RespiratoryFailure1.AbstractsRespiratoryfailure,whetheracuteorchronic,isafrequentlyfacedproblemandamajorcauseofdeathinourcountry.Forexample,mortalityfromCOPD,whichendsindeathfromrespiratoryfailure,continuestoincrease.Morethan70%ofthedeathsinpatientswithpneumoniaareattributedtorespiratoryfailure.2.DefinitionRespiratoryfailureisfunctionalacuteorchronicdisordercausedbyanyconditionthataffectsthelung’sabilitytomaintainarterialoxygenationorcarbondioxide(CO2)elimination.Itisdefinedasaconditioninwhichthisgasexchangedeterioratesbelowtheusuallevel,sothatarterialoxygentensiondecreases,withorwithoutanabnormalriseinarterialcarbondioxidetension.3.ClassificationsGenerallybothacuteandchronicrespiratoryfailuremaybedividedintotwomaincategories:TypeⅠrespiratoryfailureTypeⅠrespiratoryfailureisalsocalledhypoxicrespiratoryfailure,whichmeansthatseverelyreducesarterialoxygentension(PaO2<60mmHg),CO2retentionisnotexist.Thistypeofrespiratoryfailureiscausedbyafailureofgasexchange.TypeⅡrespiratoryfailureTypeⅡrespiratoryfailureisalsomeantthathypercapnic-hypoxicrespiratoryfailure.Arterialbloodgasvaluesshowsthatarterialcarbondioxidetensionismorethan50mmHgandarterialoxygentensionislessthan60mmHgTypeⅡrespiratoryismainlycausedbyhypoventilation.PathogenesisMainlydiscusschronicrespiratoryfailurewehaveknownthatthelungs’abilityisgasexchange.Thegasexchangeinvolvesnotonlyoxygenationbutalsocarbondioxideelimination.PathogenesisRespiratoryfailureismainlyassociatedwithpulmonarygasexchangeandpulmonaryventilation.

1.pulmonarygasexchangeismainlydeterminedbyventilation-perfusion(V/Q)ratiosanddiffuseability

V/Qmismatch:AneffectivelunggasexchangeneedsnotonlysufficientlungventilationandlungbloodvolumesbutalsoanadequateV/Qratios.Usually,thevolumeofventilationis4liters/min.Thevolumeoflungbloodis5liters/min.Sotheratiosis0.8Anyofthefactorsinfluencedtheratiosmaymainlycausehypoxemiarespiratoryfailure.Forexample,V/Q>0.8,includingemphysema,pulmonaryembolism.V/Q<0.8,includingatelectasis,severeCOPD.DiffuseabilityDiffusionabnormalitymainlyinfluenceoxygenexchange.2.PulmonaryhypoventilationItmaycausehypercapnic-hypoxicrespiratoryfailure.Pulmonaryhypoventilationincludesrestrictivehypoventilationandobstructivehypoventilation.Somediseasesinfluencedcentralnervoussystem,peripheralnervoussystem,chestwallrespiratorymusclesandpulmonarycompliancemayallcauserestrictivehypoventilation.SomecommonconditionsthatmaycauseventilatoryfailurewithhypercapneaTheseconditionsincludebrainstemlesion,alteredneuromusculartransmission(guillain-barresyndrome),muscleweakness(malnutrition,shock,hypoxemia,hypokalemia),increasedairwayresistance(upperairwayobstruction,increasedbronchialsecretionsandedema),decreasedlungcompliance(infection,atelectasis,interstitialfibrosis,acutelunginjury),decreasedchestwallcompliance(chestwalltrauma,pleuraleffusion,pneumothorax).COPDandasthmaarethemostcommondiseaseassociatedtoobstructivehypoventilation.Inourclinicalwork,multifactorsinvolveinthecourseofrespiratoryfailure.Forexample,aCOPDpatientwithseverepulmonaryinfection,hispulmonarygasexchangeabilityandpulmonaryventilationareallabnormal.PathophysiologyHypoxiaandhypercapnicmayinfluencefunctionsofmanyimportantorgansandsystems,includingrespiratorysystem,cardiovascularsystem,centralnervesystem,bloodsystemanddigestivesystemandrenalfunction.ClinicalmanifestationsClinicalsignsincludenotonlysymptomsassociatedwithprimarydiseasesbutalsothosecausedbyhypoxicandhypercapnic-hypoxicrespiratoryfailure.Hypoxemiaandhypercapniamainlyinfluencethefunctionofimportantorgans,includingrespiratorysystem,centralnervoussystem,cardiovascularsystem,digestivesystem,renalfunctions.Theunbalanceofacid-alkalosemetabolicanddielectricabnormalityareusuallyexistinthecourseofrespiratoryfailure.Table1.Clinicalmanifestationsofhypoxiaandhypercapnia.

ClinicalmanifestationsofhypoxiaandhypercapniaHYPOXEMIAHYPERCAPNIA

TachycardiaSomnolenceTachypneaLethargyAnxietyRestlessnessAlteredmentalstatusSlurredspeechConfusionHeadacheCyanosisAsterixisHypertensionPapilledemaHypotensionComaBradycardiaSeizuresLacticacidosistDiagnosisAccordingtohistory,clinicalmanifestations,physicalexaminationsandbloodgasanalysis,wecandiagnoserespiratoryfailure.Especiallyarterialbloodgasanalysismayrevealhypoxemiaandhypercapnia.DiagnosisThediagnosisstandardinclude:TypeⅠrespiratoryfailure:PaO2<60mmHgTypeⅡrespiratoryfailure:PaCO2>50mmHg,PaO2<60mmHg.Intheconditionofoxygentherapy,PaO2/FiO2<300mmHgindicatesrespiratoryfailure.TreatmentTheprincipleoftreatmentincludesprimarydiseasetreatment,airwaymaintenance,correctionofhypoxemiaandhypercapniaandmanagementofsymptomscausedbyhypoxemiaandhypercapnia.(1)AirwaymaintenanceandenhancethevolumeofventilationAssuranceofanadequateairwayiskeyinthepatientwithrespiratoryfailure.Forpatientswithchronicrespiratoryinsufficiency,theneedforintubationdependsoncriticalarterialbloodgasvaluesandthepatientsearlyacutecourse.Whenprogressivehypoxemiaorhypercapniaisobserved,intubationandmechanicalventilationareused.Tomostofthechronicrespiratoryfailure,correctlyuseofbronchodilatorsisveryimportant.

Table2.BronchodilatorsRouteDoseAlbuterolMDIandspacer400-600gq1-4hAerosolsolution2.5-7.5mgq1-4hIpratropiumMDIandspacer80-120gq4-6hMechanicalventilation

Theaimofmechanicalventilationistoimprovehypoxemiaandtopreventhypercapnia.Whendoyouselectmechanicalventilation?Thisisaquestionwealwaysmeetinourclinicalwork.1.progressiveelevationinPaCO2>70-80mmHg2.severehypoxemia,afteroxygentherapy,PaO2<40mmHg3.respiratoryrates>35perminuteorseverebreathlessness4.severemetabolicacidosisorpulmonaryencephalopathy(2)AntiinfectioustherapyRepeatedbronchialandpulmonaryinfectionisamajorcauseofchronicrespiratoryfailure.About90%ofCOPDpatientswithrespiratoryfailureiscausedbyacutebronchialorpulmonaryinfection.InfectionmayalsoincreasebronchialsecretionandCO2production.Soantiinfectioustherapyisanimportantmethodtotreatrespiratoryfailure.SelecteffectiveantibioticsAccordingtosputumculture,wecanselectsensitiveantibioticsUsingcombinedantibioticsBecauseofmultibacteriainfection,itneedsseveralkindofantibiotics.Forexample,wemaycombinesecondorthirdgenerationcephalosporintoaminoglycosideorfluoroguinolone.(3)OxygentherapyThegoalofoxygentherapyistoimprovePaO2.ItmakesPaO2>60%.Ingeneral,thelowestFiO2achievingadequateoxygenation.sometimes,arterialoxygensaturation>90%shouldbeused.Themethodsofoxygentherapy:nasalprongs1-3L/mintochronicrespiratoryfailureventimask1-3L/minFortype1respiratoryfailure,wecanelevatethepercentageofoxygentomaintainthePaO2.Wecanusehigherinspiratedfrationofoxygenintype1respiratoryfailureoxygentherapy.Butintype2respiratoryfailurewemustselectlowerinspiratedfrationofoxygen.(4)Acid-baseandelectrolytesdisturbanceTherearemanyfactorsleadtoacid-baseandelectrolytesdisturbance.Thesefactorsincludeseverepulmonaryinfection,hypoxemiaor(and)hypercapnia.Soairwaymaintenance,antibiotictherapyanduseofbronchodilatorsarebeneficialtotreatit.(5)Useofrespiratorystimulantdrugs(6)CorticosteroidsMethyprednisoneisusuallyusedtoreducetheairwayinflammation,andtoimproveFEV!.Thetreatmentisrecommendedinallpatientsbutitisnotusedforalongertime.(7)GastrointestinalbleedingtreatmentBecauseofhypoxemia,hypercapniaandbyusingcorticosteroids,gastrointestinalbleedingalwaysbehappened.Thetreatmentmathodincludecorrecthypoxemiaandhypercapnia,useofH2-blockerandsomeblockbleedingdrugs.(8)NutritionalsupporttherapyAcuteRespiratoryDistressSyndromeARDS1.DefinitionARDS,whichisafromofacutelunginjuryoftenseeninpreviouslyhealthypatients,ischaracterizedbyrapidrespiratoryratesandasensationofprofoundshortnessofbreath,andaccompaniedbyseverearterialhypoxemia.2.PathogenesisARDScanresultfrommanydisorders,includingsystemicorpulmonaryinfection,(viral,bacterial,fungal,ects.),aspiration,inhalationoftoxins,metabolicdisordersandseveresepsisorsepticshock.Theinitialinsultcausereleaseofcytokines,mediatorsfromcellmembranesandactivationofanumberofcascadeswithinjurytothepulmonaryendothelium.ARDSisinvariablyassociatedwithincreasedliquidinthelungs.Itisaformofpulmonaryedema,distinctsfromcardiogenicpulmonaryedema.Sincehydrostaticpressurearenotelevated.3.ClinicalmanifestationsTheearlymanifestationsareanincreasedrespiratoryrates.Usuallyrespiratoryratesaremorethen28perminute.Sometimesthepatientmaybefreeofrespiratorysigns.Coughandsputumproduction.Becauseofseverehypoxemia,cyanosisisacommonphysicalsignsinARDSpatients.X-rayshowsaprogressive,usuallysymmetrical,fluffyalveolarinfiltratethatprogressestoinvolveallpotionsofthelung.X-rayfeaturesofARDSmaybedividedintothreestages:Firststage-sometimesnormal,sometimessmallpatchesmaybeexistSecondstage-diffusedsmallorlargepatches,usuallyinlowerlungfieldThirdstage-pulmonaryinfiltrateinvolvedallpotionsofthelung,called‘whitelung’ArterialbloodgasanalysisshowsPaO2/FiO2<300mmHgandPaO2<60mmHg.(ALI),PaO2/FiO2<200mmHg(ARDS)4.DiagnosisThereisadisorderwhichmayleadtoARDS.Forexample,severeinfectionects.Accordingtoclinicalmanifestation,X-ray,arterialbloodgasanalysis,wecanmakeadiagnosis.Themaindiagnosisstandardincludes:AfactorwhichmayleadstoARDSTheonsetisacute.Tachypneaisexist.HypoxiaChestX-rayshowspulmonaryinfiltrateinvolvedtwolungs.PCWP<=18mmHgorexceptcardiogenicpulmonaryedema.5.TreatmentTreatmentofinitialdisorderswhichleadtoARDSImprovehypoxemiaSeverearterialhypoxemiaisacharacteristicclinicalsignofARDS.Ingeneral,thelowestinspiredfrationofoxygen(FiO2)shouldbeusedtogivethedesiredresult.TherearemultiplemeansfordeliveringO2,includingsoftnasalprongs,simplefacemasks.ButintheconditionofARDS,thesemethodsarenoteffective.Mechanicalventilatorysupportshouldbeusedearlytoimprovehypoxemia.UseofPEEPPEEPmeanspositiveendexpiratorypressure.UseofPEEPThephysiologiceffectsofPEEPinclude:1.redistributionofcapillarybloodflow,resultinginimprovedV/Qmatching;2.Therecruitmentofpreviouslycollapsedalveoliandpreventionofth