acid-base-disturbance(酸碱平衡紊乱).ppt

Acid-basedisturbanceSection1.Acid-BaseBalanceSection2.Simpletypesofacid-basedisturbanceSection3.MixedAcid-baseDisturbanceSection1.Acid-BaseBalance(1)Sourcesofacidandbase(2)Regulationofacid-basebalance(3)Laboratoryparametersofacid-basebalanceHomeostasisisveryimportantforlife.Acid-base balance is one of the majorrequirements(volume,osmolarityofthebodyfluid,etc.).Thebasicmeaningofacid-basebalanceisthestableH+inthebodyfluid.(1)SourcesofacidandbaseThemainoriginofacidandbaseisthe intracellular metabolism(catabolismofprotein,carbohydrateandfat).Twokindsofacidsareformedfrommetabolism:1)volatileacid,2)nonvolatileacid.Thevolatileacidistheacid,whichcanbeeliminatedfromlung(respiration).Thenonvolatileacidhastobeeliminatedfromkidneyswithinurine.1)VolatileacidTheCO2istheend-productofoxidativemetabolismofprotein,carbohydrateandfat.ThedailyproductionofH+(H2CO3)is1315(20)Mol.H2CO3canbedissociatedtoformhydration(H2O)andCO2.CA(carbonicanhydrase)H2CO3-H2O+CO2TheCO2canbeeliminatedfrompulmonaryexpiration,soH2CO3isvolatileacid.2)unvolatileacid(fixedacid)Uric acid,phosphoric acid(H3PO4)andsulfuric acid(H2SO4)are the products in the metabolicprocessofproteinsandnuclearacids.Lacticacidandketonicbodies(-hydroxybutyricacid-羟丁酸andacetoaceticacid乙酰乙酸)can be formed from the metabolicprocessofcarbohydrateandfatasintermediateproducts,when the oxygen supply is notsufficiency.(H+=70100mmol/perday)3)BaseThe production of acid(H2CO3,organicacids)ismuchmorethantheproductionofbase(deaminationofAANH3)fromthemetabolisminnormaldiet.The vegetables,and fruits also containssomebase(suchascitrate(柠檬酸盐)oxalate(草酸盐)theH+acceptor).Citrate+H+=citricacid(2)Regulationofacid-basebalance1)Chemicalbuffers2)Respiratoryregulation3)Renalregulation4)Cellularregulation1)ChemicalbuffersBufferpair(buffersystem)consistsofaweakacidanditsconjugatebase,suchasNaHCO3Na2HPO4Hb-Pr-HbO-2-H2CO3NaH2PO4HHbHPrHHbO2H2SO4+NaHCO3=Na2SO4+H2CO3Toconvertstrongacid(H2SO4,HCl)orstrongbaseintoaweakacidorbase.TominimizechangesofH+.Immediatelyavailable(firstdefenseline)Note,H2CO3/HCO3-systemcannotbuffervolatileacid.(Hb/HbO2system)buffersystemthe%account-HCO-3/H2CO353%Hb-/HHbHbO-2/HHbO235%Pr-/HPr7%Phosphate5%-NaHCO3canbeeffectivelyeliminatedbykidneysand(H2CO3 H2O+CO2)CO2canbeeffectivelyeliminatedbythelung.-“openbuffersystem”HCO-3/H2CO3isthemostimportantbufferpair.CO2Cl-CO2+H2OC.A.H2CO3HCO-3H+-Hb-RBCHb-/HHbandHbO-2/HHbO2buffersystem2)RespiratoryregulationAlveolarventilationiscontrolledbymedullaryrespiratorycenter,withCO2,pH,O2asitsmainstimuli.peripheralchemoreceptors(carotid/aorticbody)AlthoughthecentralchemoreceptorissensitivetothechangesofH+,H+isdifficulttodiffuseacrosstheblood-brainbarrier.AsCO2canfreelydiffuseacrosstheblood-brainbarrier,therespiratorycenterresponsesrapidlytotheperipheralchangesofPaCO2andslowlytothatofH+.IncreasedPaCO2(60mmHg,8kPa)andthedecreasedpHofESFcanstimulatetherespiratorycenterviacentralorperipheralchemoreceptorsandincreasethedepthofrespiration(hyperventilation,tidalvolumeincreased).MoreCO2canbeeliminatedfromlung,sothattheH2CO3inbloodwillfalltonormalrange,thepHwillincreasetonormalbyregulatetheratioofHCO3-andH2CO3.Characteristics(a)Timeliness.Therespiratoryresponsebeginswithinseveralminutes.Therespiratoryresponseoftentakes30minutesfortherespiratorycompensation.1224hourstogetmaximalcompensation.(b)PaCO260mmHg:stimulatesrespiratorycenter.80mmHg:inhibitsrespiratorycenter.(CO2narcosis)3)RenalregulationRenalcompensationbeginsfromseveralhoursaftertheadditionofacidload,anditmaytake35daystoreachthemaximumofthiscompensatorycapacity.KidneysplayamajorroleintheregulationofpHinthebody.Therenalregulationconsistsoftwoprocesses.(a)Excretionofacids1)SecretionofH+,NH4+2)Excreteallthenonvolatileacid(70100mmol/perday)producedfromcatabolismoffood.(b)Reabsorbproperlythebicarbonatefilteredfromglomerulus.WhenthepHisdecreased,morebicarbonateneedstobereabsorbed.IfthepHisincreased,morebicarbonatewillbeeliminated.MechanismsofH+excretionandHCO3reabsorption:inproximaltubule:ViaNa+-H+antiportor(NHE反向转运体)ViasecretionofNH3/NH4+indistaltubule+collectingductViaH+-ATPaseViasecretionofNH3/NH4+ViaCl-HCO3-exchangerinproximaltubule:Na+-H+antiportor（NHE）At end,1mol H+excretes into the lumen from tubular epithelial cells,and 1mol HCO3-is increased in the blood.CO2H2OH2CO3HCO3-HNaTubularepithelialcellTubularlumenCANaKNa-K-ATPNaHCO3-HH2CO3CO2H2OCAWhenacidosisoccur,theactivityofcarbonicanhydrase。CapillarytubeNaCO2Via secretion of NH3/NH4+H2CO3HCO3-HNaNaKNa-K-ATPNaNH4GlutamineGlutamate ketoglutarate酶酶glutamineNH3 glutamate(glutaminase)glutamateNH3-ketoglutarate(glutamatedehydrogenase)-ketoglutarate2e2HCO3-NH4TubularlumenTubularepithelialcellCapillarytubeindistaltubule+collectingductCO2H2OH2CO3HCO3-HH-ATPCl-HPO42-H2PO4-pHCAalkalineacidicAcidificationofurineDistalacidificationTubularlumenH-ATPaseCl-HCO3exchangerTubularepithelialcellCapillarytubeCO2H2OH2CO3HCO3-HH-ATPCl-CANH4NH3NH3NH3TubularlumenTubularepithelialcellCapillarytube4)Cellularregulation(a)H+-K+exchange(b)Cl-HCO3exchange(c)Utilizingofbonesalt(d)SynthesisofureafromNH3(a)H+-K+exchangeWhenHWhenH+inECFinECF(serum)isincreased,the(serum)isincreased,theH H+willmoveintothecells,willmoveintothecells,asaexchangeforelectricalasaexchangeforelectricalneutrality,Kneutrality,K+willshiftwillshiftfromICFtotheECF.SofromICFtotheECF.SothepHofECF(serum)willthepHofECF(serum)willincreasetonormal,butincreasetonormal,buthyperkalemiahyperkalemiamayoccur.mayoccur.(b)Cl-HCO3exchangeWhenCO2inECF(serum)isincreased,CO2willmoveintothecells,CO2combinesH2Otoformcarbonicacid,thenH2CO3dissociatestoformH+andHCO3,theHCO3movesoutoftheRBC,forneutrality,Clmovesintothecells.(c)UtilizingofbonesaltIn chronic metabolic acidosis,bone salt,Ca3(PO4),isalsoutilizedasabufferbase,buttheexpenseisdecalcificationofboneandosteoporosis(looseandsoftbone).Ca3(PO4)2+4H+3Ca2+2H2PO4(d)SynthesisofureafromNH3inlivercells.(3)Laboratoryparametersofacid-basebalance1)pH2)PaCO23)Standardbicarbonate(SB)Actualbicarbonate(AB)4)Bufferbase(BB)5)Baseexcess(BE)6)Aniongap(AG)1)pHpHisthenegativelogarithm(-log)ofH+inasolution.H+=40nmol/L(pH=7.4)Thenormalrangeinarteryblood=7.357.45(7.41)ThesurvivalrangeofpH=6.87.8AccordingtotheHenderson-Hasselbalchequation:The The pKapKa is the dissociation constant of carbonic acid(=6.1)is the dissociation constant of carbonic acid(=6.1)24 HCO 24 HCO3 3 metabolic factor metabolic factorpH=6.1+log -pH=6.1+log -1.2 H 1.2 H2 2COCO3 3 respiratory factors respiratory factors 20 20 =6.1+log-=6.1+1.3=7.4=6.1+log-=6.1+1.3=7.4 1 1ThepHisdeterminedbytheratioofThepHisdeterminedbytheratioof HCO HCO3 3 20 20 -=-=-H H2 2COCO3 3 1 1 Note:Note:NomatterhowtheabsoluteamountsofHCONomatterhowtheabsoluteamountsofHCO3 3 andHandH2 2COCO3 3change,oncetheratioremains20/1,thepHchange,oncetheratioremains20/1,thepHwouldbe7.4(normal).wouldbe7.4(normal).Clinicalsignificance(anticoagulantarteryblood,insulationofair)A normal range of pH may represent threedifferentsituations:acid-basebalance;compensatoryacidosisoralkalosis;amixeddecompensatoryacidosisanddecompensatoryalkalosis.pH7.45decompensatoryalkalosis2)PaCO2PaCO2isthetensionofCO2dissolvedinarterialplasma.Thenormalrange=3346(40)mmHg(mercury)(4.396.25kPa).Generallyspeaking,thePaCO2isdeterminedmainlybytherespiration,sothePaCO2iscalledthe“respiratoryfactor”.Hyperventilation-PaCO2Hypoventilation-PaCO2SignificancePaCO246mmHgPrimaryincrease:respiratoryacidosisSecondaryincrease:metabolicalkalosis(compensatedbylung)PaCO2SB(CO2retention),thereasonmustbetheeffectofrespiratoryfactor,whichindicatesrespiratoryacidosisormetabolicalkalosiscompensatedbylung.IfABSB(CO2depletion),thereasonmustbetherespiratoryfactor,whichmeansrespiratoryalkalosisorthemetabolicacidosiscompensatedbylung.4)Bufferbase(BB)SumofallbufferbasesinbloodInplasma:HCO3=24Protein=17InRBC:HbHbO2=6.3HPO42=1.0BB=4552mmol/L(48)Determinedbymetabolicfactors5)Baseexcess(BE)Under“standardcondition”(temperature3738,fullUnder“standardcondition”(temperature3738,fulloxygenationofhemoglobin,PaCO2=40mmHg),oxygenationofhemoglobin,PaCO2=40mmHg),titratethewholebloodtopH7.4withhowmuchthewholebloodtopH7.4withhowmuchacidorbase(acidorbase(mmolmmol/L)./L).Ifwithacid,thereismustmorebase(excess)intheIfwithacid,thereismustmorebase(excess)intheblood,BEisexpressedwithpositivevalueblood,BEisexpressedwithpositivevalueIfwithbase,thereismustmoreacid(deficit)intheIfwithbase,thereismustmoreacid(deficit)intheblood,BEisexpressedwithnegativevalueblood,BEisexpressedwithnegativevalueNormalBE=-3.0+3.0NormalBE=-3.0+3.0OnlymetabolicfactordeterminestheBE.OnlymetabolicfactordeterminestheBE.InmetabolicalkalosisthepositiveBEincreases.InmetabolicalkalosisthepositiveBEincreases.InmetabolicacidosisthenegativeBEincreases.InmetabolicacidosisthenegativeBEincreases.6)Aniongap(AG)UCUCUAUANa+ClCl HCOHCO3 3 DeterminedDeterminedcationcationundeterminedanionsundeterminedcationsAGisthedifferencebetweenunmeasuredanion(UA)andAGisthedifferencebetweenunmeasuredanion(UA)andunmeasuredunmeasuredcationcation(UC).AG=UA-UC(UC).AG=UA-UCDeterminedDeterminedanionanionUCUCNa+ClClHCOHCO3 3 AGUAUAn nAccordingtotheprincipleoftheAccordingtotheprincipleoftheelectroneutralityelectroneutrality:UA+HCO3+UA+HCO3+ClCl=UC+Na=UC+Na+n nTheAGcanbecalculatedby:TheAGcanbecalculatedby:AG=UA-UCAG=UA-UCandandUA-UC=NaUA-UC=Na+-(-(ClCl+HCO3+HCO3)SoAG=NaSoAG=Na+-(-(ClCl+HCO3+HCO3)n nThenormalrangeis1014Thenormalrangeis1014mmolmmol/L./L.n nAGindicatesthoseanions,AGindicatesthoseanions,otherthanHCO3otherthanHCO3 andandClCl.Actually the AG represents the proteinswithnegativecharge,phosphate,sulfateandorganicanions(lacticacid,keto-acid,etc.).An increased AG is the same meaning astheaccumulationofnonvolatileacidsinthebodyandmustbethemetabolicacidosis.Significance(a)Fortheclassificationofmetabolicacidosis1)metabolicacidosiswithnormalAG(withincreasedCl)2)metabolicacidosiswithhighAG(withnormalCl).(b)Diagnosisofmixedacid-baseimbalancesSection2.Simpletypesofacid-basedisturbanceAcidosis(acidemia)occurswhenpHdropsbelow7.35Alkalosis(alkalemia)occurswhenthepHrisesabove7.45AprimaryrespiratoryproblemisdeterminedifthePaC02islessthan33mmHg(alkalosis)orgreaterthan46mmHg(acidosis).AprimarymetabolicproblemiswhentheHC03islessthan22mEq/L(acidosis)orgreaterthan27mEq/L(alkalosis).1.metabolicacidosisconcept:theprimarydisturbanceisadecreaseofHCO-3inthearterialplasma1)causeandpathogenesis-Excessiveproductionoffixedacidslacticacidosis:ischemia,hypoxiaglycolysisheartfailure/shock/respirotoryfailureketoacidosis:diabetes,starvationlipolysis-Disordersintheexcretionofacidicmetabolitesrenal failure:GFR,elimination of fixedacidstypeIrenaltubularacidosis(RAT-I):excretionofNH41)causeandpathogenesis-ExcessivelossofHCO3-lossfromintestinaljuice:diarrhea,tubedrainage(引流),intestinalfistulas(瘘)type-IIrenaltubularacidosis(RAT-II):CA,excretionofHandreabsorptionofHCO3-Excessiveintakeofexogenousacids:NH4Cl,aspirin-Blooddilution-Hyperkalemia:H-Kexchange2)classification-NormalAGmetabolicacidosislossofHCO3fromintestinalorrenalroutes,ordepletionofHCO3bybufferingfixedacidstomaintainelectroneutrality,Cl-HighAGmetabolicacidosisfixedacids-H+unmeasuredanionbuffering,HCO3replacethenegativechargesofdecreasedHCO3thus,ClisnormalNaAGHCO3-Cl-AGHCO3-NaAGHCO3-Cl-ClHCO3-3)compensatoryregulationbuffer:first line of defenserespiratorycompensationKussmaul/hypocapniacellularcompensationhyperkalemiarenalcompensationrenal dysfunction H+:C.A.H+,NH3secretionreabsorptionofHCO34)changesofacid-baseparameterspH7.35;SB;AB;ABSBBB;negativevalueofBE;PaCO2secondarily5)effectonbody cardiovascularsystemhyperkalemiaarrhythmiaH+:contractilityperipheralresistancecentralnervoussystemH+ATP,-aminobutyricacid(somnolence嗜睡,coma)3)respiratorysystemKussmaulbreathing4)osseoussystembonegrowth,rickets(佝偻病）,osteodystrophy（骨营养不良）6)principlesoftreatmentMETABOLICACIDOSIS-metabolic balance before onset of acidosis-pH 7.4-metabolic acidosis-pH 7.1-HCO3-decreases because of excess presence of ketones,chloride or organic ions-bodys compensation-hyperactive breathing to“blow off”CO2-kidneys conserve HCO3-and eliminate H+ions in acidic urine-therapy required to restore metabolic balance-lactate solution used in therapy isconverted to bicarbonate ionsin the liver0.5102.respiratoryacidosisconcept:TheprimarydisturbanceisanelevationinplasmaH2CO31)causeandpathogenesisBarbital（镇静剂sedative）depressionofCNSheadinjuryCO2breatheparalysisofrespiratorymusclesoutdiseaseofairwayorlungchestinjuryinhalationofCO22)compensationbuffer:H2CO3 system RBC buffer respiratorycompensationcellularcompensationH+-K+exchangerenalcompensationmain,but slowacute respiratory acidosisisoftendecompensated.CO2RBCCO2H2OH2CO3HHCO3-Hb(O2)-HHb(O2)Cl-HCO3-Cl-3)changesofacid-baseparameterspH7.45;PaCO2;ABSBBBBE;ABSB4)effectsonbodyItisassameasmetabolicalkalosis,butmoreeasier.-dizziness(头晕)andconvulsion(抽搐)-neuromuscularexcitability5)principlesoftreatmentinhalationof5%CO2RESPIRATORYALKALOSIS-metabolic balance before onset of alkalosis-pH=7.4-respiratory alkalosis-pH=7.7-hyperactive breathing“blows off”CO2-bodys compensation-kidneys conserve H+ions and eliminate HCO3-in alkaline urine-therapy required to restore metabolic balance-HCO3-ions replaced by Cl-ions1.doubleacid-basedisturbance1)metabolicacidosisplusrespiratoryacidosisheartbeatHCO-3respirationstopcharacterPaCO2pH2)metabolicalkalosisplusrespiratoryalkalosishepaticfailure/feverPaCO2diuretic/vomitingcharacterHCO-3pH3)respiratoryacidosisplusmetabolicalkalosispulmonaryheartdiseasediureticpHSection3.MixedAcid-baseDisturbance4)respiratoryalkalosisplusmetabolicacidosisinfectiveshock/diabetes/renalfailurefeverpH5)metabolicacidosisplusmetabolicalkalosisketoacidosis(diabetes)vomitingpH2.tripleacid-basedisturbance1)respiratoryacidosis/metabolicacidosis/alkalosispulmonaryheartdisease;vomiting2)respiratoryalkalosis/metabolicacidosis/alkalosisfever;vomiting;diarrhea(foodpoisoning)BasicQuestionsTherearethreecriticalquestionstokeepinmindwhenattemptingtointerpretarterialbloodgases(ABGs).FirstQuestion:Doesthepatientexhibitacidosisoralkalosis?SecondQuestion:Whatistheprimaryproblem?Metabolic?orRespiratory?ThirdQuestion:Isthepatientexhibitingacompensatorystate?InordertounderstandABGanalysisandrememberwhatisabnormal,youneedtoreviewwhatisnormal.RememberDefinitionsAcidosis(acidemia)occurswhenpHdropsbelow7.35Alkalosis(alkalemia)occurswhenthepHrisesabove7.45AprimaryrespiratoryproblemisdeterminedifthePaC02islessthan35mmHg(alkalosis)orgreaterthan45mmHg(acidosis).AprimarymetabolicproblemiswhentheHC03islessthan22mEq/L(acidosis)orgreaterthan26mEq/L(alkalosis).AssessmentStep1StepOne:Determinetheacid/basestatusofthearterialblood.KeepinmindwhatisNormalIfthebloodspHislessthan7.35thisisanacidosis,andifitisgreaterthan7.45thisisanalkalosis.Youmayhearnursesordoctorssay:ThepatientisacidoticoralkaloticAssessmentStep2OnceyouhavedeterminedthepH,youcanmoveontodeterminetheprimaryproblem,orwhichsystem,respiratoryormetabolicistheprimemessenger.RespiratorySystemCarbonDioxideactsastheacidofthehumanbody,youwillbeabletodetermineiftheprimaryacid-baseimbalanceisrespiratory.Chemicallyspeaking,thereisanequilibriumbetweencarbonicacidandbicarbonate.Therefore,justrememberth