呼吸系統(tǒng)教學(xué)課件：缺氧

缺氧HypoxiaBasicLinksofRespirationAtmosphereoxygenInspiredintoalveoli,diffusedintobloodBindingtoHemoglobinTransportationUptakeandutilizationbycellsDefinitionHypoxiacanbedefinedasdeficiencyineitherthedeliveryortheutilizationofoxygen

atthetissuelevel,whichcanleadtochangesinfunction,metabolismandevenstructureofthebody.

DeficiencyinO2uptakeordelivery

HistogenousinjuryorpoisoningInsufficientO2supplyMalfunctionOfO2utilizationAbnormalFunctionMetabolismStructureSection1ParametersofBloodOxygen1.Partialpressureofoxygen,PO21.5%O2inbloodphysicallydissolvedboundtohemoglobin98.5%

PO2isthetensionproducedbyoxygenmoleculesphysicallydissolvedinplasma.

NormalValue

InfluencingFactors

SignificancePartialpressureofinspiredgasFunctionofexternalrespirationFunctionofinternalrespirationDeterminesSO2(OxygenSaturation)2.Oxygenbindingcapacity,CO2max

Maximalamountofoxygenthatcanbepotentiallyboundbythehaemoglobiniscalledoxygenbindingcapacityofhaemoglobin.Standardcondition:38°C,PO2150mmHg,PCO240mmHg

NormalValue

InfluencingFactors

SignificanceQualityofHbinBloodQuatityofHbinBloodCapacityofHbbindingtooxygenDeterminesCO2(OxygenContent)3.Oxygencontent,CO2

Thetotaloxygencontentofbloodincludesoxygenthatisboundtohaemoglobinandphysicallydissolvedinplasma.

NormalValue

InfluencingFactors

SignificancePaO2QualityofHbinBloodQuantityofHbinBloodCaO2reflectsoxygensupplyintissueCvO2reflectsoxygenutilizationintissue4.oxygensaturation,SO2

SO2isthepercentageofhaemoglobinpresentingasoxyhaemoglobin.SO2＝O2combinedwithHbCO2max╳100％

NormalValue

InfluencingFactorsPaO25.thedifferencebetweenCaO2andCvO2,Da-vO2(動靜脈氧差）A.V.19ml/dl14ml/dl5ml/dlO2O2O2O2O2

NormalValue

InfluencingFactors

SignificanceCapabilityofreleasingoxygenfromO2-HbBloodflowCapabilityofO2utilizationintissueReflectingtheamountofO2uptakebytissueTissueO2supplyTissueconsumedO2=CaO2×TissueBloodFlow=Da-vO2×TissueBloodFlowSection2Classification,Etiology&PathogenesisAtmosphereoxygenInspiredintoalveoli,diffusedintobloodBindingtoHemoglobinTransportationUptakeandutilizationbycellsLowPO2MalfunctionofexternalrespirationArteriovenousshuntHypotonicHypoxia◆Hypotonichypoxia（低張性缺氧）HypotonichypoxiaischaracterizedbythedecreaseofPaO2.Asaresult,oxygencontentinarterialbloodisalsodecreased.Italsobecalledhypoxichypoxia.Etiology1.DecreasedPO2ininspiredair：plateau海拔高度m大氣壓mmHgPiO2mmHgPAO2mmHgSaO2%076015910595100068014090942000600125709230005301106290400046098508550004058545756000366744070700031065356080002705630502.Externalrespiratorydysfunction：COPD,pulmonaryedema3.Venous-to-arterialshunts：congenitalheartdisease法洛氏四聯(lián)癥（tetralogyofFallot）

CharacteristicsofbloodO2:PaO2SO2CO2max

CaO2A-VdO2Mechanisms：LowPaO2reducesthediffusionrateColorofskinandmucousmembranes：Cynosis(紫紺）↓↓↓↓/NN★cyanosis(紫紺)Cyanosisisabluishdiscolorationoftheskin,nailbedandmucousmembranes.Itisduetotheamountofdeoxygenatedorreducedhemoglobinvisibleinthetissue.Generally,approximately5gofreducedhemoglobinper100mlbloodmustbepresentbeforecyanosisisapparent.HHbHbO2≤2.6g/dl≥5g/dlDeoxyhemoglobin≥5g/dlCyanosisHypoxiaSevereanemiaErythrocytosis(紅細(xì)胞增多癥)NotsureNotsureAtmosphereoxygenInspiredintoalveoli,diffusedintobloodBindingtoHemoglobinTransportationUptakeandutilizationbycellsLowPO2MalfunctionofexternalrespirationHypotonicHypoxiaAbnormalityofhemoglobinHemicHypoxiaAbnormalvascularconnection◆Hemichypoxia（血液性缺氧）HemichypoxiareferstothealteredaffinityofHbforoxygenordecreaseinamountofHbintheblood.-isotonichypoxiaEtiology1.Anemia:anemichypoxia2.CarbonmonoxidepoisoningCOreactswithhemoglobintoformcarbonmonoxyhemoglobin(carboxyhemoglobin,COHb),andCOHbcannottakeupO2.TheaffinityofhemoglobinforCOis210timesasitsaffinityforO2,andCOHbliberatesCOveryslowly.3.Methemoglobinemia(高鐵血紅蛋白血癥)Theironinhemoglobinisnormallyintheferrousstate(Fe2+),whenitisoxidizedtotheferricstate(Fe3+),formingmethemoglobin(HbFe3+OH)whichcannotbindoxygen.Manychemicalsanddrugsincludingnitrite(亞硝酸鹽),nitrobenzene(硝基苯),etc.,canoxidizetheironinhemoglobintoformHbFe3+OH,hypoxiamayresult.4.AffinityabnormallyincreasingAlkalosis;BankedbloodtransfusionCharacteristicsofbloodO2:Mechanisms：O2uptakingcapacityofHbreducedAffinityofO2withHbabnormallyincreasedColorofskinandmucousmembranes：Anemia:paleHbCO:cherry-redHbFe3+OH:enterogenouscyanosisN↓N↓↓/NPaO2SO2CO2max

CaO2A-VdO2AtmosphereoxygenInspiredintoalveoli,diffusedintobloodBindingtoHemoglobinTransportationUptakeandutilizationbycellsLowPO2MalfunctionofexternalrespirationAbnormalcirculationHypotonicHypoxiaAbnormalityofhemoglobinHemicHypoxiaCirculatoryHypoxia◆Circulatoryhypoxia（循環(huán)性缺氧）Circulatoryhypoxiareferstoinadequatebloodflowleadstoinadequateoxygenationofthetissues.-hypokinetichypoxiaEtiology1.Generalizedcirculatorydeficiency：shock,heartfailure2.Localcirculatorydeficiency：venousembolismCharacteristicsofbloodO2:Mechanisms：ReducedbloodsupplyLocalcongestionColorofskinandmucousmembranes：Arteriousischemia:paleVenousischemia:cynosisNNPaO2SO2CO2max

CaO2A-VdO2NN↑ReducedbloodflowinunittimeAtmosphereoxygenInspiredintoalveoli,diffusedintobloodBindingtoHemoglobinTransportationUptakeandutilizationbycellsLowPO2MalfunctionofexternalrespirationAbnormalvascularconnectionHypotonicHypoxiaAbnormalityofhemoglobinHemicHypoxiaCirculatoryHypoxiaAbnormalO2untilizationHistogenousHypoxia◆Histogenoushypoxia(組織性缺氧)HistogenoushypoxiareferstothetissuecellcannotmakeuseoftheO2suppliedtothem.-dysEtiology1.Cyanide(氰化物)poisoning:Inhibitionofmitochondrialoxidativephosphorylation2.Vitamindeficiency:thiamine(VitB1),niacin(煙酸)etc.3.Mitochondriainjury:radiation,freeradical4.TissueedemaCharacteristicsofbloodO2:Mechanisms：MalfunctionofO2utilizationColorofskinandmucousmembranes：Cyanidepoisoning:rosyredNNPaO2SO2CO2max

CaO2A-VdO2NN↓Differenttypesofhypoxia內(nèi)毒素血癥肺淤血、水腫循環(huán)障礙失血Hb組織性缺氧低張性缺氧循環(huán)性缺氧血液性缺氧HemorrhagicshockSection3FunctionalandMetabolicChangesoftheBodyinHypoxiaI.Alterationsoftissuesandcells1.Compensativecellularadaptation(1)TheabilitytouseO2↑thequantityofmitochondriaandtheirsurfacearea↑theabilitytouseO2↑enzymesintherespiratorychain↑chronichypoxia(2)Anaerobicglycolysis↑HypoxiaPhosphofructokinase(磷酸果糖激酶)anaerobicglycolysis↑ATPATP/ADP(3)myoglobin（Mb,肌紅蛋白）↑aproteininmuscle;cantakeupO2releasedbyRBCinthesystemiccapillaries,storeandtransportO2tothemetabolizingcellswhenPO2↓;hasgreateraffinityforO2

(4).reductioninmetabolicrateenergywastage↓cellularproteinsynthesisandRNAsynthesis↓cellsurvive缺氧誘導(dǎo)因子-1（hypoxiainduciblefactor-1,HIF-1）NomoxiaHypoxiaHIF-1aUbVHLE3-ligaseVonHippel-LindauOHPro564/402Prolyl-4-hydroxylase(Fe2+,O2)proteasomeHIF-1aHIF-1aHIF-1aHIF-1aHIF-1aHIF-1aVEGFbaCompensatoryresponsesregulatedbyHif12.Hypoxiccelldamage(1)CellmembraneinjuryHypoxiaCell-membranepermeability①influxofNa+

HypoxiaATP↓Na+-K+pumpinfluxofNa+↑↑cellularedema②fluxofK+fluxofK+dysfunctionofanabolismATP③influxofCa2+mitochondriaATPphospholipaseLysosomeinjuryXanthineoxidase↑freeradical↑influxofCa2+(2)Mitochondriainjury(3)LysosomeinjuryinfluxofCa2+acidosisHypoxiaActivityofphospholipaseMildhypoxiaRespiratoryfunctionofmitochondria↑SeverehypoxiaRespiratoryfunctionofmitochondria↓II.AlterationsofrespiratorysystemRateanddepthofventilation↑CompensatoryresponseHypoxia(30～60mmHg)CarotidbodyandaorticbodyPO2PeripheralchemoreceptorsrespiratorycenterHypoxiarespiratorycenterPeripheralchemoreceptorsrespiratoryfailureenergymetabolismdysfunctionrespiratorycenterSeverehypoxia(PaO2<30mmHg)III.AlterationsofcirculatorysystemHypoxia1.CardiacoutputVenousreturntoheartThoracicexpansionandcontractionHRMyocardialcontractionreflexlyactivatesympatheticnervoussystem2.Bloodredistributionperipheralvesselscatecholamine（兒茶酚胺）vasoconstrictionvasodilationαβbloodsupplyofheartandbrain↑localmetabolicproductsbloodvesselsinheartandbrainvasodilationadenosine,lacticacid,etc.3.HypoxicpulmonaryvasoconstrictionHypoxiaαsympatheticnervoussystemcatecholamine↑endothelialcell,mastcell,etc.Leukotrienes(LTs),thromboxaneA2(TXA2),etc.vasoconstictor↑Ca2+channelactivatedinfluxofCa2+缺氧性肺動脈高壓（hypoxicpulmonaryhypertension,HPH）：使得右室后負(fù)荷增加，引起右心室肥大代償、失代償、心力衰竭。4.capillaryproliferationChronichypoxiavascularendothelialgrowthfactor（VEGF）expression↑facilitateO2diffusionintocells1.RBC↑IV.AlterationsofhematologicsystemChronichypoxiakidneyErythropoietin(EPO)actingonthebonemarrowtoincreaseRBCproduction2.Rightwardshiftofoxyhemoglobindissociationc