Functional Physiology of Respiratory System

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FUNCTIONAL PHYSIOLOGY

OF RESPIRATORY SYSTEM1. MECHANICS OF BREATHING:

2. REGULATION AND CONTROL OFBREATHING:

3. VENTILATION4. LUNG VOLUMES AND PULMONARYFUNCTION TESTS

5. DIFFUSION6. PERFUSION

7. GAS TRANSPORT TO THE PERIPHERY 8. ACIDBASE REGULATION

!. RESPIRATORY SYSTEM UNDER STRESS1" RESPIRATORY FAILURE



1. MECHANICS OFBREATHING

• INSPIRATION: I#$%&'()&*# &$ )+, (-)&, %(') */ )+, 0',()+&#%'*-,$$ +&-+ &$ &#&)&(), 0 )+, respiratory control centre in me!llao"lon#ata $%rain stem&' Acti(ation o) me!lla ca!ses a contraction o) t*eiap*ra#m an intercostal m!scles leain# to an e+pansion o) t*oracicca(ity an aecrease in t*e ple!ral space press!re' T*e iap*ra#m is aome,s*ape str!ct!re t*at separates t*e t*oracic an a"ominal ca(ities

an is t*e most important m!scle o) inspiration' -*en it contracts. it mo(eso/n/ar an "eca!se it is attac*e to t*e lo/er ri"s it also rotates t*eri"s to/ar t*e *ori0ontal plane. an t*ere"y )!rt*er e+pans t*e c*estca(ity' In normal 1!ite "reat*in# t*e iap*ra#m mo(es o/n/ar a"o!t 2cm "!t on )orce inspiration3e+piration total mo(ement co!l "e !p to24cm' -*en it is paralyse it mo(es to t*e opposite irection $!p/ars&

/it* inspiration. paradoxical movement. The external intercostal musclesconnect adjacent ribs. When they contract the ribs are p!lle !p/ar an)or/ar ca!sin# )!rt*er increase in t*e (ol!me o) t*e t*oracic ca(ity' As ares!lt )res* air 5o/s alon# t*e "ranc*in# air/ays into t*e al(eoli !ntil thealveolar pressure equals to the pressure at the airway opening.



MECHANICS OFBREATHING

• EPIRATION: E%&'()&*# &$ ( %($$&, ,,#) , )* ,9($)&-',-*&9 */ )+, 9#$. H*,,' +,# ( ',()

• eal o) air *as to "e remo(e 1!ic6ly. as in e+ercise. or /*en t*eair/ays narro/ e+cessi(ely !rin#

• e+piration. as in ast*ma. t*e internal intercostal m!scles an t*e

anterior a"ominal m!scles contract• an accelerate e+piration "y raisin# ple!ral press!re'

• COUPLING OF THE LUNGS AND THE CHEST ALL: T+, 9#$(', #*) &',-)9 ())(-+, )*

• t*e c*est /all "!t t*ey c*an#e t*eir (ol!me an s*ape accorin# to

t*e c*an#es in s*ape an (ol!me• o) t*e t*oracic ca(ity' Ple!ra co(erin# t*e s!r)aces o) t*e l!n#s

$(isceral& or t*e t*oracic ca(ity

• $parietal& to#et*er /it* a t*in $74 8m& layer o) li1!i "et/een t*emcreate a li1!i co!plin#'



MECHANICS OFBREATHINGPRESSUREVOLUME RELATIONSHIPS: In t*e p!lmonary

p*ysiolo#y a"sol!te press!re means atmosp*eric press!re $9:4mm H# at sea le(els&' T*e press!res an t*e press!re i;erenceso) t*e respiratory system are e+presse as relati(e press!res tot*e atmosp*eric press!re' -*en it is sai t*at al(eolar press!re is0ero. it means t*at al(eolar press!re < atmosp*eric press!re'

I) one e+cises animal l!n# an places it in a =ar. one co!l

meas!re t*e c*an#es in (ol!me /it* a spirometer t*ro!#* acann!la attac*e to t*e trac*ea' -*en t*e press!re insie t*e =ar"elo/ atmosp*eric press!re. t*e l!n# e+pans an t*e c*an#e inits (ol!me is meas!re an t*e press!re (ol!me c!r(e is plotte'-*en t*ere is no press!re istenin# t*e l!n# t*ere is a small(ol!me o) #as in it' As t*e press!re in t*e =ar is #ra!ally re!ce.t*e (ol!me o) t*e l!n#s increases' T*is is initially a rapi e(ent"!t a)ter a certain press!re t*e c*an#es "ecome less e(ient' Itmeans t*at t*e l!n# is sti;er /*en it is e+pane an t*ere"y. t*epress!re,(ol!me c!r(es !rin# in5ation an e5ation are i;erent< hysteresis. Another important point is the volume at a given

pressure during defation isal/ays lar#er t*an !rin# in5ation'E(en /*en t*e press!re o!tsie t*e l!n# is increase a"o(e t*e




COMPLIANCE> T*e slope o) t*e press!re,(ol!me c!r(e. t*e (ol!me c*an#eper !nit press!re is

6no/n as compliance. In normal expanding range (!"# mm water$ the lung isvery dispensable%in

ot*er /ors it is (ery compliant' T*e compliance o) t*e *!man l!n# is 4'2?L3cm H7O' Ho/e(er. it

#ets sti;er $compliance smaller& as it is e+pane a"o(e t*e normal ran#e'Compliance is reduced

/*en

$2& T*e p!lmonary (eno!s press!re is increase an t*e l!n# "ecomesen#or#e /it* "loo

$7& T*ere is al(eolar oeema !e to ins!@ciency o) al(eolar in5ation

$& T*e l!n# remains !n(entilate )or a /*ile e'#' atelectasis an

$B& %eca!se o) iseases ca!sin# "rosis o) t*e l!n# e'#' c*ronic restricti(e l!n#isease'

On t*e contrary in c*ronic o"str!cti(e p!lmonary isease $COPD. e'#'emp*ysema& t*e al(eolar /alls pro#ressi(ely e#enerate. /*ic* increasesthe compliance. The lung compliance is changed according to t*e l!n#si0e> O"(io!sly t*e compliance o) a mo!se l!n# is m!c* smaller t*an a*!man l!n ' At t*e "irt* t*e l!n com liance is t*e smallest an increase




T*e stanar proce!re )or meas!rin# compliance in *!mans is toetermine t*e press!re,(ol!me relations*ip !rin# a passi(e e+piration)rom total l!n# capacity' as t*e l!n# e5ates slo/ly. al(eolar press!re ise1!al to atmosp*eric press!re. an ple!ral press!re is nearly same ast*e press!re in t*e oesop*a#!s. /*ic* is !s!ally meas!re /it* a t*in,/alle "alloon attac*e (ia a plastic t!"e to a press!re,sensor'

CHEST ALL COMPLIANCE: C*an#es in c*est /all compliance are lesscommon t*an c*an#es in t*e l!n# compliance>

$2& pat*olo#ic sit!ations pre(entin# t*e normal mo(ement o) t*e ri" ca#e.s!c* as.

istortion o) t*e spinal col!mn.$7& pat*olo#ic $cancer& or p*ysiolo#ic $pre#nancy& reasons increasin# t*e

intra

a"ominal press!re.

$& sti; c*est. s!c* as "ro6en ri"s'




• SURFACE TENSION: A )+&# ;9< */ 9&=& 9&#,$ )+, (9,*9& (# )+,$'/(-, ),#$&*# */ )+&$ ;9< &$ anot*er important )actor in t*e press!re,(ol!me relations*ip o) t*e l!n#' T*e s!r)ace tension arises "eca!se t*eattracti(e )orces "et/een a=acent molec!les o) t*e li1!i are m!c* stron#ert*an t*ose o) "et/een t*e li1!i an t*e #as' As a res!lt o) t*at t*e li1!is!r)ace area "ecomes as small as possi"le' At t*e inter)ace "et/een t*e

li1!i an t*e al(eolar #as. intermolec!lar )orces in t*e li1!i ten to ca!set*e area o) t*e linin# to s*rin6 $t*e al(eoli ten to #et smaller&' T*e s!r)acetension contri"!tes to t*e press!re,(ol!me "e*a(ior o) t*e l!n#s "eca!se/*en t*e l!n#s are in5ate /it* saline t*ey *a(e m!c* lar#er compliancet*at /*en t*ey are lle /it* air $"eca!se saline a"olis*es t*e s!r)acetension&' T*is "e*a(ior can clearly "e seen in a soap "!""le. "lo/n on t*e eno) a t!"e' T*e s!r)aces o) t*e "!""le contract as m!c* as possi"le an )orm

t*e smallest possi"le s!r)ace area. a sp*ere' T*is #enerates a press!repreicte )rom Laplaces la/> P',$$', >?4 $'/(-, ),#$&*#@ '(&$

T*e s!r)ace tension contri"!tes a lar#e part o) t*e static recoil )orce o) t*el!n# $e+piration&' T*e s!r)ace tension c*an#es /it* t*e s!r)ace area> T*elar#er t*e area t*e smaller t*e s!r)ace tension #ets'



MECHANICS OFBREATHINGS'/(-)(#)

T*e most important component o) t*is li1!i lm is s!r)actant' Itis pro!ce "y type 7 al(eolar epit*elial cells an its ma=orconstit!ent is ipalmitoyl p*osp*otiylc*oline $DPPC&. ap*osp*olipi/it* eter#ent properties' T*e p*osp*olipi DPPC issynt*esise in t*e l!n# )rom )atty acis t*at areeit*er e+tracte)rom t*e "loo or are t*emsel(es synt*esise in t*e l!n#'

Synt*esis is )ast an t*ere is a rapi t!rno(er o) s!r)actant' I) t*e"loo 5o/ to a re#ion o) l!n# is restricte !e to an em"ol!s t*es!r)actant may "e eplete in t*e e;ecte area' S!r)actantsynt*esis starts relati(ely late in )oetal li)e an premat!re "a"ies/it*o!t ae1!ate amo!nt o) s!r)actant e(elop respiratoryistress /*ic* co!l "e li)e t*reatenin#'

-*at are t*e a(anta#es o) *a(in# s!r)actant an t*e lo/ s!r)acetension

2' It increases t*e compliance o) t*e l!n#

7' It re!ces t*e /or6 o) e+panin# o) t*e l!n# /it* eac* "reat*

' It sta"ilises t*e al(eoli $t*!s t*e smaller al(eoli o not collapse at

t*e en,e+piration&



2. REGULATION AND CONTROL OF BREATHING:In orer to maintain normal le(els o) partial o+y#en an car"on io+ie press!re in "loo"ot* t*e ept* an rate o) "reat*in# are precisely re#!late' %asic elements o) t*e

respiratory control system are $2&strate#ically place sensors $7& central controller $&respiratory m!scles'

CENTRAL CONTROLLER: %reat*in# is mainly controlle at t*e le(el o) "rainstem' T*enormal a!tomatic an perioic nat!re o) "reat*in# is tri##ere an controlle "y t*erespiratory centres locate in t*e pons an me!lla' T*ese centres are not locate in aspecial n!cle!s or a #ro!p o) n!clei "!t t*ey are rat*er poor ene collection o) ne!rones'

1.M,99(' ',$%&'()*' -,#)',:

,&orsal medullary respiratory neurones are associated with inspiration' It has been proposed that spontaneo!s intrinsic perioic rin# o) t*ese ne!rones responsi"le )or t*e"asic r*yt*m o) "reat*in#' As a res!lt. t*ese ne!rones e+*i"it a cycle o) acti(ity t*at arisesspontaneo!sly e(ery )e/ secons an esta"lis* t*e "asic r*yt*m o) t*e respiration' -*ent*e ne!rones are acti(e t*eir action potentials tra(el t*ro!#* retic!lospinal tract in t*e

spinal cor an p*renic an intercostal ner(es an nally stim!late t*e respiratorym!scles'



REGULATION AND CONTROL OF BREATHING:

• ,Ventral medullary respiratory neurones areassociated with expiration. These neurones are silent!rin# 1!ite "reat*in# "eca!se e+piration is a passi(e e(ent)ollo/in# an acti(e inspiration' Ho/e(er. t*ey are acti(ate!rin# )orce e+piration /*en t*e rate an t*e ept* o) t*erespiration is increase e'#' e+ercise' D!rin# *ea(y"reat*in# increase acti(ity o) t*e inspiratory centrene!rones acti(ates t*e e+piratory system' In t!rn. t*eincrease acti(ity o) t*e e+piratory system in*i"its t*einspiratory centre an stim!lates m!scles o) e+piration'

• T*e orsal an (entral #ro!ps are "ilaterally paire ant*ere is cross comm!nication "et/een t*em' As aconse1!ence t*ey "e*a(e in sync*rony an t*e respiratorymo(ements are symmetric'



REGULATION AND CONTROL OFBREATHING:

2.A%#,$)&- C,#)',: It is locate in t*e lo/er pons' E+act

role o) t*is centre in t*e normal "reat*in# is not 6no/n'Lesions co(erin# t*is area in t*e pons ca!se a pat*olo#icrespiratory r*yt*m /it* increase apnea )re1!ency' -*atis 6no/n is ner(e imp!lses )rom t*e apne!stic centrestim!late t*e inspiratory centre an /it*o!t constant

in5!ence o) t*is centre respiration "ecomes s*allo/ anirre#!lar'

3.P#,<*)(&- -,#)',> It is locate in t*e !pper pons' T*iscentre is a #ro!p o) ne!rones t*at *a(e an in*i"itory e;ecton t*e "ot* inspiratory an apne!stic centres' It is pro"a"lyresponsi"le )or t*e termination o) inspiration "y in*i"itin#t*e acti(ity o) t*e orsal me!llar ne!rones' It primarilyre#!lates t*e (ol!me an seconarily t*e rate o) t*erespiration' %eca!se in t*e lesions o) t*is are a normalrespiration is protecte it is #enerally "elie(e t*at !pperpons is responsi"le )or t*e ne,t!nin# o) t*e respiratory

r*yt*m'




Hypoacti(ation o) Pne!mota+ic centre ca!ses prolon#eeep inspirations an "rie). limite e+pirations "y allo/in#t*e inspiration centre remain acti(e lon#er t*an normal'Hyperacti(ation o) t*is centre on t*e ot*er *an res!lts ins*allo/ inspirations' T*e apne!stic an pne!mota+iccentres )!nction in co,orination in orer to pro(ie ar*yt*mic respiratory cycle>

'

• Acti(ation o) t*e inspiratory centre stim!lates t*e m!scles

o) inspiration an also t*e pne!mota+ic centre' T*en t*epne!mota+ic centre in*i"its "ot* t*e apne!stic an t*einspiratory centres res!ltin# ininitiation o) e+piration'Spontaneo!s acti(ity o) t*e ne!rones in t*e inspiratorycentre starts anot*er similar cycle a#ain




%reat*in# in some e+tent is also controlle conscio!sly)rom *i#*er "rain centres $e'#' cere"ral corte+&'T*is controlis re1!ire /*en /e tal6. co!#* an (omit' It is alsopossi"le (ol!ntarily c*an#e t*e rate o) t*e "reat*in#'Hyper(entilation can ecrease "loo partial car"on io+iepress!re $PCO7& !e to loss o) CO7 res!ltin# in perip*eral(asoilatation an ecrease in "loo press!re' One can alsostop "reat*in# (ol!ntarily' T*at res!lts in a ecrease inarterial partial o+y#en press!re $PO7&. /*ic* pro!ces an!r#e to "reat*e' -*en e(ent!ally PCO7 reac*es t*e *i#*

eno!#* le(el it o(erries t*e conscio!s in5!ences )rom t*ecorte+ an stim!lates t*e inspiratory system' I) one *ols*is "reat* lon# eno!#* to ecrease PO7 to a (ery lo/ le(elone may loose *is conscio!sness' In an !nconscio!s persona!tomatic control o) t*e respiration ta6es o(er an t*e

normal "reat*in# res!mes' Ot*er parts o) t*e "rain $lim"icsystem. *ypot*alam!s& can also alter t*e "reat*in# pattern




SENSORS:1.MECHANORECEPTORS: T+,$, ',-,%)*'$ (', %9(-, &# )+,

(99$ */ 0'*#-+& (# 0'*#-+&*9,$ */ t*e l!n# an t*e main)!nction o) t*ese receptors is to pre(ent t*e o(erin5ation o) t*el!n#s' In5ation o) t*e l!n#s acti(ates t*ese receptors an

acti(ation o) t*e stretc* receptors in t!rn in*i"its t*e ne!rones ininspiratory centre (ia (a#!s ner(e' -*en t*e e+piration startsacti(ation o) t*e stretc* receptors #ra!ally ceases allo/in#ne!rones in t*e inspiratory ne!rones "ecome acti(e a#ain' T*isp*enomenon is calle Hering-Breuer Refex . It is particularlyimportant or inants. In adults it is )!nctional only !rin# e+ercise

/*en t*e tial (ol!me is lar#er t*an normal'2.CHEMORECEPTORS> T*e respiratory system maintains

concentrations o) O7. CO7 an t*e pH o) t*e "oy 5!is /it*in t*enormal ran#e o) (al!es' Any e(iation )rom t*ese (al!es *as amar6e in5!ence on t*e respiration' C*emoreceptors arespecialise ne!rones acti(ate "y c*an#es in O7 or CO7 le(els int*e "loo an t*e "rain tiss!e. respecti(ely




' T*ey are in(ol(e in t*e re#!lation o) respiration accorin# to t*e c*an#es inPO7 an pH' O7,sensiti(e c*emoreceptors $Perip*eral c*emoreceptors& arelocate at t*e "i)!rcation o) t*e caroti artery in t*e nec6 an t*e aorticarc*' T*ey are small (asc!lar sensory or#ans encaps!late /it* t*econnecti(e tiss!e' T*ey are connecte to t*e respiratory centre in t*eme!lla "y #lossop*arin#eal ner(e $caroti "oy c*emoreceptors& an t*e(a#!s ner(e $aortic "oy&' Central c*emoreceptors are locate "ilaterallyin t*e c*emosensiti(e area o) t*e me!lla o"lon#ata an e+pose to t*ecere"rospinal 5!i $CSF&. local "loo 5o/ an local meta"olism' T*eyact!ally respon to c*an#es in H concentration in t*ese compartments'-*en t*e "loo partial PCO7 is increase CO7 i;!ses into t*e CSF )romcere"ral (essels an li"erates H' $-*en CO7 com"ines /it* /ater )ormscar"onic aci an li"erates H an HCO& An increase in H stim!lates

c*emoreceptors res!ltin# in *yper(entilation /*ic* in t!rn re!ces PCO7 int*e "loo an t*ere)ore in t*e CSF' Cere"ral (asoilatation al/aysaccompanies an increase PCO7 an en*ances t*e i;!sion o) CO7 intot*e CSF' %eca!se CSF *as less protein t*an "loo it *as a m!c* lo/er"!;erin# capacity' As a res!lt c*an#es in pH )or a #i(en c*an#e in PCO7 isal/ays "i##er t*an t*e c*an#e in "loo'




CO7 le(el is a ma=or re#!lator o) respiration' It is m!c* more importantt*an o+y#en to maintain normal respiration' E(en (ery small c*an#es incar"on io+ie le(els $? mm H# increase in PCO7.hypercapnia$ in the bloodcause large increases in the rate and depth o respiration ("## ) increase in(entilation&' *ypocapnia% lower than normal +,- level in the blood causes in

periods in which respiratory mo(ements o not occ!r' E;ects o) PO7 $i) t*e

c*an#es occ!r /it*in t*e normal ran#e& on respiration is (ery minor' Aecrease in PO7 is calle hypoxia and only ater # ) decrease in +- can pro!ce si#nicant c*an#es in respiration' T*is is !e to t*e nat!re o) O7,H"sat!ration t*at at any PO7 le(el a"o(e 4 mm H# H" is sat!rate /it* O7'Conse1!ently only "i# c*an#es in PO7 pro!ce symptoms ot*er/ise it iscompensate "y O7. /*ic* is "o!n /it* H"'

In stro6e patients or p*ysiolo#ically at *i#* altit!e "loo PO7 le(el may

rop consiera"ly an acti(ate perip*eral c*emoreceptors an acti(atestim!lation' At *i#* altit!e "eca!se t*e a"ility o) t*e l!n# to eliminate CO7 isnot a;ecte. in response to increase respiration. "loo PCO7 is ecrease' I)PO7 rops !ner certain le(el respiratory system oes not respon an eat*/ill occ!r'




• RESPIRATORY MUSCLES:D&(%+'(< &#),'-*$)(9 <$-9,$(# )+, *)+,' (--,$$*'

',$%&'()*' m!scles /or6 in co,orination )or normal "reat*in#!ner central controller' T*ere is

e(ience s!##estin# t*at inpremat!re ne/,"orn "a"ies t*is co,orination is not mat!re eno!#* an

t*is co!l "e responsi"le )or t*e



JENTILATION• AIRAYS AND AIRFLO:

In*ale air passes t*ro!#* t*e conducting airways andeventually reac*es t*e respiratory epit*eli!m o) t*e l!n#s' T*e con!ctin# air/ays consist o) a series o) "ranc*in#t!"es /*ic* "ecome narro/er. s*orter an more n!mero!sas t*ey penetrate eeper into t*e l!n#' T*e trachea dividesinto right and let main bronchi% which in turn divide intolobar% then segmental bronchi. This process continues down

to the terminal bronchioles% which are the smallest airways/it*o!t al(eoli' Since t*e con!ctin# air/ays *a(e noal(eoli t*ey o not ta6e part in #as e+c*an#e "!t constit!tet*e anatomical dead space. Its volume is about "# ml butit varies because airways are not ri#i !rin# inspiration.

respiratory t!"es are len#t*ene an ilate. especially ineep "reat*in#' Since t*e air/ays ser(e as a "arrier as/ell. *arm)!l )orei#n material incl!in# most micro,or#anisms can not easily enter t*e lo/er respiratorypassa#es' T*e (ery rst "arrier starts at t*e (esti"!les o)

t*e nose. /*ic* contain *airs. an *ealt*y. stic6y m!c!sinterceptin# air,"orne particles' can inter)ere /it* ciliary



JENTILATION

• Co!#*in# occ!rs in response to c*emical or mec*anicalirritation o) ner(e enin#s in t*e !pper respiratory tract' T*elaryn+ an t*e "i)!rcation o) t*e trac*ea are t*e mostsensiti(e re#ions an any particles o) )orei#n matter lo#ein t*ese re#ions are remo(e /*en a co!#* sens a rapi

"last o) air s/eepin# o!t t*e respiratory tree'

• T*e al(eolate re#ion o) t*e l!n# incl!es respiratorybronchioles (divided rom terminal bronchioles an *a(e onlyoccasional al(eoli on t*eir /alls& an alveolar ducts(completely lined with alveoli$. T*is 0one is calle respiratory

/one and the gas exchange occurs here. The distance romthe terminal"ronc*iole to t*e istal al(eo!s is only a )e/mm. "!t t*e respiratory 0one ma6es !p most o) t*e l!n#. its(ol!me "ein# a"o!t 7'? to L'



JENTILATION

• %loo is "ro!#*t to t*e ot*er sie o) t*e "loo,#as "arrier)rom t*e ri#*t *eart "y p!lmonary arteries. /*ic* also)orm a series o) "ranc*in# t!"es leain# to t*e p!lmonarycapillaries an "ac6 to t*e p!lmonary (eins' T*ecapillaries lie in t*e /alls o) t*e al(eoli an )orm a ensenet/or6 t*at t*e "loo contin!o!sly r!ns in t*e al(eolar/all' At restin# not all t*e capillaries are open "!t /*ent*e press!re rises $e'#' e+ercise& recr!itment o) t*e closecapillaries occ!rs' T*e iameter o) a capillary se#ment isa"o!t 24 8m. =!st lar#e eno!#* )or a re "loo cell' T*ep!lmonary artery recei(es t*e /*ole o!tp!t o) t*e ri#*t*eart. "!t resistance o) p!lmonary circ!it is (ery lo/' T*isena"les t*e *i#* "loo 5o/ to t*e circ!it'



LUNG JOLUMES AND PULMONARYFUNCTION TESTS

•

P!lmonary )!nction can "e e+amine "y the spirometry technique.Spirometers are the traditional tools o) t*e respiratory p*ysiolo#ists' T*e s!"=ect "reat*es into a close system in /*ic* air is trappe $"ell&' Ast*e s!"=ect "reat*es air mo(ement into or o!t o) t*e mo!t*piece ca!sest*e "ell to rise $inspiration& or )all $e+piration&' Corresponin# mo(ementso) an attac*e pen re#ister t*e c*an#e in (ol!me on a rotatin# r!mrecorer' From s!c* a recorin# /e co!l meas!re

• T&(9 *9<, ?TV@: V*9<, */ (&' &#+(9, *' ,+(9, &)+ ,(-+0',()+ '&# #*'<(9 0',()+&# $4'? L&'

• I#$%&'()*' ',$,', *9<, ?IRV@: M(&<(9 *9<, */ (&' &#+(9, ())+, ,# */ ( #*'<(9 &#$%&'()&*# $ L&

• E%&'()*' ',$,', *9<, ?ERV@: M(&<(9 *9<, */ (&' ,+(9,() )+, ,# */ ( )&(9 *9<,$2'7 L&'

• I#$%&'()*' -(%(-&) ?IC@: M(&<(9 *9<, */ (&' &#+(9, (/),' (#*'<(9 ,%&'()&*# ?3.6 L@ $TJIRJ&

• F#-)&*#(9 R,$&(9 C(%(-&) ?FRC@: T+, *9<, */ ($ )+()',<(&#$ &# )+, 9# () )+, ,# */ ( passi(e e+piration' $7,7'? L or B4 Ko) t*e ma+imal l!n# (ol!me& $ERJRJ&'

• R,$&(9 V*9<, ?RV@: T+, *9<, */ ($ ',<(&#$ &# )+, 9# (/),'

<(&<(9 ,%&'()&*#. $2,2'7 L&• FRC an RJ can not "e meas!re /it* an orinary spirometer




• T*)(9 L# C(%(-&) ?TLC@: T+, <(&<(9 9# *9<, )+() -(# 0,(-+&,, *9#)('&9. ?56 L@ $IRJERJTJRJ&

• V&)(9 -(%(-&) ?VC@: T+, *9<, */ (&' <*, 0,),,# TLC (# RV. ?45L@ ?IRVERVTV@.

• M!ltiplyin# t*e tial (ol!me at rest "y t*e n!m"er o) "reat*s per min!te #i(es)+, )*)(9 <&#), *9<, ?6 L<&#@. D'&# ,,'-&$, )+, )&(9 *9<, (#

)+, #<0,' */ 0',()+$ %,' <&#), &#-',($, )*pro!ce a total min!te(ol!me as *i#* as 244 to 744 L3min'

• M,($',<,#)$ */ F#-)&*#(9 R,$&(9 C(%(-&) ?FRC@ (# R,$&(9V*9<, ?RV@: T+,', (', )* tec*ni1!es to st!y t*ese (ol!mes>

• Helium Spirometry: n this technique a su!"ect is connected to aspirometer #lled with helium which is (irt!ally insol!"le in t*e "loo' A)tersome "reat*es t*e amo!nt o) *eli!m in t*e l!n# an t*e spirometer reac*

e1!ili"ri!m' %eca!se t*ere is no loss o) #as !rin# t*e e+periment t*e amo!nt o)*eli!m "e)ore $C2 + J2& an a)ter t*e e1!ili"ri!m $C7 + J2 J7& is same'

• V1 > C2 ?V1 V2@• V2 > V1 ?C1 C2@ C2• V2 > FRC

LUNG JOLUMES AND PULMONARY




• Anot*er /ay o) meas!rin# FRC is /it* a "oy plethysmograph.

t is a !ig airtight !ox in which the s!"=ect sits' At t*e en o) anormal e+piration. t*e mo!t*piece is s*!t an t*e s!"=ect ma6esrespiratory e;orts' -*en t*e s!"=ect ma6es an inspiratory e;orta#ainst a close air/ay s3*e sli#*tly increases t*e (ol!me o)*is3*er l!n#. air/ay press!re ecreases an t*e "o+ press!reincreases>

P1V1 > P2?V1DV@ T*e press!re in t*e "o+ "e)ore $P2& an a)ter $P7& t*e respiratory

e;orts.

J> Jol!me in t*e "o+ "e)ore t*e respiratory e;orts an DJ can"e meas!re'

T*e %oyles la/ can also "e applie to t*e #as in t*e l!n#>

P3 V2 > P4 ?V2 DV@ V2 > FRC P.B> Mo!t* press!res "e)ore $P& an a)ter $PB& t*e respiratory

e;orts' I) t*e meas!rement is one )ollo/in# a )orcee+piration

V2 > RV




• TOTAL VENTILATION: T+, )*)(9 *9<, */ )+, ($ 9,(&# )+, 9# %,'#&) )&<,. I/ TV &$ 5"" <9 an t*ere are appro+imately 2? "reat*s3min t*etotal (ol!me o) t*e #as lea(in# t*e l!n#. total (entilation /ill "e ?44 + 2? <9?44 ml3min' It can "e meas!re "y *a(in# t*e s!"=ect "reat* t*ro!#* a (al(et*at separates t*e inspire air )rom e+pire air an collectin# t*e e+pire air'

ALVEOLAR VENTILATION: T+, *9<, */ )+, ($ ',(-+&# )+,

',$%&'()*' *#, */ )+, (&'($. Ho/e(er. not all o) t*e total (entilation (ol!me reac*es t*e al(eoli' 2?4 ml

o) t*e TJ $?44 ml& is le)t

"e*in in t*e air/ays. /*ic* oes not contain al(eoli. t*ere)ore oes notcontri"!te t*e i;!sion

$ Anatomic death space$. Thus% the volume o gas entering the respiratory /one% alveolar ventilation% is $?44,2?4& + 2? < ?7?4 ml3min' T*e meas!remento) al(eolar (entilation is more i@c!lt' One /ay is to meas!re t*e (ol!me o)anatomic ea space an calc!late t*e ea space (entilation' T*is t*ens!"tracte )rom t*e total (entilation' A9,*9(' ,#)&9()&*# > T*)(9,#)&9()&*# A#()*<&- ,()+ $%(-, ,#)&9()&*# A#()*<&- ,( $%(-,,#)&9()&*# > A#()*<&- ,( $%(-, *9<, ',$%&'()&*# /',=,#-




• ANATOMICAL DEAD SPACE: V*9<, */ )+, -*#-)&#(&'($. I) &$ (%%'*&<(),9 15" <9 0) its (ol!me increases/it* lar#e inspiration an epens on t*e si0e an t*e post!re o)t*e s!"=ect'

• Meas!rement o) ea space> $owler%s method: The su!"ect

!reaths pure oxygen through a &al&e !ox an a rapinitro#en analyser samples an meas!res t*e nitro#enconcentration in t*e e+pire air' A)tera sin#le inspiration o) p!reo+y#en $244 K& nitro#en concentration in t*e e+pire air isincrease as t*e #as in t*e ea space is /as*e "y p!reo+y#en' Nitro#en concentration 1!ic6ly reac*es a platea! le(el$al(eolar platea!&' T*e ea space is )o!n "y plottin# nitro#enconcentration a#ainst t*e e+pire (ol!me' T*e e+pire (ol!me !pto t*e (ertical line ra/n s!c* t*at area A < area % representst*e anatomical ea space (ol!me'



PULMONARY FUNCTION TESTS

• PULMONARY FUNCTION TESTS : P9<*#(' /#-)&*# ),$)$(', ,' $,/9 ),$)$ )* &(#*$, se(eral l!n# iseases' T*esimplest "!t one o) t*e most in)ormati(e tests o) l!n# )!nction is a'orced

• expiration.

• TESTS OF VENTILATORY CAPACITY • F*'-, E%&'()*' V*9<, ?FEV@: I) &$ )+, *9<, */ ($

,+(9, &# *#, $,-*# 0 ( /*'-, e+piration )ollo/in# a )!llinspiration $FEV1@. T+, )*)(9 *9<, */ )+, ($ ,+(9, (/),'( /99

•

inspiration represents t*e (ital capacity' Ho/e(er. t*is (al!e co!l"e sli#*tly smaller t*an t*e (ital capacity meas!re /it* a slo/$normal spee& e+piration' T*ere)ore. t*is (al!e is calle 'orced&ital capacity ($V)*. The normal ratio o' the $+V, is /o' $V).



PULMONARY FUNCTION TESTS

• F*'-, E%&'()*' F9* ?FEF2575@: T+&$ <,($',<,#) ',%',$,#)$ )+,,%&'()*' * '(), *,' )+, mile *al) o) t*e FJC $"et/een 7? 9? K&' Itis o"taine "y ienti)yin# t*e 7? K an 9? K (ol!me points o) FJC. meas!rin#t*e time "et/een t*ese points an calc!latin# t*e 5o/ rate'

• I#),'%',)()&*# */ ),$)$ */ /*'-, ,%&'()&*#: O# )+, 0($&$ */ )+,#*9,, *0)(&#, /'*< )+,$, )!nctional tests. l!n# iseases can "e

classie as restricti&e or o!structi&e.• n restricti&e lung diseases $s!c* as p!lmonary "rosis&. t*e (ital capacity

is re!ce to "elo/ normal le(els' Ho/e(er. t*e rate at /*ic* t*e (italcapacity is )orce)!lly e+*ale is normal' In o"str!cti(e l!n# isease $s!c* asast*ma. emp*ysema. "ronc*itis& t*e (ital capacity is normal "eca!se l!n#tiss!e is not ama#e an its compliance is !nc*an#e' In ast*ma t*e smallair/ays $"ronc*ioles& constrict. "ronc*oconstriction increases t*e resistance to

air5o/' Alt*o!#* t*e (ital capacity is normal. t*e increase air/ay resistancema6es e+piration more i@c!lt an ta6es lon#er time' O"str!cti(e isorersare t*ere)ore ia#nose "y tests t*at meas!re t*e rate o) )orce e+piration.s!c* as t*e FEJ2 an FEF7?,9?. A si#nicant ecrease in t*ese (al!ess!##ests an o"str!cti(e l!n# isease'



DIFFUSION

• BLOODGAS ECHANGE: O,# (# -('0*# &*&, <*,0,),,# (&' (# 09** 0 $&<%9, i;!sion> )rom an area o)*i#* to lo/ partial press!re. as simple as /ater r!ns o/n*ill' It isa passi(e process /*ic* means re1!ires no ener#y' $ic0%s law o'di1usion determines the amount o' gas mo&es across t*e

tiss!e is proportional to t*e area o) t*e tiss!e "!t in(erselyproportional to its t*ic6ness' %eca!se t*e "loo,#as "arrier in t*el!n# is e+tremely t*in an *as a (ery lar#e area $?4,244 m7&. it is/ell s!ite to its )!nction' How does the lung achie&e such alarge sur'ace area o' !lood-gas !arrier inside the limitedthoracic ca&ity2 This is achie&ed !y wrapping the

pulmonary capillaries around an enormous num!er o'small air sacs. al(eoli. an eac* a"o!t 23 mm in iameter' T*ereare a"o!t 44 million al(eoli in t*e *!man l!n#. creatin# ? m7s!r)ace area "!t *a(in# a (ol!me o) only B L'



DIFFUSION

• C(9-9()&*#$ */ O,# (# C('0*# D&*&, P(')&(9P',$$',$ D(9)*#$ L(: T*)(9 %',$$', */ ( ($<&)', ?&# *' -($, (&'@ &$ ,=(9 )* )+, $< */ )+,%',$$',$ )+() eac* #as in t*e mi+t!re /o!l *a(einepenently $P(')&(9 P',$$', */ ,(-+ ($@. P'

()<*$%+,', > PN2 PO2 PCO2 > 76" <<H Sinceo+y#en constit!tes 72 K o) t*e atmosp*ere. PO7 < 2? mmH#' nitro#en 9 PN7 < ? mmH# Inspire air also containsmoist!re an its amo!nt may (ary /it* temperat!re etc'Ho/e(er /*en t*e inspire air arri(e t*e al(eoli it is

normally sat!rate /it* /ater (apo!r' %eca!se t*etemperat!re in t*e l!n#s oes not c*an#e si#nicantly/ater (apo!r o) t*e al(eolar air co!l "e consiereconstant $B9 mm H#& P,) ()<*$%+,', > PN2 PO2 PCO2 PH2O > 76" <<H PO7 < 4'72 $9:4,B9& < 2?4

mm H# $o+y#en partial press!re o) t*e inspire air /*en itarri(es al(eoli."e)ore t*e #as e+c*an#e&'



DIFFUSION

• 3hy are the measurements o' 456 and 4)56important2 The measurement o' 456 o' arterial!lood is partic!larly important "eca!se it pro(ies a #ooine+ o) l!n# )!nction' T*e act!al amo!nt o) issol(e O7is a linear )!nction o) t*e PO7> T*e *i#*er PO7 inicates

t*at more O7 is issol(e' %loo PO7 meas!rements arenot a;ecte "y t*e O7 in re cells $"o!n /it* H"&' Anormal PO7 in t*e inspire air to#et*er /it* lo/ arterialPO7 means t*at t*e #as e+c*an#e in t*e l!n#s is impaire'In s!mmary. t*e meas!rement o) PO7 is important )or $2&

treatin# patients /it* p!lmonary iseases $7& per)ormin#sa)e s!r#ery $/*en anaest*esia is !se& $& t*e care o)premat!re "a"ies /it* respiratory istress synrome'



DIFFUSION

I#$%&', A&'A9,*9(' A&'

H2O V('&(09,47 << H

CO2 ".3 << H4" << H

O2 15! << H1"5 << H

N2 6"1 << H

568 << H



DIFFUSION

• DIFFUSION AND PERFUSION LIMITATIONS: Howdoes oxygen get into the circulation2

To ans/er t*is 1!estion /e /ill rst e+amine t/oe+treme e+amples> I) a s!"=ect "reat*es CO $car"on

mono+ie& "eca!se CO mo(es rapily across t*e "loo,#as "arrier. t*e content o) CO in re "loo cells isincrease' Ho/e(er. CO )orms (ery ti#*t "ons /it* H"t*at e(en t*o!#* lar#e amo!nt o) CO is ta6en !p "y t*ere "loo cells almost no increase in t*e CO partial

press!re is o"ser(e' T*ere)ore. t*e amo!nt o) CO t*at#ets !nto t*e "loo is limite "y t*e i;!sion propertieso) t*e "loo,#as "arrier an not "y t*e amo!nt o) "looa(aila"le> di1usion limited.



DIFFUSION

• T*e ot*er e+treme e+ample is nitro!s o+ie>Nitro!s o+ie i;!ses across t*e "arrier "!t)orms no com"ination /it* H"' As a res!lt itspartial press!re rises (ery rapily' T*e amo!nto) nitro!s o+ie ta6en !p "y "loo epens ont*e amo!nt o) "loo a(aila"le> per'usionlimited. The time course o' 56 trans)er is in"et/een' It oes "in to H" "!t not*in# li6e

t*e a(iity o) CO' In normal conitions capillaryPO7 reac*es t*at o) al(eolar #as /*en t*e recell is a"o!t 23 o) t*e /ay alon# t*e capillary.



DIFFUSION

• Thus% in normal% physiological condition oxygen transer is perusionlimited.

In pathological conitions. e'#' t*ic6enin# o) al(eolar /all. t*ere/o!l "e some i;!sion limitations as /ell'

PO7 o) t*e (eno!s "loo an t*e al(eolar air is B4 an 244 mm H#.

respecti(ely' At t*e en o) t*e capillary "loo PO7 reac*es t*e same(al!e /it* t*e al(eolar air PO7' D!rin# e+ercise t*e p!lmonary "loo5o/ is increase an t*e a(era#e tra(el time o) a re "loo cell int*e capillary is s*ortene' Ho/e(er. in normal s!"=ects still t*ere/o!l "e no i;erence "et/een t*e PO7 o) al(eolar air an t*e "looat t*e en o) t*e capillary' On t*e ot*er *an i) t*ere is t*ic6enin# o)

al(eolar /all o+y#en transport /o!l "e impaire an meas!ra"lei;erence "et/een al(eolar #as an en,capillary "loo PO7 occ!rs'

• T*e la/s o) i;!sion state t*at VG($ > A. D. ?P1 P2@ A> Area D>Di;!sion Constant



DIFFUSION

• %eca!se it is not possi"le to meas!re t*e area an t*et*ic6ness in li(in# s!"=ects one can intro!ce DL. i;!sin#capacity o) t*e l!n#'

• VG($ > DL . ?P1 P2@ DL > VG($ ?P1 P2@• %eca!se trans)er o) CO is entirely i;!sion limite it is an

ieal #as to !se )or i;!sion capacity meas!rements' DL >VCO ?P1 P2@

• Since CO in t*e capillary "loo is ne#li#i"le DL > VCO ?PACO@

• The di1using capacity o' the lung 'or )5 is the

&olume o' )5 trans'erred in mi per mm Hg o'al&eolar partial pressure. Single !reath method: 7single inspiration o' a dilute mixture o' )5 is madean t*e rate o) isappearance o) CO )rom t*e al(eolar #as!rin# a 24 sec "reat* *ol is calc!late' 0teady statemethod' A subject breathes low concentration o ,- until

steady state is reached. Then rate o) isappearance o) CO



PERFUSION

• T*e main )!nction o) t*e p!lmonary circ!lation is to "rin# systemic (eno!s"loo into contact /it* al(eoli )or #as e+c*an#e' It "e#ins at t*e mainp!lmonary artery. /*ic* recei(es t*e mi+e (eno!s "loo p!mpe "y t*eri#*t (entricle' T*is artery t*en "ranc*es s!ccessi(ely li6e t*e system o)air/ays' Eac* time t*e air/ay "ranc*es. t*e arterial tree "ranc*es t*at t*et/o parallel eac* ot*er' T*e o+y#enate "loo is collecte )rom t*e capillary

"e "y t*e p!lmonary (ein. /*ic* rains into t*e le)t atri!m' In aition.p!lmonary (essels protect t*e "oy )rom o"str!ction o) important (essels inot*er or#ans s!c* as renal or cere"ral (essels' -*en air. )at or "loo clot*senter t*e "loo stream $e'#' !rin# s!r#ery or tra!ma& p!lmonary (esselstrap t*is em"oli an enot*elial cells release "rinolytic s!"stances t*at*elp issol(e t*rom"i' T*e p!lmonary circ!lation ser(es as a "loo reser(oiran t*e (ol!me in t*e l!n# capillaries is appro+imately e1!al to t*e stro6e

(ol!me o) t*e ri#*t *eart' P!lmonary (essels also contri"!te to t*emeta"olism o) (asoacti(e *ormones' For e+ample an#iotensin I is acti(atean con(erte to an#iotensin II "y an#iotensin,con(ertin# en0yme /*ic* islocate on t*e s!r)ace o) t*e enot*elial cells o) t*e p!lmonary capillaries'



PERFUSION

• The di1erences !etween the pulmonary and the systemiccirculation:2'T*e press!res in t*e p!lmonary circ!lation are remar6a"ly lo/> T*e press!re in t*e main p!lmonary artery is 7? mm H# $systolic& an mm H#$iastolic&. in a(era#e 2? mm H#' T*is is a (ery lo/ press!re compare to t*epress!re in aorta. 244 mm H#' 7' Anot*er stri6in# property o) t*e p!lmonaryarteries is t*eir e+ceein#ly t*in /alls' T*is anatomical aaptation o) t*e l!n# iscritically important )or its )!nction> T*e l!n# is re1!ire to recei(e t*e /*ole o)t*e cariac o!tp!t at all times' eepin# t*e p!lmonary press!re as lo/ aspossi"le allo/s t*e ri#*t *eart ans/er t*is eman /it* a minim!m /or6' 'Unli6e t*e systemic capillaries. /*ic* are or#anise as t!"!lar net/or6 /it*some interconnections. t*e p!lmonary capillaries mes* to#et*er in t*e al(eolar/all so t*e "loo 5o/s as a t*in s*eet $capillary "e&' B' Anot*er !ni1!e propertyo) t*e p!lmonary circ!lation is its a"ility to ecrease resistance as cariac o!tp!tincreases' T/o mec*anisms are responsi"le )or t*is )!nction' 2' Capillaryrecr!itment> openin# o) initially close capillaries /*en cariac o!tp!t increases'7' Capillary istension> T*e ecrease in p!lmonary press!re /it* increasecariac o!tp!t +($ se(eral "enecial e;ects> It $2& minimise t*e loa on t*e ri#*t*eart. $7& pre(ents p!lmonaryoeema. $& maintains t*e ae1!ate 5o/ rate o)t*e "loo in t*e capillary an $B& increases t*e capillary s!r)ace area'



GAS TRANSPORT TO THEPERIPHERY

• How do gases mo&e to the peripheral tissues2

• OYGEN:O+y#en is carrie in t*e "loo in t/o )orms.issol(e an com"ine /it* *aemo#lo"in $H"&'8issol&ed 5xygen: The amount o' oxygen

dissol&ed in the !lood is proportional to its partial pressure $Henrys La/&' 244 ml o) arterial"loo /it* normal o+y#en partial press!re $244 mmH#& contains 4' ml o+y#en' %y t*is /ay amo!nt o)o+y#en eli(ere to t*e tiss!es is only a"o!t 4

ml3min' Ta6in# in to acco!nt t*at t*e tiss!ere1!irements are a"o!t 444 ml O+y#en3min. it iso"(io!s t*at t*is /ay o) transportin# o+y#en is notae1!ate )or *!man'




• HAEMOGLOBIN: Haemo#lo"in $H"& < Heme$iron,porp*yrin& #lo"in $protein& Glo"in *as Bprotein polypeptie c*ains> 7 alp*a $eac* *as 2B2aa& an 7 "eta $eac* *as 2B: aa&' Di;erences int*e amino aci se1!ence o) t*ese c*ains #i(e rise

to (ario!s types o) H"'H0A: N*'<(9 (9) H0H0F: F*,)(9 H0 +&-+ <(,$ %(') */ )+,)*)(9 H0 () 0&')+ (# &$ '((99 ',%9(-,0 H0A Eac* polypeptie c*ain is com"ine

/it* one *eme #ro!p' In t*e centre o) eac* *eme#ro!p t*ere is one atom o) iron. /*ic* cancom"ine /it* one o+y#en molec!le' T*!s one H"molec!le can "in B o+y#en molec!les' Hemecontains iron in t*e re!ce )orm $Fe. )erro!s

iron&' In t*is )orm t*e iron can s*are electrons an




• -*en o+y*emo#lo"in issociates to release o+y#en to t*e

tiss!es $t*e *eme iron is still in )erro!s )orm& an t*e H" iscalle ,*+,<*9*0&# ?',-, H0@. ' %eca!se t*ere!ce H" is p!rple a lo/ arterial o+y#en sat!rationca!ses cyanosis.

• O+,<*9*0&# &$ #*) $(<, &)+ *&&$, H" $or<,)+,<*9*0&#@ &# +&-+ &'*# &$ &# )+, *&&$, ?F, /,''&-@ /*'<. B,-($, <,)+,<*9*0&# lac6s t*eelectron necessary to "in o+y#en. it oes not participate ino+y#en transport' T*e o+y#en carryin# capacity o) t*e"loo is etermine "y t*e H" concentration' I) it is "elo/normal. (#(,<&( )+, *,# -*#-,#)'()&*# */ )+,

09** &$ ',-,. +,# )+, H0 -*#-,#)'()&*# &$ *i#*.%*9-)+,<&( )+, *,# -(''&# -(%(-&) */ )+,09** &$ &#-',($,. T*e H" an re "loo cell pro!ctionin t*e "oy is !ner control o) eryt*ropoietin. /*ic* ispro!ce "y t*e 6ineys' Its pro!ction is stim!late /*en

t*e amo!nt o) o+y#en eli(ere to t*e 6ineys is lo/er t*an




• ' One #ram o) H" can com"ine /it* 2' ml o+y#en an"eca!se normal "loo *as 2? # o) H"3244 ml an t*eo+y#en capacity o) t*e 244 ml "loo is $2?Q2'& 74' ml'O+y#en sat!ration o) t*e arterial "loo $PO7<244 mm H#&is 9'? K /*ile o+y#en sat!ration o) t*e (eno!s "loo

$PO7< B4 mm H#& is 9? K' 3hy is the relationship!etween 4569 56 saturation and 56 concentrationimportant2 n anaemic patients H" concentration can"e as lo/ as 24 #3244ml "loo' In s!c* patient /it*normal respiratory )!nctions $PO7<244 mm H#&. O7

capacity /ill "e lo/er $74' + 2432? < 2' ml3244 ml"loo& an t*o!#* t*e O7 sat!ration still "e 9'? K. t*eamo!nt o) o+y#en com"ine /it* H" /ill "e lo/er'



T*e o+y#en issociation c!r(e is

s*i)te to t*e ri#*t "yQ an increase in H concentration.Q an increase in PCO7 (Bohr e1ect*9Q an increase in temperat!reQ an increase in 7.,ip*osp*o#lycerate $DPG&'

G S S O O




• A ri#*t/ar s*i)t means more !nloain# o) o+y#enat a #i(en PO7 in a tiss!e capillary' DPG is an enpro!ct o) re cell meta"olism an an increaseinits concentration occ!rs in c*ronic *ypo+ia $e'#'

at *i#* attit!e or in patients /it* c*ronic l!n#isease&' %eca!se CO *as a m!c* *i#*er a@nityto H" $)orms car"o+y*emo#lo"in. COH"&. e(ensmall amo!nts o) CO "in t*e lar#e proportion o)

H" ma6in# it !na(aila"le )or o+y#en> T*e H"concentration anPO7 o) "loo may "e normal "!tits o+y#en content is #rossly re!ce'

GAS TRANSPORT TO THE




•

CARBONDIOIDE: CO7 is carrie in t*e "loo in t*ree)orms> Dissol(e CO7. as "icar"onate an as car"aminocompo!ns $com"ine /it* proteins&' &issolved ,-'1ecause ,- is more soluble than oxygen this raction o,- in the blood plays an important role in its transport$a"o!t 24K&'

• 1icarbonate' CO2 H2O H2 CO3 H HCO3 T*erst reaction is (ery )ast an in(ol(es car"onic an*yraseen0yme. /*ic* is present in re cells. /*ile t*e seconreaction oes not in(ol(e an en0yme' -*en t*econcentrations o) t*e pro!cts o) t*e car"onic aci

issociation reaction "icar"onate i;!ses into t*e "loo "!tnot *yro#en ion "eca!se t*e re cell mem"rane isrelati(ely impermea"le to t*e positi(ely c*ar#e ions' Inorer to maintain electrical ne!trality Cl, ions i;!se intot*e re cells accorin# to t*e Gi""s,Donnan e1!ili"ri!m

$chloride shi't*. Some o' the H are !ound to H!: H



GAS TRANSPORT TO THE




• ,arbamino compounds' ,- is alsobond by terminal amine groups oseveral blood proteins. 0uch as $t*e

most important one& #lo"in o) H"$car"amino,*aemo#lo"in&'In arterial"loo CO7 is carrie 4 K as

"icar"onate. ? K com"ine /it*car"amino proteins an ? K asissol(e CO7' In (eno!s "loo t*ese(al!es are :4. 4 an 24.



RESPIRATORY SYSTEM UNDER STRESS

•EERCISE: D!rin# e+ercise t*e rate an t*e ept* o) "reat*in# are

increase' T*is increase in (entilation $*yperpnea& matc*es t*esim!ltaneo!s increase in o+y#en cons!mption an car"onio+ie pro!ctiont*at t*e arterial "loo car"on io+ie an o+y#en partial press!res an pHo not c*an#e ramatically $Please note t*at *yperpnea is i;erent )rom*yper(entilation' In *yper(entilation PCO7 is ecrease&'

• T*e mec*anism !nerlyin# t*e e+ercise,in!ce c*an#es in (entilation isnot clear' A' Ne!ro#enic mec*anisms> $2& stim!lation o) respiratory systemm!scles "y sensory ner(e acti(ity )rom e+ercisin# lim"s. pro"a"ly (iaacti(atin# "rain stem respiratory centres an3or (ia spinal re5e+es' $7&stim!latory inp!ts )rom cere"ral corte+' %' C*emical mec*anisms> %eca!separtial press!res o) car"on io+ie an o+y#en o not c*an#e !rin#e+ercise it is i@c!lt to e+plain possi"le c*emical )actors' Ho/e(er. t*e)ocal c*an#es in t*ese parameters near c*emoreceptor area may contri"!te

to t*e e+ercise,in!ce c*an#es in (entilation'

RESPIRATORY SYSTEM UNDER



RESPIRATORY SYSTEM UNDERSTRESS

• A#(,'*0&- )+',$+*9> T*e ma+im!m rate o) o+y#encons!mption t*an can "e attaine "e)ore "loo lactic acile(els rise as a res!lt o) anaero"ic respiration' Lactic aciconcentration is increase !e to anaero"ic limitations int*e m!scle cells !rin# *ea(y e+ercise' T*e cario(asc!lar

system maintains an ae1!ate amo!nt o) o+y#en to t*etiss!e t*at mitoc*onria can carry o!t o+iati(ep*osp*orylation' O+iati(e p*osp*orylation is an o+y#encons!min# process "y /*ic* ener#y eri(e )rom s!"strateo+iation is store in ATP as a c*emical ener#y' -*en t*e

o+y#en cons!mption is increase $e'#' *ea(y e+ercise& orat lo/ PO7 $e'#' cell!lar *ypo+ia& anaero"ic #lycolysis"ecomes a ma=or mec*anism )or cell!lar ATP )ormation an#l!coseis re!ce to lactate'





• ACCLIMATIJATION TO HIGH ALTITUDE: I# )+, +&+ (9)&), )+,+<(# 0* -*<%,#$(),$t*e lo/ partial o+y#en press!re "yc*an#in# (entilation or a@nity o) H" to o+y#en or total H"concentration' Hypoxic &entilatory response: Hyper&entilationinduced !y the decreased partial oxygen pressure. T*is lo/erst*e arterial partial car"on io+ie press!re an ca!ses respiratory

al6alosis' T*e rise in "loo pH in t!rn set t*e (entilation to a moresta"le "!t still sli#*tly *i#*er le(els' Hyper(entilation increases t*e tial(ol!me an re!ces t*e proportion o) t*e anatomical eat* space int*e inspire air' T*is also impro(es t*e o+y#enation o) t*e "loo'Ho/e(er. in spite o) all t*ese aaptation mec*anisms. t*e partialo+y#en press!re in t*e arterial "loo can not "e increase more t*an

t*e partial o+y#en press!re in t*e inspire air' As a res!lt partialpress!re o) o+y#en in t*e arterial "loo ecreases /it* increasin#altit!e' At sea le(els arterial "loo loses 77K o) its o+y#en loa intiss!es>T*e o+y#en sat!ration o) t*e arterial an (eno!s "loo is 9Kan 9?K. respecti(ely'





• At *i#* altit!e t*e lo/ o+y#en content o) re "loo cellsstim!lates 7,DPG pro!ction an ecreases t*e a@nity o)H" to o+y#en. /*ic* in t!rn )acilitates t*e o+y#en transportto t*e tiss!es' Ho/e(er. at (ery *i#* altit!es increase in"loo pH ca!ses a s*i)t to t*e le)t in t*e o+y#en sat!ration

c!r(e an increases t*e a@nity o) H" to o+y#en' T*issecon step is inee "enecial at (ery *i#* altit!e "yincreasin# t*e o+y#enation o) t*e "loo in t*e l!n#s' D!eto lo/ o+y#en partial press!re in t*e arterial "loo at *i#*altit!e t*e tiss!e *ypo+ia occ!rs an in response t*e

6ineys secrete eryt*ropoietin *ormone' Eryt*ropoietinstim!lates t*e pro!ction o) re "loo cells res!ltin# inpolycyt*emia. /*ic* can ca!se oeema. (entric!lar*ypertrop*y an *eart )ail!re'



RESPIRATORY FAILURE

• Respiratory )ail!re is a synrome in /*ic* t*e respiratory system )ails in one or"ot* o) its #as e+c*an#e )!nctions> o+y#enation an car"on io+ieelimination' In practice. it may "e classie as eit*er *ypo+emic or*ypercapnic'

• Hypo+emic respiratory )ail!re $type I& is c*aracteri0e "y an arterial o+y#entension $Pa O7& lo/er t*an :4 mm H# /it* a normal or lo/ arterial car"on

io+ie tension $Pa CO7&' T*is is t*e most common )orm o) respiratory )ail!re.an it can "e associate /it* (irt!ally all ac!te iseases o) t*e l!n#. /*ic*#enerally in(ol(e 5!i llin# or collapse o) al(eolar !nits' Some e+amples o)type I respiratory )ail!re are cario#enic or noncario#enic p!lmonary eema.pne!monia. an p!lmonary *emorr*a#e'

• Hypercapnic respiratory )ail!re $type II& is c*aracteri0e "y a PaCO7 *i#*er t*an

?4 mm H#' Hypo+emia is common in patients /it* *ypercapnic respiratory

)ail!re /*o are "reat*in# room air' T*e pH epens on t*e le(el o) "icar"onate./*ic*. in t!rn. is epenent on t*e !ration o) *ypercapnia' Commonetiolo#ies incl!e r!# o(erose. ne!rom!sc!lar isease. c*est /alla"normalities. an se(ere air/ay isorers $e#. ast*ma anc*ronic o"str!cti(e p!lmonary isease COPD&'

http://emedicine.medscape.com/article/300157-overview






RESPIRATORY FAILURE

• Respiratory )ail!re may "e )!rt*er classie as eit*er ac!te orc*ronic' Alt*o!#* ac!te respiratory )ail!re is c*aracteri0e "yli)e,t*reatenin# eran#ements in arterial "loo #ases an aci,"ase stat!s. t*e mani)estations o) c*ronic respiratory )ail!re areless ramatic an may not "e as reaily apparent'

•

Ac!te *ypercapnic respiratory )ail!re e(elops o(er min!tes to*o!rs t*ere)ore. pH is less t*an 9'' C*ronic respiratory )ail!ree(elops o(er se(eral ays or lon#er. allo/in# time )or renalcompensation an an increase in "icar"onate concentration'

T*ere)ore. t*e pH !s!ally is only sli#*tly ecrease'

• T*e istinction "et/een ac!te an c*ronic *ypo+emicrespiratory )ail!re cannot reaily "e mae on t*e "asis o)arterial "loo #ases' T*e clinical mar6ers o) c*ronic *ypo+emia.s!c* as polycyt*emia or cor p!lmonale. s!##est a lon#,stanin#isorer'



RESPIRATORY FAILURE

• Arterial "loo #ases s*o!l "e e(al!ate in all patients /*o areserio!sly ill or in /*om respiratory )ail!re is s!specte' C*estraio#rap*y is essential' Ec*ocario#rap*y is not ro!tine "!t issometimes !se)!l' P!lmonary )!nctions tests $PFTs& may "e*elp)!l' Electrocario#rap*y $ECG& s*o!l "e per)orme to assess

t*e possi"ility o) a cario(asc!lar ca!se o) respiratory )ail!re italso may etect ysr*yt*mias res!ltin# )rom se(ere *ypo+emiaor aciosis' Ri#*t,sie *eart cat*eteri0ation is contro(ersial $see-or6!p&'

• Hypo+emia is t*e ma=or immeiate t*reat to or#an )!nction' A)tert*e patients *ypo+emia is correcte an t*e (entilatory an

*emoynamic stat!s *a(e sta"ili0e. e(ery attempt s*o!l "emae to ienti)y an correct t*e !nerlyin# pat*op*ysiolo#icprocess t*at le to respiratory )ail!re in t*e rst place' T*especic treatment epens on t*e etiolo#y o) respiratory )ail!re



RESPIRATORY FAILURE

• Respiratory )ail!re can arise )rom an a"normality in any o) t*ecomponents o) t*e respiratory system. incl!in# t*e air/ays. al(eoli.central ner(o!s system $CNS&. perip*eral ner(o!s system. respiratorym!scles. an c*est /all' Patients /*o *a(e *ypoper)!sion seconary tocario#enic. *ypo(olemic. or septic s*oc6 o)ten present /it* respiratory)ail!re'

• Jentilatory capacity is t*e ma+imal spontaneo!s (entilation t*at can "emaintaine /it*o!t e(elopment o) respiratory m!scle )ati#!e'Jentilatory eman is t*e spontaneo!s min!te (entilation t*at res!lts ina sta"le Pa CO7'

• Normally. (entilatory capacity #reatly e+cees (entilatory eman'Respiratory )ail!re may res!lt )rom eit*er a re!ction in (entilatory

capacity or an increase in (entilatory eman $or "ot*&' Jentilatorycapacity can "e ecrease "y a isease process in(ol(in# any o) t*e)!nctional components o) t*e respiratory system an its controller'Jentilatory eman is a!#mente "y an increase in min!te (entilationan3or an increase in t*e /or6 o) "reat*in#'



RESPIRATORY FAILURE T*e act o) respiration en#a#es processes>

• Trans)er o) o+y#en across t*e al(eol!s• Transport o) o+y#en to t*e tiss!es

•Remo(al o) car"on io+ie )rom "loo into t*e al(eol!s an t*en into t*e en(ironment

Respiratory )ail!re may occ!r )rom mal)!nctionin# o) any o) t*ese processes' In orerto !nerstan t*e pat*op*ysiolo#ic "asis o) ac!te respiratory )ail!re. an!nerstanin# o) p!lmonary #as e+c*an#e is essential'

2as exchange

•Respiration primarily occ!rs at t*e al(eolar capillary !nits o) t*e l!n#s. /*eree+c*an#e o) o+y#en an car"on io+ie "et/een al(eolar #as an "loo ta6es place'A)ter i;!sin# into t*e "loo. t*e o+y#en molec!les re(ersi"ly "in to t*e *emo#lo"in'Eac* molec!le o) *emo#lo"in contains B sites )or com"ination /it* molec!lar o+y#en2 # o) *emo#lo"in com"ines /it* a ma+im!m o) 2': mL o) o+y#en'

• T*e 1!antity o) o+y#en com"ine /it* *emo#lo"in epens on t*e le(el o) "looP

a O

7' T*is relations*ip. e+presse as t*e o+y#en *emo#lo"in issociation c!r(e. is not

linear "!t *as a si#moi,s*ape c!r(e /it* a steep slope "et/een a P a O7 o) 24 an ?4

mm H# an a 5at portion a"o(e a Pa O7 o) 94 mm H#'



RESPIRATORY FAILURE

• T*e car"on io+ie is transporte in main )orms> $2& in simplesol!tion. $7& as "icar"onate. an $& com"ine /it* protein o)*emo#lo"in as a car"amino compo!n'

• D!rin# ieal #as e+c*an#e. "loo 5o/ an (entilation /o!lper)ectly matc* eac* ot*er. res!ltin# in no al(eolar,arterial

o+y#en tension $PO7& #raient' Ho/e(er. e(en in normal l!n#s.not all al(eoli are (entilate an per)!se per)ectly' For a #i(enper)!sion. some al(eoli are !ner(entilate. /*ile ot*ers areo(er(entilate' Similarly. )or 6no/n al(eolar (entilation. some!nits are !nerper)!se. /*ile ot*ers are o(erper)!se'

• T*e optimally (entilate al(eoli t*at are not per)!se /ell *a(e a

lar#e (entilation,to,per)!sion ratio $J3& an are calle *i#*,J3!nits $/*ic* act li6e ea space&' Al(eoli t*at are optimallyper)!se "!t not ae1!ately (entilate are calle lo/,J3 !nits$/*ic* act li6e a s*!nt&'

RESPIRATORY FAILURE



RESPIRATORY FAILURE Alveolar ventilation

• At steay state. t*e rate o) car"on io+ie pro!ction "y t*etiss!es is constant an e1!als t*e rate o) car"on io+ie

elimination "y t*e l!n#' T*is relation is e+presse "y t*e )ollo/in#e1!ation>

JA < JCO73 Pa CO7

/*ere is a constant $4':&. JA is al(eolar (entilation. an

JCO7 is car"on io+ie (entilation' T*is relation etermines

/*et*er t*e al(eolar (entilation is ae1!ate )or meta"olic neeso) t*e "oy'

• T*e e@ciency o) l!n#s at carryin# o!t o) respiration can "e )!rt*ere(al!ate "y meas!rin# t*e al(eolar,arterial PO7 #raient' T*is

i;erence is calc!late "y t*e )ollo/in# e1!ation>

PA O7 < FI O7 $P% PH7 O& PA CO73R /*ere PA O7 is al(eolar PO7. FI O7 is )ractional concentration o)

o+y#en in inspire #as. P% is "arometric press!re. PH7 O is /ater

(apor press!re at 9C. PA CO7 is al(eolar PCO7 $ass!me to "e

e1!al to Pa CO7&. an R is respiratory e+c*an#e ratio' R epens on

o+y#en cons!mption an car"on io+ie pro!ction' At rest. t*eratio o) JCO7 to o+y#en (entilation $JO7& is appro+imately 4''



RESPIRATORY FAILURE

H%*,<&- ',$%&'()*' /(&9',• T*e pat*op*ysiolo#ic mec*anisms t*at acco!nt )or t*e *ypo+emia o"ser(e in a /ie(ariety o) iseases are J3 mismatc* an s*!nt' T*ese 7 mec*anisms lea to /ienin# o)t*e al(eolar,arterial PO7 #raient. /*ic* normally is less t*an 2? mm H#' T*ey can "e

i;erentiate "y assessin# t*e response to o+y#en s!pplementation or calc!latin# t*es*!nt )raction a)ter in*alation o) 244K o+y#en' In most patients /it* *ypo+emicrespiratory )ail!re. t*ese 7 mec*anisms coe+ist'

345 mismatch•J3 mismatc* is t*e most common ca!se o) *ypo+emia' Al(eolar !nits may (ary )rom lo/,J3 to *i#*,J3 in t*e presence o) a isease process' T*e lo/,J3 !nits contri"!te to*ypo+emia an *ypercapnia. /*ereas t*e *i#*,J3 !nits /aste (entilation "!t o not a;ect#as e+c*an#e !nless t*e a"normality is 1!ite se(ere'

• T*e lo/ J3 ratio may occ!r eit*er )rom a ecrease in (entilation seconary to air/ay orinterstitial l!n# isease or )rom o(erper)!sion in t*e presence o) normal (entilation' T*eo(erper)!sion may occ!r in case o) p!lmonary em"olism. /*ere t*e "loo is i(erte tonormally (entilate !nits )rom re#ions o) l!n#s t*at *a(e "loo 5o/ o"str!ction seconaryto em"olism'

•Aministration o) 244K o+y#en eliminates all o) t*e lo/,J3 !nits. t*!s leain# tocorrection o) *ypo+emia' Hypo+emia increases min!te (entilation "y c*emoreceptorstim!lation. "!t t*e Pa CO7 #enerally is not a;ecte'



RESPIRATORY FAILURE

0hunt •S*!nt is ene as t*e persistence o) *ypo+emia espite 244K o+y#en in*alation' T*eeo+y#enate "loo $mi+e (eno!s "loo& "ypasses t*e (entilate al(eoli an mi+es /it*o+y#enate "loo t*at *as 5o/e t*ro!#* t*e (entilate al(eoli. conse1!ently leain# to are!ction in arterial "loo content' T*e s*!nt is calc!late "y t*e )ollo/in# e1!ation>

S3 T < $CC O7 Ca O7&3CC O7 C( O7&

/*ere S3 T is t*e s*!nt )raction. CC O7 is capillary o+y#en content $calc!late )rom

ieal PA O7&. Ca O7 is arterial o+y#en content $eri(e )rom Pa O7 "y !sin# t*e o+y#enissociation c!r(e&. an C( O7 is mi+e (eno!s o+y#en content $ass!me or meas!re "y

ra/in# mi+e (eno!s "loo )rom a p!lmonary arterial cat*eter&'

•Anatomic s*!nt e+ists in normal l!n#s "eca!se o) t*e "ronc*ial an t*e"esian circ!lations./*ic* acco!nt )or 7,K o) s*!nt' A normal ri#*t,to,le)t s*!nt may occ!r )rom atrial septale)ect. (entric!lar septal e)ect. patent !ct!s arterios!s. or arterio(eno!s mal)ormationin t*e l!n#'

•

S*!nt as a ca!se o) *ypo+emia is o"ser(e primarily in pne!monia. atelectasis. an se(erep!lmonary eema o) eit*er cariac or noncariac ori#in' Hypercapnia #enerally oes note(elop !nless t*e s*!nt is e+cessi(e $V :4K&' Compare /it* J3 mismatc*. *ypo+emiapro!ce "y s*!nt is i@c!lt to correct "y means o) o+y#en aministration'



RESPIRATORY FAILURE

• H%,'-(%#&- ',$%&'()*' /(&9',• At a constant rate o) car"on io+ie pro!ction. Pa CO7 is etermine "y t*e

le(el o) al(eolar (entilation accorin# to t*e )ollo/in# e1!ation $a restatemento) t*e e1!ation #i(en a"o(e )or al(eolar (entilation&>

Pa CO7 < JCO7 3JA

/*ere is a constant $4':&' T*e relation "et/een Pa CO7 an al(eolar

(entilation is *yper"olic' As (entilation ecreases "elo/ B,: L3min. Pa CO7 risesprecipito!sly' A ecrease in al(eolar (entilation can res!lt )rom a re!ction ino(erall $min!te& (entilation or an increase in t*e proportion o) ea space(entilation' A re!ction in min!te (entilation is o"ser(e primarily in t*esettin# o) ne!rom!sc!lar isorers an CNS epression' In p!re *ypercapnicrespiratory )ail!re. t*e *ypo+emia is easily correcte /it* o+y#en t*erapy'

• Hypo(entilation is an !ncommon ca!se o) respiratory )ail!re an !s!ally occ!rs

)rom epression o) t*e CNS )rom r!#s or ne!rom!sc!lar iseases a;ectin#respiratory m!scles' Hypo(entilation is c*aracteri0e "y *ypercapnia an*ypo+emia' Hypo(entilation can "e i;erentiate )rom ot*er ca!ses o)*ypo+emia "y t*e presence o) a normal al(eolar,arterial PO7 #raient'

Functional Physiology of Respiratory System

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