酸中毒和碱中毒课件

酸中毒和碱中毒酸中毒和碱中毒1CaseCase2CaseA22-year-oldwomanwhohadbeeninjuredinanaccidentreceived6litersofisotonicsaline,Theplasma[Na]135mmol/l,[K]3.8mmol/l,[Cl]115mmol/l,and[HCO3]18mmol/l.ThebloodpH7.28,andthePaCO239mmHg.Theurinarysodium65mmol/l,potassium15mmol/l,andchloride110mmol/l.Thepatient’sserumalbumin2.7g/dlaftertheinfusionofsaline.Herbloodpressurewas98/52mmHg,andherpulseratewas102beats/m.Shehadbeenhealthybeforetheaccident,wasreceivingnomedications,anddidnotuseanyillicitdrugs.Theaccidentoccurredwhenaspeedingcarranthrougharedlight,hittinghercaronthedriver’sside.Theaccidenthascausedmultipleribfractures,acompoundleftfemoralfracture,apelvicfracture,andnumerousbruises.Sheisintheemergencydepartmentforstabilizationofherconditionbeforeshecanbesenttotheoperatingroomforstabilizationofherlegandpelvis.CaseA22-year-oldwomanwhoha3CaseA22-year-oldwomanwhohadbeeninjuredinanaccidentreceived6litersofisotonicsaline,Theplasma[Na]135mmol/l,[K]3.8mmol/l,[Cl]115mmol/l,and[HCO3]18mmol/l.ThebloodpH7.28,andthePaCO239mmHg.Theurinarysodium65mmol/l,potassium15mmol/l,andchloride110mmol/l.Thepatient’sserumalbumin2.7g/dlaftertheinfusionofsaline.Herbloodpressurewas98/52mmHg,andherpulseratewas102beats/m.Shehadbeenhealthybeforetheaccident,wasreceivingnomedications,anddidnotuseanyillicitdrugs.Theaccidentoccurredwhenaspeedingcarranthrougharedlight,hittinghercaronthedriver’sside.Theaccidenthascausedmultipleribfractures,acompoundleftfemoralfracture,apelvicfracture,andnumerousbruises.Sheisintheemergencydepartmentforstabilizationofherconditionbeforeshecanbesenttotheoperatingroomforstabilizationofherlegandpelvis.什么酸碱紊乱？代谢、呼吸？AG酸中毒、高氯性简单/复杂性？CaseA22-year-oldwomanwhoha4酸中毒和碱中毒课件5酸中毒和碱中毒课件6AcidproductioninthebodyCarbonicacid: themetabolismofcarbohydratesandfats(primarilyderivedfromthediet)resultsintheproductionofapproximately15,000mmolofCO2perday.Non-carbonicacid:Organic:lactate,metabolizedbytheliverandkidneyInorganic: themetabolismofproteinsandothersubstancesresultsinthegenerationofnoncarbonicacids(50–100mEq,1mEq/kg).

Methionine—>glucose+urea+SO4(2-)+2H+ Arginine+—>glucose(orCO2)+urea+H+ R-H2PO4+H2O—>ROH+0.8HPO42-/0.2H2PO4-+1.8H+AcidproductioninthebodyCar7Thehomeostaticresponsetoacidload

Chemicalbufferingbytheextracellularandintracellularbuffers.ChangesinalveolarventilationtocontrolthePCO2.AlterationsinrenalH+excretiontoregulatetheplasmaHCO3-concentration.Thehomeostaticresponsetoac8ChemicalbufferingExtracellularbuffersIntracelluar:boneChemicalbufferingExtracellula9Henderson-Hasselbalchequation(Eq.1)H++HCO3-<—>H2CO3<—>H2O+CO2PCO2(Eq.2)[H+]=24x————[HCO3-]orbytheHenderson-Hasselbalchequation[HCO3-](Eq.3)pH=6.10+log———————0.03PCO2Henderson-Hasselbalchequation10Henderson-Hasselbalchequation(Eq.1)H++HCO3-<—>H2CO3<—>H2O+CO2PCO2(Eq.2)[H+]=24x————[HCO3-]orbytheHenderson-Hasselbalchequation[HCO3-](Eq.3)pH=6.10+log———————0.03PCO2Acidosis:PCO2=1.5XHCO3+8

Henderson-Hasselbalchequation11ChemicalbufferingExtracellularbuffersIntracelluarbuffer:bone,Ca++release,osteoclastactivationChemicalbufferingExtracellula12Thehomeostaticresponsetoacidload

Chemicalbufferingbytheextracellularandintracellularbuffers.ChangesinalveolarventilationtocontrolthePCO2.

AlterationsinrenalH+excretiontoregulatetheplasmaHCO3-concentration.Thehomeostaticresponsetoac13Thehomeostaticresponsetoacidload

Chemicalbufferingbytheextracellularandintracellularbuffers.

ChangesinalveolarventilationtocontrolthePCO2.

AlterationsinrenalH+excretiontoregulatetheplasmaHCO3-concentration.Thehomeostaticresponsetoac14酸中毒和碱中毒课件15RENALHYDROGENEXCRETION(1)reabsorptionofthefilteredHCO3-(2)excretionofthe50to100meqofH+producedperdayFormationoftitratableacidExcretionofNH4+intheurineRENALHYDROGENEXCRETION(1)re16CollectingtubuleTubularLumenPeritubularcapillaryH+H2O2OH-+CO23HCO3-CAH+Cl-ATPaseATPaseH+K+ExcretionofH+inaintercalatedcellsH+H+CollectingtubuleTubularLumen17CollectingtubuleTubularLumenPeritubularcapillaryH+H2O2OH-+CO23HCO3-CAH++HPO42-H2PO4Cl-ATPaseATPaseH+K+ExcretionofH+inaintercalatedcellsCollectingtubuleTubularLumen18CollectingtubuleTubularLumenPeritubularcapillaryH+H2O2OH-+CO23HCO3-CAH++NH3NH4+Cl-H+-ATPaseNH3ExcretionofH+inaintercalatedcellsCollectingtubuleTubularLumen19CanbestimulatedbylowKCanbestimulatedbylowK20Acid-basebalanceThekidneysmustexcretethe50to100meqofnoncarbonicacidgeneratedeachday.ThedailyacidloadisexcretedasNH4+andH2(PO4).ThedailyacidloadalsocannotbeexcretedunlessvirtuallyallofthefilteredHCO3-hasbeenreabsorbed,becauseHCO3-lossintheurineisequivalenttoaddingH+ionstothebody.Regulation:TheextracellularpHtheeffectivecirculatingvolume,aldosterone,andtheplasmaK+concentrationCanbeindependentofserumpHAcid-basebalanceThekidneysm21Stepsinacid-basediagnosisObtainarterialbloodgas(ABGs)andelectrolytessimultaneouslyCompare[HCO3-]onABGsandelectrolytestoverifyaccuracyCalculateaniongap(AG)Know4causesofhighAGacidosisKetoacidsisLacticacidacidosisRenalfailureToxinsKnow2causesofhyperchloremicornongapacidosisBicarbonatelossfromGI,RTAEstimatecompensatoryresponseCompareΔAGandΔHCO3-Comparechangein[Cl]withchangein[Na]Stepsinacid-basediagnosisOb22Henderson-Hasselbalchequation(Eq.1)H++HCO3-<—>H2CO3<—>H2O+CO2PCO2(Eq.2)[H+]=24x————[HCO3-]orbytheHenderson-Hasselbalchequation[HCO3-](Eq.3)pH=6.10+log———————0.03PCO2Acidosis:PCO2=1.5XHCO3+8

Henderson-Hasselbalchequation23酸中毒和碱中毒课件24酸中毒和碱中毒课件25酸中毒和碱中毒课件26MetabolicacidosisInfluxoforganicacidintoplasma(highaniongap)KetoacidosisLacticacidosisPoisoningAccumulationofendogenousacids(highaniongap)RenalfailureExternallossesofbicarbonate(normalaniongap;hyperchloremic).GIlossRenallossMetabolicacidosisInfluxofor27AnionGapAG=Na+-Cl--HCO3-=12±2albumin:negativecharged.LowserumalbuminwillreduceAG.Paraprotein(Igorlightchains,MM):positivecharged.PresenceoflargeamountofparaproteinreducesAG.AnionGapAG=Na+-Cl--HCO3-=1228AnionGapAnionGap29CausesofaHighAnionGapMetabolicAcidosisCausesofaHighAnionGapMet30TypesandCausesofLacticAcidosisTypesandCausesofLacticAci31TypesandCausesofLacticAcidosisTypesandCausesofLacticAci32RenalfailureWithmildtomoderatereductionsinGFR,theacidosisreflectsdecreasedammoniagenesisandisthereforehyperchloremic.Askidneyfailureworsens,thekidneylosesitsabilitytoexcretevariousanions,andtheaccumulationofsulfate,phosphate,andotheranions,producesanelevatedAG.RenalfailureWithmildtomode33RenalfailureDespiteadailynetpositiveacidbalance,itisunusualfor[HCO3−]tofalllowerthan15mmol/L.Thebufferingofprotonsbyboneresultsinlossofcalciumandanegativecalciumbalance.Chronicacidosiscausesproteinbreakdown,musclewasting,andanegativenitrogenbalance.Maintenanceoftheacid-basebalanceclosetonormalcanpreventtheseconsequencesRenalfailureDespiteadailyn34TreatmentAlkalireplacementNaHCO3SodiumcitrateTreatmentAlkalireplacement35HyperchloremicMetabolicAcidosisCauses:Renallossofalkali–RTAGIlossofalkaliReciprocalchangesin[Cl]and[HCO3]resultinnormalAGIntheabsenceofsucharelationshipsuggestsamixeddisturbanceHyperchloremicMetabolicAcido36DiarrheaMetabolicacidosisMetabolicacidosisandhypokalemiaincreaserenalsynthesisandexcretionofNH4+,thusurinarypHisaround6UrinaryNH4levelsarehigh:urineaniongapisnegativeDiarrheaMetabolicacidosis37酸中毒和碱中毒课件38ProximalRTA(type2)ThethresholdforHCO3-reabsorptionintheproximaltubuleislower(normal:26-28mmol/l).ThedistalnephronhasalowcapacityforHCO3reabsorption.Self-limitedbicarbonaturiaInthesteadystate,theserumHCO3concentrationusuallyis16–18mmol/l,whenallthefilteredHCO3isreabsorbed.Despitesystemicacidemiadevelopment,theurinepHisalkaline.Howeverundersteadystate,theurinecanbeacidifiedtoapHoflessthan5.5.ProximalRTA(type2)Thethres39HCO3HCO3HCO3HCO3HCO3HCO340ProximalRTA:hypokalemiaIncreaseddistalNa+delivery(NaHCO3)Increasedaldosteronelevels(dehydrationbecauseoflossofNaintheurine).TreatmentofacidosiswithHCO3improvestheacidosisbutworsensthedegreeofhypokalemia.ProximalRTA:hypokalemiaIncre41CausesofProximalRTAInheritedpRTA:NBCe1/SLC4A4)mutation,accompaniedbyocularabnormalitiessuchascataracts,glaucoma.Carbonicanhydraseinhibitor:acetazolamideFanconisyndrome:inheritedandacquiredAdultwithFanconi:dysproteinemicconditionsuchasmultiplemyelomaCausesofProximalRTAInherite42dRTA(type1)SystemicacidosisindRTAtendstobemoreseverethaninpatientswithaproximalRTA(serumHCO3-canreachaslowas10mmol/lvs16to18mmol/l)Hypokelemiacanalsobesevere:musculoskeletalweaknessNephrolithiasisandnephrocalcinosisdRTA(type1)Systemicacidosis43HCO3HCO3HCO3HCO3HCO3HCO344dRTA:kidneystoneUrinarycalciumexcretionishighAcidosisinducedbonemineraldissolutionLowintraluminalconcentrationofHCO3-becauseofacidosisUrinarycitratelevelsarelow–citrateserveasthemajorCa++chelatorintheurineHighurinepHdecreasethesolubilityofcalciumphosphatecomplexes.dRTA:kidneystoneUrinarycalc45dRTAPrimary:idiopathicorinherited(SLC4A1mutation)Systemicdisease:SjogrensyndromedRTAPrimary:idiopathicorinh46dRTA-diagnosisNH4ClFurosemide+mineralocorticoid(fludrocortisone)dRTA-diagnosisNH4Cl47dRTAHyperchloremicacidosisKidneystoneHypokalemiaSjogrensyndromedRTAHyperchloremicacidosis48Type4RTARenalfunctioncompromisedHyporeninemichypoaldosteronismHyperkalemiaUrinaryammoniumexcretiondepressedType4RTARenalfunctioncompr49MetabolicAlkalosisAnelevatedarterialpHAnincreaseintheserum[HCO3-]andaincreaseinPCO2OftenaccompaniedbyhypochloremiaandhypokalemiaMetabolicAlkalosisAnelevated50PathogenesisGenerativestage:lossofacidMaintenancestage:volumecontraction,alowGFRordepletionofClorKPathogenesisGenerativestage:51DifferentialdiagnosisMineralocorticoidexcessBartter’sorGitelman’sDiureticsDifferentialdiagnosisMineralo52MetabolicalkalosisassociatedwithECFVcontraction,Kdepletion,andsecondaryhyperreninemichyperaldosteronismGastrointenstinalHCO3retention+volumecontractionRenaloriginDiureticsNonreaborbableanionsandmagnesiumdeficiencyPotassiumdepletionAftertreatmentoflacticacidosisorketoacidosisposthypercapniaMetabolicalkalosisassociated53MetabolicalkalosiswithECFVexpansion,hypertensionandhyperaldosteronismMineralocorticoidadministrationorexcessproductionSymptoms:changesincentralandperipheralnervoussystemfunction:confusion,obtundation,apredispositintoseizures…Relatedelectrolyteabnormalities:hypokalemiaTreatmentCorrectingtheunderlyingstimulusforHCO3generationRemovingthefactorsthatsustainHCOreabsorption(ECFVcontraction)MetabolicalkalosiswithECFV54RespiratoryacidosisSeverepulmonarydisease,respiratorymusclefatigueorabnormalitiesinventilatorycontrolAcute:immediatecompensatoryelevationinHCO3,whichincreases1mmol/Lforevery10mmHgincreaseinpCO2Chronic(>24h):renaladaptationincreasesthe[HCO3]by4mmol/LRespiratoryacidosisSeverepul55ClinicalfeaturesTheclinicalfeaturev