofacid-basebalanceTheimportantroleofpotassium DecreasedH+andK+exchange,IncreasedH+andNa+exchangeinrenaltubuleParadoxicalacidurineMetabolicalkalosisisaggravated SensibleacidsareexcretedviathelungHCI＋NaHCO3NaCI＋H2CO3H2O＋CO2Theimportantroleofthelung InsensibleacidsexcretedbykidneyInorganicacidanions（hydrochloric、sulfuric、phosphoricacids）－withhydrogen（H+－Na+exchange）－ammoniumsalts（H+＋NH3→NH4-）Theimportantroleofthekidney organicacidanions（lactic、keto、pyruvicacids）－Bemetabolized－Somerenalexcretion（withhighlevels） BHCO3-pH＝pK＋logH2CO327mmol/L＝6.1＋log1.35mmol/L20＝6.1＋log1＝6.1＋1.3=7.4Henderson-Hasselbalchequation 氧离曲线与组织的缺氧Bohr效应（H+、CO2、O2三者与Hb的关系）HHbO2+H++CO2Hb+O2CO2组织肺部 氧饱和度(SaO2)氧分压(PaO2)正常右移左移HbO2的O2解离曲线(S型) MetabolicAcidosis(pH<7.35) DefectsLossofbasebicarbonate(Aniongapnormality)CauseDiarrhea,Smallbowel,pancreaticfistulasCompensationRenal(slow):RetentionofHCO3-,Excretionofacidsalts,ammoniaformation,ChlorideintoRBC MetabolicacidosisClinicalmanifestationsIncreasedindepth&frequencyofrespiration(Kussmaulbreathing)Peripheralvesselsdilated，Circulatoryshock,Ceriselip Decreasedmusculartension&tendonreflexmergedUnconsciousness MetabolicacidosisTreatmentsPrinciplesTherapyforbasicdiseaseAlkalitreatment:doseinitials1/3~1/2requisiteamountPre-treatment:serumK+&Ca++ TheamountofAlkalinecessary-（normalCO2-CPserumCO2-CP）×TBW（Kg）×0.4-（BE＋3）×BW（Kg）×0.4-（normalSBobservedSB）×BW（Kg）×0.4＝Lossofbase(mEq)MetabolicacidosisTreatment SomeofalkalescentsolutioncontainsHCO3-1gmNaHCO3＝12mmolHCO3-1ml-11.2%NaC3H5O3＝1mmolHCO3-1ml-3.63%THAM(三羟甲基氨基甲烷)＝0.3mmolHCO3-MetabolicacidosisTreatment RespiratoryAcidosis(pH<7.35) RespiratoryAcidosisClinicalmanifestationAdvancedrespiratoryinsufficiency(Apnea)Metabolicencephalopathy(headache,drowsiness,stuporandcoma,papilledema) Bloodpressureelevated→reducedVentricularfibrillation(hyperkalemia) RespiratoryAcidosisTreatmentTreatmentofCausesToimproveventilationAlkalescentsolutionisharmful!! Metabolicalkalosis(pH>7.45) PeripheralvesselconstrictedMentalsymptoms:Delirium,DrowsinessMetabolicalkalosisClinicalmanifestations Decreasedindepth&frequencyofrespirationTetany&tendonreflexaccentuation TherapyforbasicdiseaseCorrectionoftheunderlyingdisturbancesLossofgastricfluidreplacedwithNSorGNSpotassiumdeficitcorrectionofhypokalemiaSerumHCO3－,45～50mmol/L，pH>7.650.1MhydrochloricacidsolutionIVMetabolicalkalosisTreatment Hydrochloricacid（mmol）＝[actualserumHCO3--normalserumHCO3-（mmol/L）]×BW（kg）×0.4＝[normalplasmaCI－-actualplasmaCI－（mmol）]×BW（kg）×0.2×0.6Theinitialdoseofhydrochloricacid:1/2doseofabovementionedMetabolicalkalosisTreatment Respiratoryalkalosis(pH>7.45) IncreasedrateanddepthofbreathingMentalsymptomParesthesiawithTetanyRespiratoryalkalosisClinicalmanifestation TherapyforbasicdiseaseIncreasepulmonarydeadspace5%CO2addedtotheinspiredair－Dangerous!!!RespiratoryalkalosisTreatment Howtodifferentiatethefourtypesofacid-baseimbalanceArterialbloodgasestestAB:actualbicarbonate(Bothmetabolismandrespiration)SB:Standardbicarbonate(Onlymetabolism) SB：38℃760mmHgPCO240mmHgfullyoxygenatedHbBE:Baseexcess Thefourtypesofacid-basedisturbances