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Anatomy and Physiology of Respiratory System Relevant To Anaesthesia
Anatomy and Physiology of Respiratory System Relevant To Anaesthesia
IndianJAnaesth.2015Sep59(9):533541. PMCID:PMC4613399
doi:10.4103/00195049.165849
Anatomyandphysiologyofrespiratorysystemrelevanttoanaesthesia
ApekshPatwa1,2andAmitShah1,2
1
KailashCancerHospitalandResearchCentre,MuniSevaAshram,Goraj,Vadodara,Gujarat,India
2
DepartmentofAnaesthesia,VadodaraInstituteofNeurologicalSciences,Vadodara,Gujarat,India
Addressforcorrespondence:Dr.ApekshPatwa,B31/32,KailashParkDuplex,AimsOxygenLane,AksharChowk,OldPadraRoad,Vadodara390
020,Gujarat,India.Email:apekshpatwa@gmail.com
Copyright:IndianJournalofAnaesthesia
ThisisanopenaccessarticledistributedunderthetermsoftheCreativeCommonsAttributionNonCommercialShareAlike3.0License,whichallows
otherstoremix,tweak,andbuildupontheworknoncommercially,aslongastheauthoriscreditedandthenewcreationsarelicensedundertheidentical
terms.
Abstract Goto:
Clinicalapplicationofanatomicalandphysiologicalknowledgeofrespiratorysystemimprovespatient'ssafety
duringanaesthesia.Italsooptimisespatient'sventilatoryconditionandairwaypatency.Suchknowledgehas
influenceonairwaymanagement,lungisolationduringanaesthesia,managementofcaseswithrespiratory
disorders,respiratoryendoluminalproceduresandoptimisingventilatorstrategiesintheperioperativeperiod.
Understandingofventilation,perfusionandtheirrelationwitheachotherisimportantforunderstandingrespiratory
physiology.Ventilationtoperfusionratioalterswithanaesthesia,bodypositionandwithonelunganaesthesia.
Hypoxicpulmonaryvasoconstriction,animportantsafetymechanism,isinhibitedbymajorityoftheanaesthetic
drugs.Ventilationperfusionmismatchleadstoreducedarterialoxygenconcentrationmainlybecauseofearly
closureofairway,thusleadingtodecreasedventilationandatelectasisduringanaesthesia.Variousanaestheticdrugs
alterneuronalcontrolofthebreathingandbronchomotortone.
Keywords:Anatomy,bronchomotortone,functionalresidualcapacity,physiology,respiratorysystem,
tracheobronchialtree,ventilationperfusion
INTRODUCTION Goto:
Accurateknowledgeofanatomyandphysiologyoftherespiratorytractisimportantnotonlyinthefieldof
pulmonologybutalsoinanaesthesiologyandcriticalcare.About7080%ofthemorbidityandmortalityoccurring
intheperioperativeperiodisassociatedwithsomeformofrespiratorydysfunction.[1]Generalanaesthesiaand
paralysisareassociatedwithalterationsintherespiratoryfunction.[2,3]Dynamicanatomicalchangesand
physiologicalalterationhappeningduringanaesthesiamakeitimperativeforananaesthesiologisttohavesound
knowledgeoftherespiratorysystemandapplyitforsafeandsmoothconductofanaesthesia.Suchknowledgehas
influenceonclinicalpracticeofairwaymanagement,lungisolationduringanaesthesia,managementofcaseswith
respiratorydisorders,respiratoryendoluminalproceduresandsurgeries,optimisingventilatorstrategiesin
perioperativeperiodanddesigningairwaydevices.
ANATOMYOFRESPIRATORYSYSTEM Goto:
Therespiratorysystem,functionally,canbeseparatedintwozonesconductingzones(nosetobronchioles)forma
pathforconductionoftheinhaledgasesandrespiratoryzone(alveolarducttoalveoli)wherethegasexchange
takesplace.Anatomically,respiratorytractisdividedintoupper(organoutsidethoraxnose,pharynxandlarynx)
andlowerrespiratorytract(organwithinthoraxtrachea,bronchi,bronchioles,alveolarductandalveoli).
Thediscussionismainlyconcentratedonthelowerrespiratorytractandtherelatedphysiology.
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Noseandnasalcavityaredividedintotwohalvesbythenasalseptum.Thelateralwallofthenoseconsistsofthree
turbinatesorconchae(superior,middleandinferior).Thepassageinferiortoinferiorturbinateispreferredpassage
fornasotrachealintubation.[4]Thepharynxisatubelikepassagethatconnectstheposteriornasalandoralcavities
tothelarynxandoesophagus.Itisdividedintonasopharynx,oropharynxandlaryngopharynx.Increaseinsoft
tissuewithinbonyenclosureofpharynxordecreaseinbonyenclosuresizewouldresultinanatomicalimbalance
andcauselimitationofspaceavailableforairway[Figure1].[5]
Figure1
Excessivesofttissue(obesity)infixbonyenclosureleadstocompromised
pharyngealpassage
Therearethreenarrowestportionsofpharynxpassageposteriortothesoftpalate(retropalatalspace),passage
posteriortothetongue(retroglossalspace)andpassageposteriortoepiglottis(retroepigloticspace).Thereis
significantreductionofthesespaceswithsedationandanaesthesia[6]whichwouldleadtoupperairway
obstruction.
ANATOMICALFACTORSWHICHCOMPROMISESPHARYNGEALPATENCY Goto:
Inefficientcontractionofpharyngealdilatormuscles[Figure2]
Figure2
Upperairwayshowingpharyngealdilatormusclesandpharyngealairway
space
(1)Thetensorpalatineretractsthesoftpalateawayfromtheposteriorpharyngealwall,therebymaintainingretro
palatalpatency.(2)Thegenioglossusmovesthetongueanteriorlytoopentheretroglossalspace.(3)Hyoidmuscles
(geniohyoid,sternohyoidandthyrohyoid)makethehyoidmoveanteriorlyandstabilisetheretroepiglotic
laryngopharynx.Excessivefatdepositionaroundthesemuscleswouldresultininefficientcontractionofpharyngeal
dilatormuscles.Thiswouldleadtopharyngealairwayobstructionduringsedationandanaesthesia.[7]
Anatomicalimbalanceoforopharyngealsofttissue
Enlargedtongue(inthecaseofacromegalyorobesity)innormalbonyenclosureoforopharynxorasmallerbony
enclosure(recedingmandible)oforopharynxwouldbeunabletoaccommodatethetongueintooropharynxand
thusshiftthetongueintohypopharynx(laryngopharynx).Hypopharyngealtonguedecreaseslaryngopharyngeal
airwaypatency.Thisisonereasonforobstructivesleepapnoeaanddifficultmaskventilationduringanaesthesia.[8]
Trachealtug
Thereisconstanttractionontrachea,pharynxandlarynxduringinspirationbecauseofnegativeintrathoracic
pressurewhichelongatespharyngealairwayduringinspirationthatwouldresultindecreasedpharyngealluminal
spaceinobesepatients.Thisisalsooneofthereasonsfordifficultmaskventilationandobstructivesleepapnoea.
[9]
Larynx
Itservesasasphincter,transmittingairfromoropharynxandnasopharynxtotrachea.
TRACHEOBRONCHIALTREE Goto:
Itisacomplexsystemthattransportsgasesfromthetracheadowntotheacini,thegasexchangeunitsofthelung.It
ispartitionedinto23generationsofdichotomousbranching,extendingfromtrachea(generation0)tothelastorder
ofterminalbronchioles(generation23).Ateachgeneration,eachairwayisbeingdividedintotwosmallerdaughter
airways[10][Figure3].
Figure3
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Tracheobronchialtreeshowing23generations
Fromthetracheatotheterminalbronchioles(generation1516),theairwaysarepurelyconductingpipes.Sinceno
gasexchangestakeplaceinthisregion,thevolumeinthesepipesiscalledasthedeadspacevolume(average150
ml).Theterminalbronchioles(generation16)divideintorespiratorybronchiolesortransitionalbronchioles
(generations1719)astheyhaveoccasionalalveoliatthewalls.Theserespiratorybronchiolesfurtherdivideinto
alveolarducts(generations2022)whicharecompletelylinedwithalveoli.Thisregionisknownasacinus
(generations1623).Theacinusiscomprisedofrespiratoryairwaysandformsfunctionaltissues(gasexchange
units)oflung.Thealveolarductsaresmalltubessupportedbyarichmatrixofelasticandcollagenfibres.Thedistal
endsofalveolarductsopenintothealveolarsacwhichismadeupbyalveoli.
TRACHEAANDRIGHT/LEFTMAINBRONCHUS Goto:
Thetracheaisahollowconduitforgasesandbronchialsecretions.ItextendsfromthelevelofC6(cricoid
cartilage)tothecarina,approximatelylocatedatthelevelofT4T5.[11]Inadults,itslengthisapproximately1113
cm,with24cmbeingextrathoracic.[12]Thetracheahas16to22horseshoebands(cshaped)ofcartilages.The
posteriortrachealwalllackscartilageandissupportedbythetrachealismuscle.Dependingonthelevelof
inspiration,theposteriorwallofthetracheabecomesflat,convexorslightlyconcave.[13,14]Theposteriorwallof
thetracheaeitherflattensorbowsslightlyforwardduringexpiration.Innormalsubjects,thereisupto35%
reductioninanteroposteiortracheallumeninforcedexpiration,whereasthetransversediameterdecreasesonlyby
13%.[15]Thetracheaisgenerallymidlineinposition,oftendisplacedslightlytotherightandposteriorlyasit
approachescarina.Theangleofthetrachealbifurcationiscalledasthecarinal/subcarinalangle,whichismeasured
commonlyas73(3590).[16,17,18]Thecarinalangleiswiderinindividualswithanenlargedleftatrium,in
femalesandobesepatients.
Thetracheadividesatcarinaintotherightandleftmainbronchus.Thedistanceofthecarinafromtheteethvaries
markedlywithchangeinneckpositionfromflexiontoextension(tracheallengthvariationis2cm),bodyposition
andpositionofdiaphragm.[19]Thisexplainsthechangeinpositionofendotrachealtubeduringchangeinposition
ofpatientorflexionextensionofneck.Therightmainstembronchushasamoredirectdownwardcourse,is
shorterthantheleftandbeginstoramifyearlierthantheleftmainbronchus.[11]Thisleadstohigherchancesof
rightendobronchialintubation.Therightmainstembronchusdividesinto(secondarybronchi)rightupperlobe
bronchusandbronchusintermediuswhichfurtherdividesintorightmiddleandlowerlobebronchus.Theleft
bronchuspassesinferolaterallyatagreateranglefromtheverticalaxisthantherightbronchus.Theleftmainstem
bronchusdividesinto(secondarybronchi)theleftupperandlowerlobebronchi.
BRONCHOPULMONARYSEGMENT Goto:
Bronchopulmonarysegmentmaybedefinedasanareaofdistributionofanybronchus[Figure4].Eachlobar
bronchidividesintosegmentalbronchi(tertiarybronchi),whichsupplythebronchopulmonarysegmentofeach
lobe.Technically,therearetenbronchopulmonarysegmentsineachlung,butinleftlung,someofthesesegments
fuseandthereareasfewaseightbronchopulmonarysegments.Thebronchicontinuetodivideintosmallerand
smallerbronchiupto23generationsofdivisionsfrommainbronchus.Asbronchibecomesmaller,theirstructure
changes:
Figure4
Tracheobronchialtreewithbronchopulmonarysegments
Cartilaginousringbecomesirregularandthendisappear.Whenbronchiloseallcartilaginoussupport,the
airwayisthenreferredasbronchioles
Theepitheliumchangesfrompseudostratifiedcolumnartocolumnartocuboidalintheterminalbronchioles
Therearenociliaandmucousproducingcellsinbronchioles
Theamountofsmoothmuscleinthetubewallincreasesastheairwaybecomessmaller.
DIMENSIONSOFTRACHEOBRONCHIALTREE[TABLE1]
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DIMENSIONSOFTRACHEOBRONCHIALTREE[TABLE1] Goto:
Table1
Dimensionsandfeaturesoftracheobronchialtree
Ascertainingtheparametersoftracheobronchialtreesuchaslength,diametersandangulationshelpsoptimizing
proceduressuchasintubation,lungisolationtechniquesandjetventilationduringinterventionalendoscopic
surgeriesoftracheaorbronchi.[20]
Tracheobronchialanatomicalvariations
Tracheobronchialtreeexhibitsawiderangeofvariationsanditsprevalenceis4%.[28]Themostcommonmain
bronchusanomaliesarethetrachealbronchusandtheaccessorycardiacbronchus.Knowledgeoftracheobronchial
variantsisimportantforclinicalaspectinpreoperativeevaluationinviewofintubation,lungisolationtechniques
andotherendobronchialprocedures.
Trachealbronchus Thisisabronchususuallyoriginatingfromtherightsideofthetracheaabovethecarinaand
within26cmfromit.[29]Righttrachealbronchushasaprevalenceof0.12%andleftbronchushasaprevalence
of0.31%.[30,31,32,33,34]Thetrachealbronchusmaycausecomplicationssuchasatelectasisorpneumothoraxin
thecasesofobstructiontoitsentranceortubeenteringintoitduringintubation.[35,36,37]
Accessorycardiacbronchus Itisacongenital,shortandthinbronchustowardspericardiumoriginatingeither
fromrightbronchusorintermediatebronchus.Itsprevalenceis0.08%.[31]Itisassociatedwithrecurrentinfections
infewcases.[38]
PHYSIOLOGYOFRESPIRATORYSYSTEM Goto:
Movementofinspiredgasintoandexhaledgasoutoflungiscalledasventilation.Understandingoflungvolumes,
lungcompliance,ventilationperfusionandbronchomotortoneareessentialforclinicalapplicationofrespiratory
physiologyinanaesthesiaandcriticalcare.
Lungvolumes[Figure5]
Figure5
Lungvolumes
Normalrequirementsofthebodycanbeeasilymetbynormaltidalventilationwhichisapproximately48ml/kg.
Bodyhaskeptmechanismtoprovideextraventilationintheformofinspiratoryreservevolumeandexpiratory
reservevolumewheneverrequired(e.g.,exercise).Whenanindividual,aftertidalexpiration,takesfullinspiratory
breathfollowedbyexpirationtoreservevolume,itiscalledasvitalcapacitybreathandis45Linanaverage70
kgindividual.Thereisalwayssomeamountofairremaininginthealveoliwhichpreventsitfromcollapsing.The
volumeremaininginthelungsaftervitalcapacitybreathiscalledasresidualvolume.
Residualvolumewithexpiratoryreservevolumeiscalledasfunctionalresidualcapacity(FRC).FRCisbasically
theamountofairinthelungsafteranormalexpiration.Gasesremaininginthelungsattheendofexpirationnot
onlypreventalveolarcollapsebutalsoitcontinuestooxygenatethepulmonarybloodflowingthoughthe
capillariesduringthistimeperiod.[39]ReportedFRCvaluesvarywithvariousreportsbutonaverageitisbetween
2.8and3.1L[40]instandingposition.FRCvarieswithchangeofposition,anaesthesiaandbodyweight.FRCis
thereservewhichprolongsnonhypoxicapnoeatime.
Theportionoftheminuteventilationwhichreachesalveoliandtakespartinthegasexchangeiscalledasalveolar
ventilation.Normalvalueofalveolarventilationisapproximately5L/minwhichissimilartothevolumeofblood
flowingthroughthelung(cardiacoutput5L/min).Thismakesalveolarventilationtoperfusionratioapproximately
one.[39]
RESPIRATORYMECHANICS Goto:
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Lungsarelikeinflatableballoonwhichdistendactivelybypositivepressureinsideand/ornegativepressurecreated
inpleuralspace.Innormalrespiration,negativepleuralpressure(Ppl)issufficienttodistendthelungsduring
inspiratoryphase.Understandingofdistendingpressureisveryimportanttounderstandtherespiratorymechanics.
Distendingpressurecanbeknownastranspulmonarypressure(Ptp),whichisexpressedbythefollowingequation:
Ptp=PawPpl,(Ptp=transpulmonarypressure,Paw=alveolarpressure,Ppl=Pleuralpressure).
Complianceandventilationoflung
ComplianceisexpressedasthedistensionoflungforagivenlevelofPtp.Itisusually0.20.3L/cmH2O.[41]
Compliance(abilityoflungtodistend)dependsuponthevolumeofthelung.Complianceislowestatextremesof
FRC.Itimpliesthatexpandedlungandcompletelydeflatedlunghaslowercapacitytodistendtoagivenpressure[
Figure6].Intheuprightlung,intraPplvariesfromthetoptothebaseofthelungs.IntraPplbecomes0.2cmH2O
positiveforeverycentimetredistancefromapextobaseoflung.Averageheightoflungisabout35cm.Inquite
breathing,theintraPplatapexisabout8cmofH2Owhileatbaseitis1.5cmofH2O.Thismeansthatthe
alveoliattheapexareexposedtoagreaterdistendingpressure(PAPpl=0(8)=8cmH2O)comparedtothose
atthebase(PAPpl=0(1.5)=1.5cmH2O).Asalreadydistended,apicalregionbecomeslesscompliantthan
otherareaoflung.Thisexplainsthepreferentialdistributionofventilationtothealveoliatthebaseofthelungsin
uprightposture.DistributionofventilationchangeswiththepositionofindividualbecauseofthechangeofPpl
withthegravity.
Figure6
Transpulmonarypressure
Airwayclosureduringexpirationisnormalphenomenon,withreopeningofairwaysduringthesucceeding
inspiration.[42]ThevolumeremainingabovetheresidualvolumewhereexpirationbelowFRCclosessome
airwaysistermedasclosingvolumeandthisvolumeaddedtotheresidualvolumeistermedastheclosingcapacity.
Inuprightposition,closingcapacityapproachesnearFRCinolderindividual(6570years)whichwouldresultin
airwayclosureevenatnormaltidalexpiration.Changeinbodypositionfromuprighttosupine,lateralorprone
reducesFRC.ReductioninFRCpromotesairwayclosureindependentlungregions.Earlyairwayclosurethus
decreasesventilationinthedependentregions.Sincelungbloodflowpassespreferentiallytodependentregions,
matchingbetweenventilationandperfusionisimpeded.[43]
Perfusionoflung
Pulmonarycirculationdiffersfromsystemiccirculation.Thepulmonaryvesselsarethinwalledandhaveless
musculaturetoassistfastdiffusionofgases.Theyaresubjectedtolesspressurecomparedtosystemiccirculation.
Becauseoflesspressureandstructuraldifferencesofpulmonaryvasculaturetoassistdiffusion,theyaresubjected
toPawinsidethethoraxandgravity.[44]
Onthebasisoftheinfluenceofgravity,perfusionoflungisdividedintothreezones.[45]Thedistributionofblood
flowinthesezonesdependsuponthreefactors:Alveolarpressure(PA),pulmonaryarterialpressure(Pa)and
pulmonaryvenouspressure(Pv).
ApicalregionwherePAcanbehigherthanPaandPvisconsideredaszoneI.SincePA>Pa>PvinzoneI,no
arterialbloodflowoccursandthiszoneisconsideredasphysiologicaldeadspace.ThoughsuchzoneIdonotexist
inhealthysubjectundernormalperfusionpressure,inconditionofhaemorrhageorpositivepressure,ventilation
zoneImaybecomerealityandaddstodeadspaceventilation.
InmiddlezoneorzoneII,differenceofPatoPAdecidestheperfusion(Pa>PA>Pv)whileinlowerzoneorzone
III,differenceofPatoPv(Pa>Pv>PA)decidestheperfusion.Fewstudiesalsoinclude4thzoneoflessblood
supplybecauseofthecompressionofvesselsduetotheweightoflungs.[46]
Thezonesdescribedearlierarepurelyphysiologicalandnotanatomical.Thebordersbetweenzoneschangeswith
manyphysiologicalandpathophysiologicalalterationsorconditions.Pawchangesareminimalduringthecourseof
aquietbreathbuttheyaremuchgreaterduringspeech,exerciseandotherconditions.Thepatientsonpositive
pressureventilationwithpositiveendexpiratorypressure(PEEP)mayhavesubstantialzoneIduetohighPAs.Pa
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alterswithseverehaemorrhageorduringgeneralanaesthesiaresultinginzoneIconditions.Pulmonaryartery
pressureishighduringexercise,eliminatinganyexistingzoneIintozoneIIandmovingtheboundarybetween
zonesIIIandIIupward
Ventilationtoperfusionmatching
Thealveolarpartialpressureofoxygenandcarbondioxidearedeterminedbytheratioofventilation(V)to
perfusion(Q).Asdiscussedearlier,ventilationandperfusionbothincreasefromtoptobottominlungs,but
perfusionincreasesmoreincomparisontoventilation.
Proportionately,ratioofventilationtoperfusionismoreinupperlungandlesstowardsthebaseoflungs[Figure7].
Thisgradientoccursinverticalaxisofthelungfieldsirrespectiveofbodypositions.(i.e.,ifpatientisinupright
posture,apexhasmoreventilationwhilebasehasmoreperfusion.Ifpatientisinlateralposture,nondependentlung
getsmoreventilationwhiledependentlunggetsmoreperfusion).
Figure7
Ventilationperfusionratiofromapextothebaseoflung
HYPOXICPULMONARYVASOCONSTRICTION Goto:
Hypoxicpulmonaryvasoconstriction(HPV)iscompensatorybloodflowawayfromhypoxiclungregionstobetter
oxygenatedregions.HPVoccursinresponsetolowalveolaroxygentension.ThismechanismimprovestheV/Q
mismatch.Allinhalationagentsexceptneweragents,sevofluraneanddesflurane,inhibittheHPV.[39]
PHYSIOLOGICALVARIATIONWITHPOSITIONANDANAESTHESIA Goto:
Supineposition
Generalanaesthesiapromotesbasalatelectasisirrespectiveofthemodesofventilation(spontaneousorcontrolled)
ordrugs(intravenousorinhalation)used.Nearly,1520%ofthelungisatelectaticduringgeneralanaesthesia.
Atelectasisdecreasestowardstheapex,whichusuallyremainsaerated.[42]Theareaofatelectasisbecomesthearea
ofshuntwherenogasexchangeoccursinspiteofperfusion.Earlyairwayclosureintidalbreathingwithsupine
position,promotesventilationperfusionmismatch(V/Q<1)andimpairmentofgasexchange.Thecombinationof
atelectasisandairwayclosureexplainsabout75%oftheoverallimpairmentinoxygenationinanaesthetised
subject.[47]
Lateralpositionandonelungventilation
Anaesthesiainlateralpositioncausesventilationperfusionmismatchwhereupperornondependentlungreceives
moreventilationandlowerordependentlungreceiveshigher(6065%)perfusion.Dependentlungalsoexhibits
signsofearlyairwayclosureandformationofatelectasis.WithadditionofPEEP,almost80%ofbloodflowis
directedtolowerdependentlung.[47]Duringonelungventilation,HPVcandivertbloodflowawayfromthenon
ventilatedlung.OneshouldavoiddrugscausinginhibitionofHPV.
Proneposition
Pronepositiondecreasesventilationperfusionmismatchandimprovestheoxygenation.Variousreasons(e.g.,
uniformverticaldistributionofperfusion,betterventilationdistributionbecauseofsmallerverticalpleuralgradient,
increasedFRC,moreuniformgasdistributionandlesslungcompressionbyheart)havebeenproposedbydifferent
authorsforimprovementinventilationwithproneposition.Therearenoreportsofatelectasisinproneposition,
probablybecauseweightofhearttransferredonthesternuminsteadoflungsasopposedtosupineposition.[42]
NEUROLOGICALCONTROLOFBREATHING Goto:
Therespiratorycentresarelocatedinponsandmedulla.Theycontaindifferenttypesofinspiratoryandexpiratory
neuronsthatfireduringthethreephasesoftherespiratorycycle,namelyinspiratoryphaseofsuddendischargeof
signalstoinspiratorymusclesandthedilatormusclesofthepharynx,followedbygradualdeclineofsignalsinpost
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inspiratoryphase.Inspirationisfollowedbynosignalsinexpiratoryphaseexceptinforcedexpirationorhigh
minuteventilation.[48]Inhalationalagentsinfluencerate,rhythmandintensityofdischargefromtherespiratory
centreswhichreceiveinputsfromthechemoreceptors,cortex,hypothalamus,pharyngealmechanoreceptors,vagus
nerveandotherafferents.Peripheralchemoreceptorsrespondquicklytohypoxia,hypercapniaandhydrogenion
concentration.Thecentralchemoreceptorsareslowrespondersrelativetoperipheralchemoreceptors.
BRONCHOMOTORTONE Goto:
Bronchomotortoneisthestateofcontractionorrelaxationofthesmoothmuscleinthebronchialwallsthat
regulatesthecalibreoftheairways.Numberoffactorsinfluencesthechangeofbronchomotortone,e.g.depthof
anaesthesia,drugsandvariousproceduresonairway,respiratorydiseases(bronchialasthma)andinhalational
agents.Usingcomputedtomography,Brownetal.hadshowedthathalothanecausesgreaterbronchodilatation
thanisofluraneatlowconcentrations.[49]Sevoflurane(1minimumalveolarconcentration)reducedrespiratory
systemresistance(determinedusinganisovolumetechnique)by15%inpatientsundergoingelectivesurgery.In
contrast,desfluranedidnotsignificantlyalterresistance.[50]
SUMMARY Goto:
Clinicalapplicationoftheanatomicalknowledgeofrespiratorysystemdefinitelyimprovessafetyofconductof
anaesthesiaandalsooptimisespatientventilatoryconditionandairwaypatency.Suchknowledgehasinfluenceon
theclinicalpracticeofairwaymanagement,lungisolationduringanaesthesia,managementofcaseswithrespiratory
disorders,respiratoryendoluminalproceduresandsurgeries,optimisingventilatorstrategiesinperioperativeperiod,
applyingjetventilationduringemergencyandendoluminalsurgeriesanddesigningairwaydevices.
AnanaesthesiologistshouldunderstandthatFRCisthemostimportantparameter.Itsrelationwithclosingcapacity
isanimportantdeterminantofventilationofpatient.Ventilationandperfusionbothareaffectedbythegravity.
Overallventilationtoperfusionratiois1butitalterswithanaesthesia,bodypositionsandwithonelung
anaesthesia.HPV,animportantsafetymechanism,isinhibitedbymajorityofanaestheticdrugs.Ventilation
perfusionmismatchleadingtoreducedarterialoxygenconcentrationismainlybecauseofearlyclosureofairway
leadingtodecreasedventilationandatelectasisoccurringwiththeanaesthesia.Variousanaestheticdrugsalter
neuronalcontrolofthebreathingandbronchomotortone.
Financialsupportandsponsorship
Nil.
Conflictsofinterest
Therearenoconflictsofinterest.
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