ABG 简明血气分析课件

ABGINTERPRETATION血气分析解读,SIMCICULiu,Objectives,WhatsanABG?UnderstandingAcid/BaseRelationshipGeneralapproachtoABGInterpretationClinicalcausesAbnormalABGsCasestudies,WhatisanABG,ArterialBloodGas动脉血气Drawnfromartery-radial,brachial,femoral由动脉取样一般取桡动脉、肱动脉、股动脉Itisaninvasiveprocedure.这是侵入性检查Cautionmustbetakenwithpatientonanticoagulants.有凝血功能障碍的患者慎用Helpsdifferentiateoxygendeficienciesfromprimaryventilatorydeficienciesfromprimarymetabolicacid-baseabnormalities协助区分缺氧/通气不足和酸碱代谢异常,WhatIsAnABG?,pHH+PCO2PartialpressureCO2PO2PartialpressureO2HCO3BicarbonateBEBaseexcessSaO2OxygenSaturation,Acid/BaseRelationship,Thisrelationshipiscriticalforhomeostasis酸碱平衡对内环境是非常重要的SignificantdeviationsfromnormalpHrangesarepoorlytoleratedandmaybelifethreatening酸碱严重失衡后果严重，甚至可能致命AchievedbyRespiratoryandRenalsystems一般由呼吸系统和肾脏决定,CaseStudyNo.1,60y/omalecomesERc/oSOB.Tachypneic,tachycardic,diaphoreticandCyanotic.Dxacuteresp.failureandABGsShowPaCO2wellbelownl,pHabovenl,PaO2isverylow.ThebloodgasdocumentResp.failureduetoprimaryO2problem.60岁男性进入急诊室。查体见呼吸过速、心动过速、大汗、发绀，诊断急性呼衰。动脉血气分析结果PaCO轻度降低，PH升高，PaO2非常低。结果显示其主要问题为缺氧,CaseStudyNo.2,60y/omalecomesERc/oSOB.Tachypneic,tachycardic,diaphoreticandCyanotic.Dxacuteresp.failureandABGsShowPaCO2veryhigh,lowpHandPaO2ismoderatelylow.ThebloodgasdocumentResp.failureduetoprimarilyventilatorinsufficiency.60岁男性进入急诊室。查体，呼吸过塑，心动过速，大汗，发绀，诊断急性呼衰。动脉血气分析结果显示PaCO2非常高，PH降低，PaO2中度降低。结果显示其主要问题为通气不足。,Buffers,TherearetwobuffersthatworkinpairsH2CO3NaHCO3CarbonicacidbasebicarbonateThesebuffersarelinkedtotherespiratoryandrenalcompensatorysystem两者和呼吸、肾脏代偿密切相关,RespiratoryComponent,functionofthelungsCarbonicacidH2CO3Approximately98%normalmetabolitesareintheformofCO2CO2+H2OH2CO3excessCO2exhaledbythelungs,MetabolicComponent,FunctionofthekidneysbasebicarbonateNaHCO3ProcessofkidneysexcretingH+intotheurineandreabsorbingHCO3-intothebloodfromtherenaltubules肾脏将H+排泄至尿液，并从肾小管重吸收HCO3-1)activeexchangeNa+forH+betweenthetubularcellsandglomerularfiltrate在肾小管和肾小球主动用Na+交换H+2)carbonicanhydraseisanenzymethataccelerateshydration/dehydrationCO2inrenalepithelialcells可以加速CO2在肾上皮细胞的水化和脱水反应,Acid/BaseRelationship,H2O+CO2H2CO3HCO3+H+,NormalABGvalues,pH7.357.45PCO23545mmHgPO280100mmHgHCO32226mmol/LBE-2-+2SaO295%,Acidosis酸中毒Alkalosis碱中毒,pH45HCO37.45PCO226,RespiratoryAcidosis,ThinkofCO2asanacid把二氧化碳想象成酸failureofthelungstoexhaleadequateCO2肺无法排出足够的二氧化碳pH45CO2+H2CO3pH,CausesofRespiratoryAcidosis,Emphysema肺气肿drugoverdose药物过量narcosis麻醉respiratoryarrest呼吸暂停airwayobstruction气道阻塞,MetabolicAcidosis,failureofkidneyfunctionbloodHCO3whichresultsinavailabilityofrenaltubularHCO3forH+excretionpH26,CausesofMetabolicAlkalosis,lossacidfromstomachorkidney由胃或肾脏过量丢失酸性物质hypokalemia低血钾excessivealkaliintake过量碱性物质摄入,HowtoAnalyzeanABG,PO2NL=80100mmHgpHNL=7.357.45Acidotic7.45PCO2NL=3545mmHgAcidotic45Alkalotic26,Four-stepABGInterpretation,Step1:ExaminePaO2&SaO2DetermineoxygenstatusLowPaO2(80mmHg)&SaO2meanshypoxiaPaO2和SaO2降低提示缺氧NL/elevatedoxygenmeansadequateoxygenation正常或更高的数值表明氧合充分,Four-stepABGInterpretation,Step2:pHacidosis7.45,Four-stepABGInterpretation,Step3:studyPaCO2&HCO3respiratoryirregularityifPaCO2abnl&HCO3NL呼吸系统异常会显示PaCO2异常，HCO3正常metabolicirregularityifHCO3abnl&PaCO2NL代谢系统异常会显示HCO3异常，PaCO2正常,Four-stepABGInterpretation,Step4:DetermineifthereisacompensatorymechanismworkingtotrytocorrectthepH.判断机体是否在进行代偿ie:ifhaveprimaryrespiratoryacidosiswillhaveincreasedPaCO2anddecreasedpH.CompensationoccurswhenthekidneysretainHCO3.例如：如果主要是呼吸性酸中毒的话会导致PaCO2升高，PH降低。当肾脏仍有足够的HCO3时会进行代偿,PaCO2pHRelationship,807.20607.30407.40307.50207.60,ABGInterpretation,Compensated,Respiratory,Acidosis,CO2,MoreAbnormal,Respiratory,Acidosis,CO2,Expected,Mixed,Respiratory,Metabolic,Acidosis,CO2,LessAbnormal,CO2Change,c/w,Abnormality,Metabolic,MetabolicAcidosis,CO2,Normal,Compensated,Metabolic,Acidosis,CO2Change,opposes,Abnormality,Acidosis酸中毒,ABGInterpretation,Compensated,Respiratory,Alkalosis,CO2,MoreAbnormal,Respiratory,Alkalosis,CO2,Expected,Mixed,Respiratory,Metabolic,Alkalosis,CO2,LessAbnormal,CO2Change,c/w,Abnormality,Metabolic,Alkalosis,CO2,Normal,Compensated,Metabolic,Alkalosis,CO2Change,opposes,Abnormality,Alkalosis,RespiratoryAcidosis,pH7.30PaCO260HCO326,RespiratoryAlkalosis,pH7.50PaCO230HCO322,MetabolicAcidosis,pH7.30PaCO240HCO315,MetabolicAlkalosis,pH7.50PCO240HCO330,Whatarethecompensations?,RespiratoryacidosismetabolicalkalosisRespiratoryalkalosismetabolicacidosisInrespiratoryconditions,therefore,thekidneyswillattempttocompensateandvisaversa.Inchronicrespiratoryacidosis(COPD)thekidneysincreasetheeliminationofH+andabsorbmoreHCO3.TheABGwillShowNLpH,CO2andHCO3.Bufferskickinwithinminutes.Respiratorycompensationisrapidandstartswithinminutesandcompletewithin24hours.Kidneycompensationtakeshoursandupto5days.,MixedAcid-BaseAbnormalities,CaseStudyNo.3:56yoneurologicdzrequiredventilatorsupportforseveralweeks.SheseemedmostcomfortablewhenhyperventilatedtoPaCO228-30mmHg.Sherequireddailydosesoflasix（速尿）toassureadequateurineoutputandreceived40mmol/LIVK+eachday.On10thdayofICUherABGon24%oxygen&VS:,ABGResults,pH7.62BP115/80mmHgPCO230mmHgPulse88/minPO285mmHgRR10/minHCO330mmol/LVT1000mlBE10mmol/LMV10LK+2.5mmol/L,Interpretation:Acutealveolarhyperventilation(resp.alkalosis)andmetabolicalkalosiswithcorrectedhypoxemia.,CasestudyNo.4,27yoretardedwithinsulin-dependentDMarrivedatERfromtheinstitutionwherehelived.OnroomairABG&VS:pH7.15BP180/110mmHgPCO222mmHgPulse130/minPO292mmHgRR40/minHCO39mmol/LVT800mlBE-30mmol/LMV32L,Interpretation:Partlycompensatedmetabolicacidosis.,CasestudyNo.5,74yowithhxchronicrenalfailureandchronicdiuretictherapywasadmittedtoICUcomatoseandseverelydehydrated.On40%oxygenherABG&VS:pH7.52BP130/90mmHgPCO255mmHgPulse120/minPO292mmHgRR25/minHCO342mmol/LVT150mlBE17mmol/LMV3.75L,Interpretation:Partlycompensatedmetabolicalkalosiswithcorrectedhypoxemia.,CasestudyNo.6,43yoarrivesinER20minutesafteraMVAinwhichheinjuredhisfaceonthedashboard.Heisagitated,hasmottled,coldandclammyskinandhasobviouspartialairwayobstruction.Anoxygenmaskat10Lisplacedonhisface.ABG&VS:pH7.10BP150/110mmHgPCO260mmHgPulse150/minPO2125mmHgRR45/minHCO318mmol/LVT?mlBE-15mmol/LMV?L.,Interpretation:Acuteventilatoryfailure(resp.acidosis)andacutemetabolicacidosiswithcorrectedhypoxemia,CasestudyNo.7,17yo,48kgwithknowninsulin-dependentDMcametoERwithKussmaulbreathingandirregularpulse.RoomairABG&VS:pH7.05BP140/90mmHgPCO212mmHgPulse118/minPO2108mmHgRR40/minHCO35mmol/LVT1200mlBE-30mmol/LMV48L,Interpretation:Severepartlycompensatedmetabolicacidosiswithouthypoxemia.,CaseNo.7contd,Thispatientisindiabeticketoacidosis.IVglucoseandinsulinwereimmediatelyadministered.AjudgementwasmadethatsevereacidemiawasadverselyaffectingCVfunctionandbicarbwaselectedtorestorepHto7.20.Bicarbadministrationcalculation:BasedeficitXweight(kg)430X48=360mmol/LAdmin1/2over15min&4repeatABG,CaseNo.7contd,ABGresultafterbicarb:pH7.27BP130/80mmHgPCO225mmHgPulse100/minPO292mmHgRR22/minHCO311mmol/LVT600mlBE-14mmol/LMV13.2L,CasestudyNo.8,47yowasinPACUfor3hourss/pcholecystectomy.Shehadbeenon40%oxygenandABG&VS:pH7.44BP130/90mmHgPCO232mmHgPulse95/min,regularPO2121mmHgRR20/minHCO322mmol/LVT350mlBE-2mmol/LMV7LSaO298%Hb13g/dL,CaseNo.8contd,Oxygenwaschangedto2LN/C.1/2hourpt.readytobeD/CtofloorandABG&VS:pH7.41BP130/90mmHgPCO210mmHgPulse95/min,regularPO2148mmHgRR20/minHCO36mmol/LVT350mlBE-17mmol/LMV7LSaO299%Hb7g/dL,CaseNo.8contd,Whatisgoingon?,CaseNo.8contd,Ifthepicturedoesntfit,repeatABG!pH7.45BP130/90mmHgPCO231mmHgPulse95/minPO287mmHgRR20/minHCO322mmol/LVT350mlBE-2mmol/LMV7LSaO296%Hb13g/dL,Technicalerrorwaspresumed.,CasestudyNo.9,67yowhohadclosedreductionoflegfxwithoutincident.FourdayslatersheexperiencedasuddenonsetofseverechestpainandSOB.RoomairABG&VS:pH7.36BP130/90mmHgPCO233mmHgPulse100/minPO255mmHgRR25/minHCO318mmol/LBE-5mmol/LMV18LSaO288%,Interpretation:Compensatedmetabolicacidosiswithmoderatehypoxemia.Dx:PE,CasestudyNo.10,76yowithdocumentedchronichypercapniasecondarytosevereCOPDhasbeeninICUfor3dayswhilebeingtxforpneumonia.Shehadbeenstableforpast24hoursandwastransferredtogeneralfloor.Ptwason2Loxygen&ABG&VS:pH7.44BP135/95mmHgPCO263mmHgPulse110/minPO252mmHgRR22/minHCO342mmol/LBE+16mmol/LMV10LSaO286%.,Interpretation:Chronicventilatoryfailure(resp.acidosis)withuncorrectedhypoxemia,CaseNo.10contd,Shewasplacedon3Landmonitoredfornextho