呼吸科呼吸系統(tǒng)課件1

Unit5:RespirationDefinitionofRespirationTheprocessthathumanbodyexchangesgaseswiththeatmosphere.

orTheprocessoftakingupoxygenandremovingcarbondioxidefromcellsinthebody.2/1/20231Dyspnea&ApneaDyspneameansthatthereisairhunger.Apneameansnobreathing.Whenyoucan’tbreathe,nothingelsemattersSloganoftheAmericanLungAssociation2/1/20233MainTopics5.1.Pulmonaryventilation

Theventilatorypump Mechanicsofventilation Elasticandnon-elasticresistances Staticlungvolume Dynamiclungventilation

5.2.Gasexchange

Gasdiffusion Factorsthataffectgasexchange Ventilation-perfusionratio(VA/Q)5.3.Gastransportintheblood

Oxygen,carbondioxide,carbonmonoxidepoisoning5.4.Thecontrolofventilation

Respiratorycenterandthebasicrespiratorypattern Voluntarycontrol Chemosensoryreflexes Mechanicalreflexes2/1/202342023/2/1WhoamI?Name:詹仁知E-mail:zhan0001@Location:6-3385網(wǎng)上學(xué)習(xí)材料復(fù)旦大學(xué)上海醫(yī)學(xué)院生理學(xué)精品課程/第五章自測(cè)題庫(kù)/document/tkch-5.pdf2/1/20236ConductingZoneandRespiratoryZoneType1alveolarcellsThesecellsarederivedfromtypeIIalveolarcellsandprovideathinlayerofcytoplasmwhichcoversabout80%ofthegasexchangezone.TypeIIalveolarcellsThesecellsallowtheformationofsurfactantandotherenzymes.TypeIIIalveolarcellsThesecellsarethemainlungdefencesystem–theyarethealveolarmacrophages.MainFunctionalEventsofRespiration2/1/20239TerminologyPulmonaryventilation（肺通氣）Theinflowandoutflowofairbetweentheatmosphereandthelungalveoli.Gasexchange（肺換氣)Diffusionofoxygenandcarbondioxidebetweenthealveoliandthebloodinsidethepulmonarycapillaries.Gastransportintheblood（氣體在血液中的運(yùn)輸）Transportsofoxygenandcarbondioxideinthebloodandbodyfluidtoandfromthetissuecells.Tissuegasexchange（組織換氣）Theexchangeofoxygenandcarbondioxidebetweenbloodandcellsindifferenttissues.2/1/202310Terminology-ContinuedExternalRespiration(外呼吸)Exchangeofgasesbetweentheatmosphereandthebloodinpulmonarycapillaries.Itconsistsofpulmonaryventilationandgasexchange.InternalRespiration(內(nèi)呼吸)Theexchangeofoxygenandcarbondioxidebetweenbloodandcellsindifferenttissues.Itconsistsoftissuegasexchangeandbiologicaloxidation.2/1/202311Summary1.Breathingisessentialtolife.2.Theprimaryfunctionofrespirationistoprovideoxygenformetabolicneedsandtoremovecarbondioxidefromcellsinthebody.3.Themainfunctionaleventsofrespirationarepulmonaryventilation,gasexchange,gastransportinthebloodand

tissuegasexchange.2/1/2023125.1.PulmonaryVentilationDefinitionPulmonaryventilationreferstotheinflowandoutflowofairbetweentheatmosphereandthelungalveoli.2/1/202313TwoPhasesoftheBreathingCycleInspirationorinhalation（吸氣）InspirationisthemovementofairintothelungsExpirationorexhalation（呼氣）Expirationisthemovementofairoutofthelungs2/1/2023142023/2/115NormalQuietBreathingvs.ForcedBreathing（平靜呼吸vs.用力呼吸）PatternFeatureInspiratoryMusclesExpiratoryMusclesNormalquietbreathing(Eupnea)Quiet,smooth

unlaboredventilationinrestingconditions(12beats/min)Diaphragm(main);externalintercostalmuscles(minor)NoneForcedbreathing(Deepbreathing)Laboredventilation(Canbesloworfaster)Diaphragm;externalintercostalmuscles;accessorymusclesAbdominalmuscles;internalintercostalmusclesAbdominalBreathingvs.ThoracicBreathing（腹式呼吸vs.胸式呼吸）PatternExpansionMusclesInvolvedSeeninAbdominalTheabdomenDiaphragmInfantsThoracicThechestExternalintercostalmusclese.g.,peritonitis（腹膜炎）MixedTheabdomenandchestDiaphragmandexternalintercostalmusclesNormaladults2/1/202316LungVentilation（肺通氣）DrivingforceAgainstResistance2/1/2023175.1.1.TheVentilatoryPumpChestwall（胸壁）Spine,ribsandsternumRespiratorymusclesThediaphragm（膈?。㏕hemaininspiratorymuscleTheintercostalmuscles（肋間?。㏕heexternalintercostalmuscles(inspiratorymuscles)Theinternalintercostalmuslces(expiratorymuscles)Pleuralcavity（胸膜腔）2/1/202318ThePleuralCavity（胸膜腔）Thepleuralcavityisthepotential

spacebetweenthelungsandthechestwall,containingasmallamountofpleuralfluid2/1/202319RespiratoryMuscles（呼吸?。?.InspiratoryDiaphragm（膈?。〦xternalintercostalmuscles（肋間外?。?.Accessory（輔助）Scalene（斜角?。㏒ternocleidomastoidmuscles（胸鎖乳突?。?.ExpiratoryAbdominalmusclesInternalintercostalmuscles（肋間內(nèi)?。?/1/202320TheDiaphragm（膈肌）ThemostimportantmuscleforinspirationContractionofthediaphragmpushestheabdominalcontents（腹腔內(nèi)容物）

downwardandliftstheribs（肋骨）

upwardandoutward,increasingthevolumeofthethoraciccavityin3directions.2/1/202321PressuresinDifferentCompartmentsBarometricpressure（大氣壓）Theatmospheretheairwebreatheandlivein,expertsapressureknownasbarometricpressure(PB).Pleuralpressureorintrapleuralpressure（胸膜腔內(nèi)壓）Thepressureinthepleuralspacebetweenthelungandthechestwallispleuralpressure(Ppl).Adecreaseinpleuralpressurecausesthelungstoexpand.Thepleuralpressurestartstodecreaseinthebeginningofuntiltheendofinspiration.Alveolarpressureorintrapulmonarypressure（肺內(nèi)壓）Alveolarpressureisthepressureinsidethealveoli;itdeterminesinwardoroutflowofair.Transpulmonarypressure（跨肺壓）Transpulmonarypressureisthepressuredifferenceacrossthelungwall(PA–Ppl).2/1/202322TheNegative(subatmospheric)PleuralPressureInnormalquietbreathing,thepleuralpressureisnegative(lowerthantheatmospphericpressure).Elasticrecoil（彈性回縮）ofthelungsandchestwallresultsinnegativepleuralpressure.Thepleuralpressurechangesaccordingtobreathingcyclewiththemaximalnegativepleuralpressurereachesjusttheendofinspirationduetothebiggestelasticrecoilofthelungs.Forcedexpirationcanresultinapositivepleuralpressure.2/1/202323WindblowsWhenpressuredifferencebetweentwoadjacentcompartmentsexists

2/1/202324FromPressureDifferencestoAirflowThedifferencebetweenalveolarpressureandbarometricpressureisthedirectdrivingforceforventilation.Inspiratorymusclecontractionistheprimarydrivingforceforventilation.Negativealveolarpressure(lowerthantheatmosphericpressure)

resultsininspirationwhereaspositivealveolarpressurecausesexpiration.Foranygivencycleofbreathing,thereisatimepointwherealveolarandthebarometricpressuresareequal(theendofispirationorjustbeforeexpiration)2/1/202325

1.Thepleaural(orintrapleaural)pressurereachesitsmaximumnegativelevelattheendofinspiration.2.Attheendofispirationorjustbeforeexpiration,thealveolarandthebarometricpressuresareequal.3.Flowrateincreases(ordecreases)inparallelwithalveolarpressure.ConclusionsDrawnfromtheLeftFigure

2/1/202326Boyle’sLaw2/1/202327InspiratoryMusclesContractThoracicCavityExpandsPleuralPressureBecomesmoreNegativeTranspulmonaryPressureIncreasesAlveolarPressureBecomesSubatmosphericAirFlowsintotheLungsuntilAlveolarPressureEqualsAtmosphericPressureP1XV1=P2XV2Boyle’sLawSequentialEventsOccurduringInspirationLungstendtoInflate2/1/202328SequentialEventsOccurduringExpirationRelaxationofDiaphragmThoracicCavityShrinksNegativePleuralPressureDecreasesTranspulmonaryPressureBecomesSmallAlveolarPressureRisesabovetheAtmosphericPressureLungVolumeTendstoDecreaseAirFlowsouttheLungsuntilAlveolarPressureEqualsAtmosphericPressureP1XV1=P2XV2Boyle’sLaw2/1/202329TheSignificanceofaNegativePleuralPressureKeepsthelungstobeinflatedasitisdemonstratedinpneumothorax(氣胸).Promotesthereturnsofvenousbloodandlymphaticfluid

(淋巴液).2/1/202330Pneumothorax(氣胸)Aconditioninwhichairhasenteredandexpandedthenormallyclosedpleuralspace,drivingpleuralpressureuptowardatmosphericpressure,andresultinginpartialorcompletecollapse

ofthelung.

2/1/202331ConsequencesofPneumothoraxHypoxia（缺氧）duetoshunt(bloodpassesthroughthosecollapsedalveoli).Decreaseinvenousbloodreturnduetocompressionofvenacava,resultinginlowercardiacoutputandconsequentlyhypotension(circulatorycollapse).2/1/202332CasesofPneumothoraxCase1:Apatientwhounderwentstomachsurgeryunderepiduralanesthesiahassymptomsofanxiety,intensifiedabdomenbreathingandlowbloodpressurewithdecreasedpulsepressure.Case2:ApatientwithhistoryofemphysemapresentedtoERwithdifficultbreathingandcyanosis.ChestX-rayshowednosignsofcollapsedlung.2/1/202333SummaryonDrivingForcesforVentilationThenegativepleuralpressureresultsfromtheelasticrecoilofthelungsandthechestwall,keepingthelungstobeinflated.Chestwallmovementcausedbythecontractionofinspiratorymusclesmainlythediaphragmistheprimarydrivingforceforventilation,leadingtochangesinalveolarpressure.Thepressuredifferencebetweenthealveoliandtheatmosphereisthedirectdrivingforcefor

ventilation,leadingtoinhalationorexhalation.2/1/202334InspiratoryMusclesContractThoracicCavityExpandsPleuralPressureBecomesmoreNegativeTranspulmonaryPressureIncreasesAlveolarPressureBecomesSubatmosphericAirFlowsintotheLungsuntilAlveolarPressureEqualsAtmosphericPressureP1XV1=P2XV2Boyle’sLawSequentialEventsOccurduringInspirationLungstendtoInflate2/1/202335SequentialEventsOccurduringExpirationRelaxationofDiaphragmThoracicCavityShrinksNegativePleuralPressureDecreasesTranspulmonaryPressureBecomesSmallAlveolarPressureRisesabovetheAtmosphericPressureLungVolumeTendstoDecreaseAirFlowsouttheLungsuntilAlveolarPressureEqualsAtmosphericPressureP1XV1=P2XV2Boyle’sLaw2/1/202336SequentialEventsOccurduringExpirationRelaxationofDiaphragmThoracicCavityShrinksNegativePleuralPressureDecreasesTranspulmonaryPressureBecomesSmallAlveolarPressureRisesabovetheAtmosphericPressureLungVolumeTendstoDecreaseAirFlowsouttheLungsuntilAlveolarPressureEqualsAtmosphericPressureP1XV1=P2XV2Boyle’sLaw2/1/2023375.1.2.MechanicalPropertiesoftheLungsandChestWallHowthelungsinflateanddeflatenotonlydependontranspulmonarypressurebutalsoelasticpropertiesoflungsandchestwall.Threeterms(elasticrecoil,stiffnessanddistensibility)areusedtodescribetheelasticpropertiesofthelungsandchestwall.2/1/202338Stiffness,DistensibilityandElasticRecoilStiffness（硬度）isdefinedasresistancetobestretchedorinflated.Distensibility（可擴(kuò)張性）isthetermappliedtotheeasewithwhichthelungscanbestretchedorinflated.Elasticrecoil（彈性回縮）isdefinedastheabilityofastretchedorinflatedlungtoreturntoitsrestingvolume(FRC).Distensibiltyandelasticrecoilareinverselyrelatedtoeachother.2/1/202339LungCompliance

(CL)Lungcompliance(CL)isameasureofdistensibility.CLisdefinedbychangeinvolumeperchangeinpressure.ItcanbewrittenasCL=volume/pressure.Wherevolumeequalschangeinvolumeandpressureequalschangeinpressure.CListheslopeofthepressure–volumecurve.2/1/202340MeasurementofCLinHumans2/1/202341FactorsthatAffectCLElasticrecoilInverselyrelatedLungvolumeProportionallyrelatedSurfacetension(willbeanalyzedlater)Inverselyrelated2023/2/142PathologicalConditionsThatAreAssociatedwithReducedCLDamageofelastinfiberse.g.,COPDFibrosisPulmonaryhypertension/congestionIncreasesstiffnessofthelungsAlveolaratelectasise.g.afterprolongedperiodofventilationReducedsurfactant(increasedsurfacetension)e.g.artificialventilation,prematurity2/1/202343ObstructiveandRestrictiveDisorders

AffectCLdifferently2023/2/144ObstructivediseaseRestrictivediseaseRestrictivelungdiseasesareassociatedwithincreasedcollagenfibers(膠原纖維).Obstructivelungdiseases(emphysemaandCOPD)areassociatedwithdamageofelastinfibers(彈性纖維).Smokingdamageselastinfibers,causingemphysema

(肺氣腫).ElasticRecoilofChestWallThechestwallhaselasticproperty.Theoutwardofelasticrecoilofthechestwallaidslongexpansionwhereastheinwardofelasticrecoiloflungpullsinthechestwall.Atabout67%oftotallungcapacity,chestwallisinitsnaturalposition.Iflungvolumeislessthan67%ofTLC,thechestwalltendstorecoiloutward.Iflungvolumeismorethan67%ofTLC,ittendstorecoilinward.2/1/202345ChangesinChestWallComplianceAreLessCommonPathologicsituationspreventingthenormalmovementoftheribcage,suchasdistortionofthespinalcolumn,Pathologic(cancer)orphysiologic(pregnancy)reasonsincreasingtheintraabdominalpressure,Stiffchest,suchasbrokenribs.2/1/202346WhatisSurfaceTension?Surfacetensionisapropertyofthesurfaceofaliquid.Itiswhatcausesthesurfaceportionofliquidtobeattractedtoanothersurface,suchasthatofanotherportionofliquid.Inalveoli,thesurfaceofalveolarmembraneismoistandisincontactwithair,producingalargeair-liquidinterface.Thesurfacetensionpreventstheexpansionofalveoliandrisesresistanceforventilation.2/1/202347HowDoesSurfaceTensionAffectLungCompliance？Theexperimentwasdoneinanisolatedlung.Thelungwasinflatedanddeflatedinastepwisefashion,firstwithairandthenwithsaline.Withair-filledlungs,thegas-liquidinterfacecreatessurfacetension(therelationisdifferentforinspirationandexpiration).Inthesaline-filledlung,air-liquidinterfaceiseliminatedasitssurface.2/1/202348WorksareNeededtoExpandtheLungsSurfacetensioncausesadecreaseinlungcompliance.Twothirdsoftheworkrequiredtoinflatethelungisspenttoovercomesurfacetension(grayarea).ToexpandthelungFirsttoovercomethesurfacetension(grayarea)Thentoovercometheelasticrecoil(bluearea).2/1/202349SurfaceTensionAffectsAlveolarStability*Pindicatesinternalpressurethatisneededtokeepanalveolustobeinflated.*Tindicatessurfacetension*

Ristheradiusofanalveolus2/1/202350拉普拉斯(1749-1827)PulmonarySurfactant:Source&ChemistryPulmonarysurfactantisalipoproteinrichinphospholipid(磷脂).Theprincipalagentresponsibleforitssurfacetension-reducingpropertiesisdipalmitoylphosphatidylcholine(DPPC,二磷脂酰卵磷脂).AlveolartypeIIcellssynthesizeandstorelungsurfactant.Infantsbornbeforegestationalweek26producelittlesurfactant.2/1/202351PhysiologicalFunctionsofSurfactantIncreaseslungcomplianceandconsequentlyreducesventilatoryresistanceStabilizesalveoliKeepsthealveoli“dry”2/1/2023522023/2/153InfantRespiratoryDistressSyndrome/radio/topic710.htm.SummaryonLungComplianceLungcompliance(CL)isdefinedaschangeinvolumeperchangeinpressure.CLisameasureoflungdistensibility;itisinverselyrelatedtostiffness.Abnormallylowlungcomplianceindicatesastifflung,whichmeansmoreworkisneededtoinflatethelungtobringinanormaltidalvolume.Abnormallyhighlungcomplianceresultsinincreasedstaticvolumes(RV,VC,FRCetc).2/1/202354SummaryonSurfaceTensionThesurfacetensionisaforcethatpreventsalveolitobeopenedandrisesresistanceforventilation2/1/202355SummaryonSurfactantProductionPulmonarysurfactantisalipoproteinrichinphospholipid(mainlydipalmitoylphosphatidylcholine,DPPC)andismanufacturedbythealveolarepithelialtypeIIcells.FunctionSurfactantreducessurfacetensionwithinthealveoliwhichhelpstoincreasethecomplianceofthelungandthuslowerrespiratoryresistanceItimprovesalveolarstabilityItkeepsalveolidrybyopposingwatermovementfromthepulmonaryinterstitium5.1.3.VentilatoryResistanceElasticresistance(70%oftotal)Itisastaticresistancethatpreventsthelungstobeinflated.Itresultsfromelasticrecoil(30%)andsurfacetension(70%).Non-elasticresistance(30%oftotal)Itisadynamicresistance,resultingfromthemovementofair.Itconsistsofinertialresistance(慣性阻力),viscousresistance(粘滯阻力)andairwayresistance(80%ofnon-elasticresistance).2/1/202357SurfaceTensionandElasticRecoilMakeUpElasticResistanceToexpandthelung1.Firsttoovercomethesurfacetension(grayarea)2.Thentoovercometheelasticrecoil(bluearea)Twothirdsoftheworkrequiredtoinflatethelungisspenttoovercomesurfacetension.Onethirdoftheworkrequiredtoinflatethelungisspenttoovercometheelasticrecoil.Elasticresistanceconsistsoftwocomponents:surfacetensionandelasticrecoil.2/1/202358AirwayResistanceItmakesthelargestproportion(>80%)ofnon-elasticresistance.IcanbeestimatedbyRaw=P(PA-PB)/V(gasflow)2/1/202359FactorsthatAffectAirwayResistanceThediameteroftheairwaysThenumberofairwaysThelungvolume2/1/202360WhereDoestheAirwayConstitutetheSiteofLargestAirwayResistance?Themedium-sizedairways(2mm)?OrThesmallairways(<2mm)?2/1/202361Themedium-sizedbronchi(2mm)actuallyconstitutethesideofhighestresistancealongthebronchialtree.Althoughthesmallradiiofbronchioles(<2mm)mightpredictthattheywouldhavethelargestresistance,theydonotbecauseoftheirparallelarrangement.Earlychangesinresistanceinthesmallairwaysmaybe“silent”andgoundetectedbecauseoftheirsmalloverallcontributiontoresistance.2/1/202362NeurohumoralControloftheAirwaysMichoudetal2/1/202363TheSmoothMuscleToneofAirwaysisControlledbyNervesSympatheticadrenergicfibersBronchialdilation&inhibitionofglandsecretion.ParasympatheticcholinergicpostganglionicfibersBronchialconstriction&increasedmucussecretionNon-adrenergicnon-cholinergicneuronalfibersBronchcoconstrictoryeffects(tachykinins,substancePorneurokininetc.)Bronchodilatatorypathway(nitricoxideandvasoactiveintestinalpeptide)2/1/2023642-adrenergicReceptorsandcholinergicMuscarinicReceptors

Stimulationofsympatheticadrenergicfiberscausesdilationofbronchialandbronchiolarairwaysvia2adrenergicreceptoractivationandinhibitionofglandsecretion.2-adrenergicagonistsareusedfortreatmentofasthma.Stimulationofparasympatheticcholinergicpostganglionicfiberscausesbronchialconstrictionaswellasincreasedmucussecretionviamuscarinicreceptor(M2/M3)activation.Mreceptorantagonistsareusedfortreatmentofasthma.

2/1/202365LungVolumeinverselyRelatestoAirwayResistance2/1/202366SummaryonVentilatoryResistancesElasticresistance(70%oftotalventilatoryresistance)Itisastaticresistance.Itresultsfromelasticrecoil(30%)andsurfacetension(70%).

Non-elasticresistance(30%oftotal)Itisadynamicresistance.Itconsistsofinertialresistance,viscousresistanceandairwayresistanceTheairwayresistanceaccounts80%ofnon-elasticresistance2/1/202367Respiratoryresistanceelasticresistance(70%)thoracicelasticresistancelungelasticresistanceelasticrecoil(1/3)surfacetension(2/3)inertialresistanceviscousresistanceairwayresistance(80%-90%)non-elasticresistance(30%)SummaryonRespiratoryResistance2/1/2023685.1.4.StaticandDynamicLungVolumesLungvolumesdeterminedbyanatomicalsizesofthepulmonarytract2/1/2023692023/2/1702023/2/1702023/2/170StaticLungVolume（靜態(tài)肺容積）

Spirometry(肺量計(jì)),adevicethatisusedtomeasurethevolumeofairthatisbreathedinoroutofthelungs.Notalllungvolumescanbemeasureddirectlybyspirometry(e.g.RVanditsrelatedFRCandTLC)

2023/2/1712023/2/1712023/2/1712023/2/171“Volume”vs.“Capacity”Lungvolume（肺容積）

andlungcapacity（肺容量）

areusedindifferentterms.Volumeisusedwhenonlyonevolumeisinvolved,andcapacityisusedwhenavolumecanbebrokendownintotwoormore.Forexample,thefunctionalresidualcapacity(FRC)isthesumofERVandRV.ImportantPulmonaryVolumesThetidalvolume(潮氣量,VT)isthevolumeofairinspiredorexpiredwitheachnormalbreath.Theinspiratoryreservevolume(補(bǔ)吸氣量或吸氣儲(chǔ)備量,IRV)istheextravolumeofairthatcanbeinspiredoverandabovethenormaltidalvolume.Theexpiratoryreservevolume(呼氣儲(chǔ)備量或,補(bǔ)呼氣量，ERV)isthemaximumextravolumeofairthatcanbeexpiredbyforcefulexpirationaftertheendofnormaltidalexpiration.Theresidualvolume(余氣量或殘氣量,RV)isthevolumeofairremaininginthelungsaftermaximumexpiration.2023/2/172ImportantLungCapacitiesTheinspiratorycapacity(吸氣容量或深吸氣量,IC)isthevolumeofgasthatcanbetakenintothelungsinafullinhalation,startingfromtherestinginspiratoryposition;ICisequaltothetidalvolumeplustheinspiratoryreservevolume(IRV).Thefunctionalresidualcapacity(功能殘氣量，F(xiàn)RC)isthevolumeofairremaininginthelungsafteranormalexpiration;FRC=REV+RV.Thevitalcapacity(VC)isthemaximumamountofairapersoncanexpelfromthelungsafterfillingthelungstothemaximumextentandthenexpiringtothemaximumextent;VC=IRV+VT+ERV.Thetotallungcapacity(肺總量,TLC)isthemaximumamountofairinthelungattheendofgreatestpossibleeffort;TLC=VC+RV.2023/2/173InterrelationsFRC=ERV+RVFRC:functionalresidualcapacity;ERV:expiratoryreservevolume;RV:residualvolumeVC=IRV+VT+ERV=IC+ERVVC:vitalcapacity;IC:inspiratorycapacity(IRV+VT);ERV:expiratoryreservevolume;IRV:inspiratoryreservevolumeTLC=IC+FRC=VC+RVTLC:totallungcapacity;IC:inspiratorycapacity(IRV+VT);FRC:functionalresidualcapacity;RV:Residualvolume2/1/2023742023/2/1752023/2/175FunctionalResidualCapacity(FRC)

Itisthevolumeofairremaininginthelungsafteranormalexpiration;itisthesumofERVandRV.Itcannotbemeasuredbyspirometrydirectly.Itdullsoxygenandcarbondioxideconcentrationfluctuationsinthealveoliduringarespiratorycycle.ClinicalConditionsthatAffectFRCFactorsthatreduceFRCAgePosture–supinepositionAnesthesia–musclerelaxantsSurgery-LaparoscopicPulmonaryfibrosisFactorsthatincreaseFRCCOPDEmphysemaSmoking2023/2/1772023/2/1772023/2/177VitalCapacityandItsRelatedThevitalcapacity(VC)isthemaximumamountofairapersoncanexpelfromthelungsafterfillingthelungstothemaximumextentandthenexpiringtothemaximumextent(VC=IRV+VT+ERV).Whenexpirationisperformedasrapidlyandasforciblyaspossible,VCiscalledforcedvitalcapacity(FVC).Forcedexpiredvolumeinonesecond(FEV1):Thevolumeexpiredinthefirstsecondofmaximalexpirationafteramaximalinspiration.Itisoneofmostreliablespirometrymeasurements.FEV1/FVCistheFEV1tobeexpressedasapercentageofFVC,whichcorrectsfordifferencesinlungsize.Normally,FEV1/FVCis0.8.FVCIsaUsefulMeasurementinAssessingVentilatoryFunction2023/2/1782023/2/178MinuteVentilation（分鐘通氣量）2023/2/179DefinitionTheamountofairisbroughtinoroutofthelungsinaminute.ItcanbewrittenasVE=VTXfVE=minuteventilation;VT=tidalvolume;f=breathingrate.Inadults,thetidalvolume(VT)is500mlandbreathingrateis12beats/min,thustheminuteventilation(VE)is6,000ml.NotalloftheInspiredAirParticipatesinGasExchange2023/2/180Deadspace(無效腔或死腔，VD)TheportionofeachtidalvolumethatdoesnottakepartingasexchangeVDisaresultoftheanatomyoftheairways;itisreferredtoasanatomicVDAsVT=Tidalvolume（潮氣量)VD=Deadspacevolume（無效腔容積）VA=Alveolarventilation（肺泡通氣量）

VT=VD+VA

81Anatomicaldeadspace:Thetotalvolumeoftheconductingairwaysfromthenoseormouthdowntotheleveloftheterminalbronchioles.

Alveolardeadspace:Inspiredairthatisdistributedtoalv