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RevisiononPulmonaryPhysiologyand
Disorders
Dr. YeungManNga,Mandy
Rm423,SchoolofNursing
Tel:39176684
Email:mandyymn@hku.hk 1
Whatiselasticrecoil?
Tendencyofanelasticobjecttoreturntoitsoriginalshapeafteritis
deformedbyanexternalforce.
Atequilibrium,recoilpressurehasthesamemagnitudeastheforceapplied,
buttheyareofoppositedirection.
2
Elasticrecoiloftherespiratorysystem
Ifyouwanttoinflatethelungs,youhavetoovercometheelasticrecoilofthe
respiratorysystem
1. Elasticrecoilofthelung
a. Whatisthenaturalpositionofthelungs? Collapsed(thelungsarealways
expandedinsidechestcavity)
b. Whatcontributestotherecoilpressureofthelungs?
i. Elasticityoflungtissue
ii. Surfacetensioninalveoli
2. Elasticrecoilofthechestwall
a. Whatisthenaturalpositionofthechestwall?
b. Whatcontributestotherecoilpressureofthechestwall?
3
Surfacetensionoftheairliquidinterface
Capillary
TypeIalveolarcells
(respiratorysurface) TypeIIalveolarcells
(secretessurfactant)
https://beyondthedish.wordpress.com/2011/11/21/ 4
Elasticrecoiloftherespiratorysystem
Ifyouwanttoinflatethelungs,youhavetoovercometheelasticrecoilofthe
respiratorysystem
1. Elasticrecoilofthelung
a. Whatisthenaturalpositionofthelungs? Collapsed(thelungsarealways
expandedinsidechestcavity)
b. Whatcontributestotherecoilpressureofthelungs?
i. Elasticityoflungtissue
ii. Surfacetensioninalveoli
2. Elasticrecoilofthechestwall
a. Whatisthenaturalpositionofthechestwall? 60%Vitalcapacity
b. Whatcontributestotherecoilpressureofthechestwall?
i. Elasticityofthechestwalltissue
5
Lungvolumesandcapacities
Lungvol.(L) Maximalinspiration
Chestwall
expanded
6.0
60%VC
3.0
compressed
Chestwall
2.5
1.5
Maximalexpiration
6
Q3.Lungvolumeat______________isconsideredthenaturalposition
oftherespiratorysystem. Noenergyexpenditureis
requiredtomaintainthis
A. tidalvolume position(i.e.nomuscle
B. residualvolume contractionneeded)
C. totallungcapacity
D. functionalresidualcapacity(Endexpiratorypositionatrest)
Outwardrecoilofchestwall= inwardrecoiloflungs
Intrapleuralpressure(Pip)= 4mmHg
7
Q4.Whenlungvolumeisatresidualvolume,
A. thelungsarerecoilingoutward.
B. thechestwallisrecoilingoutward.
C. inspiratorymusclesareactively
contractingtomaintainthisposition.
Chestwallrecoil> lungrecoil
D. transpulmonary pressureatthis Energy neededtoovercome
positionislargerthanwhenlung therecoilpressuredifference
volumeisattotallungcapacity.
Pressuredifference
betweeninside&
outsideofthelungs 60%VC
= Palv Pip
= forcethatexpands
thelungs NP
RV
8
Q5.Lungcompliance
A. isconstantatanylungvolume.
B. increaseswithincreasinglungvolume.
C. ishigherinsupineposition.lungvol.,pulmonarybloodow
D. ishigherinpatientwithemphysema.lungtissuedestruction
E. ishigherinpatientwithpulmonaryfibrosis scarringoflungtissue
F. decreaseswithage. lung ssue
Lungtissueisverystretched
highrecoilpressure
9
Q6.Airwayresistance(Raw) 1/r4
A. isthelowestinthetracheaasithasthe Lowesttotalcross
largestradius. sectionalarea
B. isthehighestinthesmallbronchiolesas Highesttotalcross
theyhavethesmallestradii. sectionalarea
C. isconstantthroughoutarespiratorycycle.lungvol. Raw
lungvol. Raw
D. isdecreasedincaseofpulmonaryfibrosis.
lungcompliance
elas crecoil Radialtraction
radialtraction
Air
way
10
Lungfunctiontests
Q1.Whichofthefollowingstatementsabout
vitalcapacityis/arecorrect?
A. Itcanbemeasuredbyusinga
simplespirometer.
Measuresall lungvol.andcapacities
B. Itcanbemeasuredbyusing bymeasuringtheamountofN inthe
2
nitrogenwashouttechnique. lungsatthebeginningoftest.
C. Increaseinvitalcapacitymay Expansionoflungsisrestricted
indicaterestrictivelungdiseases. (e.g.pulmonaryfibrosis)
D. Patientwithemphysemawillshow
increasedforcedvitalcapacity.
11
Normallungs Characteristics:
1. lungcompliance
2. alllungvolumes&
capaci es
IC
Pulmonaryfibrosis ERV
ERV
RV
http://en.wikipedia.org/wiki/Idiopathic_pulmonary_fibrosis#mediaviewer/File:Ipf_NIH.jpg 12
Lungfunctiontests
Q1.Whichofthefollowingstatementsaboutvitalcapacity
is/arecorrect?
A. Itcanbemeasuredbyusinga
simplespirometer.
Abletomeasurealllungvol.
B. Itcanbemeasuredbyusing andcapacities.Principleof
nitrogenwashouttechnique. testistomeasuretheamount
ofN2 inthelungs.
C. Increaseinvitalcapacitymay Expansionoflungsisrestricted
indicaterestrictivelungdiseases. (e.g.pulmonaryfibrosis)
D. Patientswithemphysemahave
increasedforcedvitalcapacity. Obstructivedisease
(airwayobstruction)
13
Normal Emphysema
IC
ERV
IC
RV
Characteristics:
1. ___________ofalveolarwall
destruction
enlarged lungcompliance TLC
2. ________alveolidueto________________
narrowing radialtraction ERV,RV
3. __________ofsmallairwaysduetoreduced_____________
http://www.acbrown.com/lung/Lectures/RsVntl/RsVntlPthpEmph.htm 14
Lungfunctiontests
Q1.Whichofthefollowingstatementsaboutvitalcapacity
is/arecorrect?
A. Itcanbemeasuredbyusinga
simplespirometer.
Abletomeasurealllungvol.
B. Itcanbemeasuredbyusing andcapacities.Principleof
nitrogenwashouttechnique. testistomeasuretheamount
ofN2 inthelungs.
C. Increaseinvitalcapacitymay Expansionoflungsisrestricted
indicaterestrictivelungdiseases. (e.g.pulmonaryfibrosis)
D. Patientswithemphysemahave Obstructivedisease
increasedforcedvitalcapacity. (airwayobstruction)
decreased Standardtestforassessing
airwayobstruction:
=FEV1/FVCratio(<0.8)
15
Matchingalveolarventilationwithperfusion
MostefficientwaytoloadO2 andremoveCO2
1. everyalveolushasfreshairsupply(ventilation)
2. capillarybloodflowisavailableforeachalveolus(perfusion)
Matchedventilationandperfusion(@normalrestingstate)
. .
alveolarventilation/perfusionratio(VA/Q)~ 0.8
PartlyregulatedbyalveolarPO2
Ifthereisanymismatch inventilationandperfusion
changeinalveolarventilation/perfusionratio
ventilationperfusioninequality(chiefcauseofhypoxemiainvariousdisease)
inefficientgasexchange
affectarterialpartialpressures
16
Ventilationperfusioninequality
1. Alveolusisnotventilatedandthereissufficientbloodsupply
. .
VA/Q=0(shunt)
a. WhathappenstoalveolarPO2 andPCO2?
PO2 ________;PCO
2_________
b. WhathappenstoPO2 andPCO2ofeffluentblood?
eventuallythesameasthatofthemixedvenousblood
c. WhathappenstoarterialPO2 andPCO2?
PaO2 _______;PaCO
2________
NormalmixedvenousPO2 =40
NormalmixedvenousPCO2 =45
17
Ventilationperfusioninequality
2. Alveolusiswellventilated,butnobloodsupply
. .
VA/Q=
a. WhathappenstoalveolarPO2 andPCO2?
PO2 ________;PCO
2_________
b. WhathappenstoPO2 andPCO2ofeffluentblood?
eventuallythesameasthatoftheinspiredair(ifthereisanyblood)
NormalalveolarPO2 =100
NormalalveolarPCO2 =40
AtmosphericPO2 =160
alveolus AtmosphericPCO2 =0.3
NormalmixedvenousPO2 =40
NormalmixedvenousPCO2 =45
18
Howdoesventilationperfusioninequality
affectarterialPO2?
Littlebloodflow
1. PO2 inbothalveoliand
Littleventilation blood
1. PO2 inbothalveoli 2. little intotalO2 carried
andblood permlblood(HbO2 curve)
2. totalO2 carried
permlblood
PaO2 isdetermined
bytherelative
amountofblood
thatcomefromthe3
typesofalveoli
19
Howdoesventilationperfusioninequality
affectarterialPCO2?
Littlebloodflow
PCO2 inbothalveoli
Littleventilation andblood
PCO2 inbothalveoli
andblood
PaCO2 isdetermined
bytherelativeamount
ofbloodthatcome
fromthe3typesof
alveoli
20
OveralleffectofV/Qmismatch
DecreasedPaO2 (hypoxemia)andincreasedPaCO2(hypercapnia)
AnincreaseinPaCO2 triggerschemoreceptorreflex
increasesventilation(respiratorycompensation)
PaCO2 returnstonormal
butPaO2 cannotreturntonormalvalue
(duetohighO2 saturationatPO2 >60mmHg)
97.5%
21
cerebrum
Regulationofbreathing
Limbicsystem
Q1.Respiratorycontrolcentres Hypothalamus
arelocatedinthe
A. midbrainandpons. Central
B. ponsandmedulla. Pneumotaxic chemoreceptors
centre
C. midbrainandmedulla. Apneustic
D. hypothalamusand centre
medulla. CNIXandX
Peripheral
chemoreceptors
Baroreceptors CNX Inspiratory
Q2.Apneusticcentre Stretch
centre
receptors Expiratory
centre
A. stimulatesinspir.centre
B. inhibitsinspir.centre
C. stimulatesexpir.centre
D. inhibitsexpir.centre
22
Q3.Whichofthefollowingreceptorsisinvolvedinregulationof
breathinginresponsetochangesinpH?
A. TypeJreceptors Pathologicalconditions(e.g.pulmonaryoedema)
B. Stretchreceptor HeringBreuerreflexforfeedback
C. Irritantreceptors regulationofbreathingrhythm
D. Chemoreceptors
1. central(medullaoblongata)
2. peripheral(aorticandcarotidbodies)
23
Q4.Whichofthefollowingstatementsiscorrectaboutthechangesin
respiratorysysteminresponsetodiabeticketoacidosis?
high H+ in blood
A. Centralchemoreceptorsareactivatedleadingtoa
largeincreaseinventilation. NotactivatedasH+ ionscannotcross
bloodbrainbarrierreadily
B. Bothcentralandperipheralchemoreceptorsare
activatedleadingtoalargeincreaseinventilation.
C. Centralchemoreceptorsareinhibitedwhile DuetoPCO2 as
peripheralchemoreceptorsareactivated ventilationincreases
resultinginaslightincreaseinventilation.
D. Centralchemoreceptorsareactivatedwhile
peripheralchemoreceptorsareinhibited
resultinginaslightincreaseinventilation.
24
Q5.Concerningtheperipheralchemoreceptors:
A. TheyrespondtochangesinarterialPO2
butnotpH.
B. Theyarethemostimportantreceptors
thatcauseincreaseinventilationin Central chemoreceptorasCSF
havelittlebufferingcapacityso
responsetoariseinPCO2. thatslightchangesinPCO2
resultsinalargerchangeinpH.
C. TheirresponsetochangesinPCO2 is
slowerthanthatofthecentral Fasterastheyareinclose
chemoreceptors. proximitywitharterialblood
D. Undernormalcondition,theirresponse
tochangesinPO2 isverysmall.
25
WhenPCO2 iskeptconstant@40mmHg
PO2 willcausealargeincreasein
ventilationesp.whenPO2 <60mmHg
Therefore,theoveralleffectofPO2
=aslightincreaseinventilation
26
Q6.Themostpowerfulstimulusforbreathinginaheathypersonis
A. lossofO2 intissues.
B. increaseinCO2.
C. pH(acidosis).
D. pH(alkalosis).
Respiratoryfailure
Definition:
Respiratoryfailureoccurswhenthelungsfailtooxygenatethearterial
bloodadequatelyand/orfailstopreventCO2 retention
Generalindicationforrespiratoryfailure:
1. PaO2 lowerthan60mmHg(hypoxemia)and/or
2. PaCO2 greaterthan50mmHg(hypercapnia)
28
TypeIandTypeIIRespiratoryFailure
TypeIfailure TypesIIfailure
Causes Gas exchangefailure Ventilationfailure
1. Impairedgasdiffusion 1. Hypoventilation
2. V/Qmismatch
Problemwithbreathing
Mostlungdiseases(e.g.fibrosis, apparatus(e.g.complianceis
COPD,pulmonaryoedema) toolow,neurodepression,
weaknessinrespiratory
muscles)
Presence ofrespiratory
compensation Yes No orinsufficient
(chemoreceptorreflex)
AlterationinPO2 Low,< 60mmHg Low,<60mmHg
1. normal
AlterationinPCO2 High,>50mmHg
2. normal 50mmHg
29
Impaired diffusion V/Qmismatch Ventilation failure
AlterationinPO2
Normal(asCO2
AlterationinPCO2 diffusion is20Xfaster
thanO2)
Presence of
Yesdueto
respiratory YesduetolowPO2 No orinsufficient
PCO2
compensation
PO2 Towards normal Towardsnormal
PCO2 Normal
Hypoventilation