呼吸衰竭.ppt

RespiratoryFailure,Dr.SatSharmaUnivofManitoba,RESPIRATORYFAILURE,“inabilityofthelungtomeetthemetabolicdemandsofthebody.Thiscanbefromfailureoftissueoxygenationand/orfailureofCO2homeostasis.”,RESPIRATORYFAILURE,DefinitionRespirationisgasexchangebetweentheorganismanditsenvironment.FunctionofrespiratorysystemistotransferO2fromatmospheretobloodandremoveCO2fromblood.ClinicallyRespiratoryfailureisdefinedasPaO250mmHg.,Respiratorysystemincludes:,CNS(medulla)Peripheralnervoussystem(phrenicnerve)RespiratorymusclesChestwallLungUpperairwayBronchialtreeAlveoliPulmonaryvasculature,PotentialcausesofRespiratoryFailure,HYPOXEMICRESPIRATORYFAILURE(TYPE1),PaO250mmHgHypoxemiaisalwayspresentpHdependsonlevelofHCO3HCO3dependsondurationofhypercapniaRenalresponseoccursoverdaystoweeks,AcuteHypercapnicRespiratoryFailure(TypeII),AcuteArterialpHislowCauses-sedativedrugoverdose-acutemuscleweaknesssuchasmyastheniagravis-severelungdisease:alveolarventilationcannotbemaintained(i.e.Asthmaorpneumonia)Acuteonchronic:ThisoccursinpatientswithchronicCO2retentionwhoworsenandhaverisingCO2andlowpH.Mechanism:respiratorymusclefatigue,CausesofHypercapnicRespiratoryfailure,Respiratorycentre(medulla)dysfunctionDrugoverdose,CVA,tumor,hypothyroidism,centralhypoventilationNeuromusculardiseaseGuillain-Barre,MyastheniaGravis,polio,spinalinjuriesChestwall/Pleuraldiseaseskyphoscoliosis,pneumothorax,massivepleuraleffusionUpperairwaysobstructiontumor,foreignbody,laryngealedemaPeripheralairwaydisorderasthma,COPD,ClinicalandLaboratoryManifestation(non-specificandunreliable),Cyanosis-bluishcolorofmucousmembranes/skinindicatehypoxemia-unoxygenatedhemoglobin50mg/L-notasensitiveindicatorDyspnea-secondarytohypercapniaandhypoxemiaParadoxicalbreathingConfusion,somnolenceandcomaConvulsions,ASSESSMENTOFPATIENT,CarefulhistoryPhysicalExaminationABGanalysis-classifyRFandhelpwithcause1)PaCO2=VCO2x0.863VA2)P(A-a)02=(PiO2-PaCO2)PaO2RLungfunctionOVPvsRVPvsNVPChestRadiographEKG,Clinical&LaboratoryManifestationsCirculatorychanges-tachycardia,hypertension,hypotensionPolycythemia-chronichypoxemia-erythropoietinsynthesisPulmonaryhypertensionCor-pulmonaleorrightventricularfailure,ManagementofRespiratoryFailurePrinciples,HypoxemiamaycausedeathinRFPrimaryobjectiveistoreverseandpreventhypoxemiaSecondaryobjectiveistocontrolPaCO2andrespiratoryacidosisTreatmentofunderlyingdiseasePatientsCNSandCVSmustbemonitoredandtreated,OxygenTherapy,SupplementalO2therapyessentialtitrationbasedonSaO2,PaO2levelsandPaCO2GoalistopreventtissuehypoxiaTissuehypoxiaoccurs(normalHb&C.O.)-venousPaO260mmHg(SaO290%)orvenousSaO260%O2doseeitherflowrate(L/min)orFiO2(%),RisksofOxygenTherapy,O2toxicity:-veryhighlevels(1000mmHg)CNStoxicityandseizures-lowerlevels(FiO260%)andlongerexposure:-capillarydamage,leakandpulmonaryfibrosis-PaO2150cancauseretrolentalfibroplasia-FiO235to40%canbesafelytoleratedindefinitelyCO2narcosis:-PaCO2mayincreaseseverelytocauserespiratoryacidosis,somnolenceandcoma-PaCO2increasesecondarytocombinationofa)abolitionofhypoxicdrivetobreatheb)increaseindeadspace,MECHANICALVENTILATION,NoninvasivewithamaskInvasivewithanendobronchialtubeMVcanbevolumeorpressurecycledForhypercapnia:-MVincreasesalveolarventilationandlowersPaCO2,correctspH-restsfatiguesrespiratorymusclesForhypoxemia:-O2therapyalonedoesnotcorrecthypoxemiacausedbyshunt-Mostcommoncauseofshuntisfluidfilledorcollapsedalveoli(Pulmonaryedema),POSITIVEENDEXPIRATORYPRESSURE(PEEP),PEEPincreasestheendexpiratorylungvolume(FRC)PEEPrecruitscollapsedalveoliandpreventsrecollapseFRCincreases,thereforelungbecomesmorecompliantReversalofatelectasisdiminishesintrapulmonaryshuntExcessivePEEPhasadverseeffects-decreasedcardiacoutput-barotrauma(pneumothorax,pneumomediastinum)-increasedphysiologicdeadspace-increasedworkofbreathing,PULMONARYEDEMA,PulmonaryedemaisanincreaseinextravascularlungwaterInterstitialedemadoesnotimpairfunctionAlveolaredemacauseseveralgasexchangeabnormalitiesMovementoffluidisgovernedbyStarlingsequationQF=KF(PIV-PIS)+(IS-IV)QF=rateoffluidmovementKF=membranepermeabilityPIV&PISareintravascularandinterstitialhydrostaticpressuresISandIVareinterstitialandintravascularoncoticpressuresreflectioncoefficientLungedemaisclearedbylymphatics,AdultRespiratorydistressSyndrome(ARDS),VarietyofunrelatedmassiveinsultsinjuregasexchangingsurfaceofLungsFirstdescribedasclinicalsyndromein1967byAshbaugh&PettyClinicaltermssynonymouswithARDSAcuterespiratoryfailureCapillaryleaksyndromeDaNangLungShockLungTraumaticwetLungAdulthyalinemembranedisease,RiskFactorsinARDS,Sepsis3.8%Cardiopulmonarybypass1.7%Transfusion5.0%Severepneumonia12.0%Burn2.3%Aspiration35.6%Fracture5.3%Intravascularcoagulopathy12.5%Twoormoreoftheabove24.6%,PATHOPHYSIOLOGYANDPATHOGENESIS,Diffusedamagetogas-exchangingsurfaceeitheralveolarorcapillarysideofmembraneIncreasedvascularpermeabilitycausespulmonaryedemaPathology:fluidandRBCininterstitialspace,hyalinemembranesLossofsurfactant:alveolarcollapse,CRITERIAFORDIAGNOSISOFARDS,ClinicalhistoryofcatastrophiceventPulmonaryorNonpulmonary(shock,multisystemtrauma)ExcludechronicpulmonarydiseasesleftventricularfailureMusthaverespiratorydistresstachypnea20breath/minuteLaboredbreathingcentralcyanosisCXR-diffuseinfiltratesPaO2O.6Compliance50ml/cmH2Oincreasedshuntanddeadspace,ARDS,MANAGEMENTOFARDS,Mechanicalventilationcorrectshypoxemia/respiratorya