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Physiology Kerry > 4.3 Non respiratory functions lung & shunt > Flashcards

4.3 Non respiratory functions lung & shunt Flashcards

1
Q

What is the fxn of type 2 alveolar cells

A

Production of surfactant

Stemm cell production type 1 cells

Type 1 are produced from type 2

Type 1 are thin
no signif barrier to gas exch

No ogranelles
dont divide

Lung damage -
2 divide to produce replacement

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2
Q

How are alveolar epithelial cells affected by oxygen toxicity

A

Thin Type 1 - easily damage high levels of oxygen
larger type 2 more resistant

Alveolar epithelium becomes thciker than normal - impariment of gas exchange

Oxygen conc return normal - type 2 prolif to replace 1`

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3
Q

What is surfactant

constitituents

A

Reduces surf tension - air liquid interface alveoli - redution larger in small alveoli

Stored type 2 alv cell - lamellar body
secreted into alveoli

Surfcat composite
Plip 80% - dipalmitoyl phophatdiyl choline

Neutral lipids 10%

Plasma proteins 4 %

Carbs 2%

severeal surfactant protiens 4%

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4
Q

What is the chemi feat dipalmitoly phophatdiyl choline - gives surface tension reduction activity

A

Ampipathic -
Charged Hydrophilic head - choline
hydrophobic tail - two palmitoyl groups

Struct feat - important orinetant of moleculs at air liq interface

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5
Q

What are the functions of surfactant

A

Reduce surface tension alveoli

  • reduce effort
  • mag dep conc on surf of fluid layer lining

when smaller - surf area smaller - conc surf - interface higher

radially dependent seufrace tension red agent - mag reduction tesnion depened radius aloveli
countract effects pred law lpalace - small alveoli higher pressure than large

improve stability

assist keeping dry
Oppose movement water from interstit to alveolar space
reducing collapse alvoli - reduce hydrostaitc pressure in tissue outside capillary

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6
Q

Roles surfactant proteins

A

4 specific protien found a- d
sp a sp b sp c sp d

sp b sp c - hydrophobic - neccessary spreading phospholipid into a monolayer lining alveoli

Sp a sp d -hydrophilic 
sp a-
faciltate spread sp b - break lamellar body
prevent plasma pro entry into fluid
macophage enhancement
regul8 surfactant turnover
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7
Q

Non respiratory fxn lung

A 
1 Blood resevor
2 blood filtration - thrombi removed b4 brain
3 Metabolic
-surfactant
-protein collagen + elastin
-r/o proteases a1at
- metabol vasoactives
4 immunlog - macopahge iga
5 heat reg
6 air flow - facil speech
7 Drugs - rout admin some drugs -
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8
Q

Mech as blood resevoir

Vol lying
standing
vol capillary

A

Increase in PA pressure - increase vol blood lung - increase bentral blood vol
Recuitment - more vessels open
distenion - open bet bigger

Vol 450 lying
standing 250

Vol capillary 80

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9
Q

What is central blood volume

A

Volume blood in heart and lungs

errect 15%
lungs 450. heart 350 = 800

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10
Q

What way is pulmonary circ different?

A

1 Whole of CO - RV
Most blood traverese capillary
lung receives venous efflent whole body - mix ven blood
cap bed filter whole VR - only capillary bed capable of same

Second
Pulmonary circulation reacts low Po2 - constricting - HPV
Redirect blood away poorly vent alveoli
response system opp - vdilates
Perip vdil aim increase o2 supply / blood flow

Higher flow at lower pressure and vascular resistance

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11
Q

What is converting enzyme

A

ACE located pul cap endothel cell
2 fxn

1 Converts Ang I to active ang II - ang convertin enxyme
drugs which inhib ace - useful antihtn

Inactivaing bradkinin - inhib of fxn - lead ace side effect
eg angioed cough

Widely distrib body - lower conc than capillary

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12
Q

How are the vasoactives handled by lung

A

Activate aAng I

Inact Bradykin

Taken up 5HT, PGE2, PGF2, LK

Unaffected AngII pGA ADH, Adrenaline

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13
Q

What is the role in heat regulation

A

Upper resp tract fxn

upper aiwrway warm and humidfy gas to inspire gas to body temp

Obiltory loss of heat by route - latent heat vpa
req for evap water

eheat loss .58kcals per gram water ecap
daily resp insense water loss 400mls heat loss 230 kcal day
12%

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14
Q

What are major defency mech protect lung

A

Physical
1 upper airway filter mech & particle impaction
2 Airway reflex cough sneeze
3 Mucocillary escalator

Cellular mech
Alveolar macrophage
Iga - immun fact

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15
Q

Respiratory response to altitude
what is percent o2 air at 5500m
380mmhg where ambient pressure 1/2 sea level

A

Percent oxygen still 21%

Partial pressure oxygen air less
as ambient pressure is half
ambient po2 is 80 (.21x380) in dry
or 69 in saturated

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16
Q

What Po2 would you predict if alveolar vent was same as sea level

A

PAO2 = Pi - PACO2/r

= .21 (380-47) - 40/.8
= 20mmHg in absence in change of centilation

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17
Q

What vent response to asecnt to 5500

A

Hypoxameia - stim periph chemo rec - ventilation increase signifcantly

Resultts fall PaCo2 - acts central cehemo rec - inhibt chemorec in resp centre - limit vent rise

Action of fall in art Pco2 - d/t local brain ECF [H]
over days - bec equil accross bbb - preogres resotre ecf H to normal

Inhbi to increase in vent progress removed

vent rises marfkedy increase alveolar Po2 - decrease PCo2 - typcall takes secereal days before max response achieved (can inc x5)

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18
Q

What else involved acclimiatisation to altitude hypoxia

A

Increase oxygen uptake

increase tport and delivery

the above 2
increase Hb conc - hypx stim epo - may increase >20

Increase caplarry in muscle to failatte perfusion

Positon ODC alter -
left shift - hypocap
right shift inc 2 3 dpg -

Oxygen loading - decrease combo low alverolar po2 and right shift cyrve

Polycthtme - incr blood viscosity
HPV d/t low alv Po2 - increase PA pressures

Both - increase work / strain rihgt heart

PHTN & RV hypertrophy may occur

CO increase by 20 to 50% on ascent to altitude
as vent and Hb inc - co return normal

people live life altitude - high conc oxidative enzymes - great ability utilise oxygen

increase oxygen utilisation

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19
Q

Functions nose

what structural features assist

A

Pathway for bulk flow gas

smell

conditioning ventilated gas

Minimisation water loss resp tract

Eustachian tube enter nose

Major process condition inspired gas -

Humidification
Warming
removal particulate matter

All - assisted turbulent flow
increase surf area - turbinates

min water loss during expiate
moisture condense during expiration
-would lose 75% daily water intake if turbinates mechansim

warming and humid related - increase in temp increase amt water vapour req fully sat the air

Processes involved removing particulate
filtration:
hair

impaction on muscoa

sedimentation lim nose -
important in trachea and large bronchi

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20
Q

How much total airways resistance d/t the nose -

A

Major contributr and ressitance increase and insp flow rate increase

Mouth function low resistance bypass - short activation time

Resistance slows expiration help main lung vol and prevent atelectasis - phys peep

resistant - internal shape and feautres - favour turbulent flow

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21
Q

Functions of rbcs

A

1 Tport of oxygen

2 co2 tport

3 a b buffer

4 package hb

hb also carry NO - affinity reduc deoxy = release NO periph

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22
Q

How are function interrelated

A

Hb - 3 roles -
Haldane effect of o2 sat of hb on co2 tport

hb carbamino - imporant co2 tport

Bohr effect- pco2 and ph on o2 tport

hb buffer - imporntant co2 tport and ab balance

buffering affect degree sat - hb

carbonic anhydrase inside rcc

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23
Q

What are advantage of having Hb locate in RCC

package of hb

A

Protect fo filt

enverino raise p50 26.6 - allosteric effect 2 3 dpg which phys more advant

avoid icnrease plasma oncotic pressure if hb in solution

assist mainta as stable teatrae - posit coop

main same locn carbonic anyhdrase

return methb - back to hb - methb reduct in rcc cyto

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24
Q

Role RCC CO2 tport

A

Co2 tport in 3 forms in blood70% bic lelavce1 dissolved 2 bic 90% - accounbts 60% av diff co2 content 3 carbamino

RCC import
1 anyhdrase in red cell not plasma
2 Hb forms carbamino compoinds
3 hb buffer H production bic

Bic formed from co2 and water - carbon anhydrase catalyses
Fast

70% bic leaves RCC - hambuger- exchange Cl (cl shif)
Maintain elec neutraility

Hion production reaction
increase H disav - not removed limit bic production ( las mass action)

Addit low ph inhib prod 2 3 dpg
H is buffer by Hb

oxygen unloading facilate process - deoxy is ab tetr buffer than oxy
imidazole grooup 6.8 pka - histdine responsible most buffer

hb large no histidine residue (38) - designed buffer

Carbammino comnpound account 5% CO2 carriage contib 30% av diff co2 content
more imporrartant tport in venous blood -
compound formed combo co2 terminal aminos

Net prod H low pka carbamic acid

Formed with hb nad plasma protein
hb presnet 2x conc pl portein

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25
Haldane effect
- increase co2 carry at same pco2 in deoxy v oxy doexy 3/5 x more carbamino compared to oxy - account 70% haldane effect Secon dfacotr - ncrease buffering ability deox- mops H+ formed production bic More bic formed because of buffering some dissolved co2 present co2
26
Role RCC in AB meatbolsim
Hb - high contc many histide reside - suiot pka buffer phys ph doexy better buffer - than oxy buffer H prod from carb anyhdrse in rcc bic buffer cant buffer itsekf
27
What is role of RCC membrane
Gas tfer - oxy co tfer bic to plamsa cl shift prote hb - glom fil stable immunolog function rcc naito abo
28
Mechanics breathing What are the muscle involved in ventilation?
Inspiration is active - d/ tcontract diaphragm - contract Ex IC also cintrib Diaphr respo 70% TV - traonctacion msucle causes intrapleeural - more eng - decrease alveolar pressure gradient for inspiration dfiff alveolar and mouth pressure Diaphr lower rib c3-c5 External contract ribs move up and forward buckel hand increase tb diagram pump handle increase AP dap TV not impair if ext IC paralysed
29
How much does dipahgram desed during tv and vc
TV - 1 cm | VC 10c,
30
What is oxygen cost normal TV at rest
3mls o2 min | 1% consump
31
Why do we breath out How diff exercise
Normal exp - passive no active contraction - active require energy energy elastic recoil lungs during inspiration elastic potentinal energy in lung increase with expriation - elastic potential energy used gen pressure gradient driving expiration - pull chest wall back to FRC work expiration powered by inspiratory muscle - intermed store elastic pot energy lungs exercise rectas abd int ext obliq tv and inter itercostal
32
What pressure gradient driving expiration
diff alvoelar press and mouth pressure Normal TB peak alveolar +1cm mouth pressure atm - 0 gauge
33
Whats respons for elastic recoil of lung
Factors responsible - 1 Surface tension of thin film of fluid lining alveolus 70% surfactant - reduces reduction marked smaller size 2 Stretch elastic fibre in lung parenchyma fibres elastin collagent
34
Alveolar Arterial pO2 gradient | What is A a gradient
Num diff alve and art po2 PiO2 - PaO2 Ox tension difference ref to dA-aO2
35
What is ideal alveolar Po2
Ideal alveolar pO2 - Po2 present in alveoli - No V/Q inequality in lung + Lung exchange gas same rate resp exchange ratio as real lung Calc from alveolar gas eqn
36
What is use of A-a gradient
Index amt v/q mm and shunting
37
What need to know calc Aa
Inspired Oxy blood gas result pAo2 - alve gas eqn pao2 measured from blood gas
38
What factors affecting A-a Normal values What causes this gradient
VQ mm Shunt Diffiusion abnorm Usually 5mmHg in young fit health values 15mmHg - breathing room air acceptable Value - higher in healthy elderly - no disease state V/Q mm or scatter vq ratio Shunt - small amount noirmal shunt bornch circ and thebesian vein drain left heart diffusion End pulm cap same Po2 alveolus - wall pases extreme stress - path A-A d.t diffusion prob -
39
Is Aa same in adults and pead
Neotates higher 30mmhg increase venous admix shunt v/q scatter Amount intrapulmonary shunt higerh - unexpaind / fluid alveoli alveoili low vq common Frc < CC - gas trapping occurs - normal tv Art Po2 neonates - lower above but effect o2 delivery offset Increase affinity Hbf Increase CO Increase HB after birth HbF - 80% hb in neonates Neoanates higher o2 consump 6mls kg min vs 3-3.5
40
How does v/q MM cause increase a-a grad
Lungs unit at apex - high v/q end cap blood high Po2 not signif increase from blood - hb alm cmplete sat Lungs base - lower v/q conseq end cap blood drain lower Po2 than apex lower po2 -a/w lower oxygen content as o2 sat of hb sligh decrease total perfusion of basal units higher - perfusion base lower o2 content contrib more toal flow lower Pv art Po2 - SUMMARY High V/Q apex - not contrib extra oxygen - flat curve also doesnt contrib much flow Low v/q base contrib flow at lower Po2 base most imporant effect and causes lowering art PO2 - increase Aa grad Flow apex - not compenaste lowering - high po2 doesnt contrib compenaste increase oxygen apical flow small
41
In patients w/ lung disease and icnreased scatter of V/Q rations do unit high v/q ratios and units low v/q ratio contribute to increased Aa grad
Yes maginutide contribute lung units to increase Aa can be estimated Contribution units low Cq - assesd mesaure phys shunt w/ shunt eqn Cintrib high v/q - assesed measure phs dead space -using bohr Type analysis - approximation based asusmption lung
42
Increased Aa gradeint - decrease art po2 a/w increase pco2?
No Increase art pco2 - sense central and perip increase vent resore art pco2 normal pco2 only eleveated additional factor impar pco2 feedback control Reason icnrease alve vent restore pco2 - linear slope co2 dissoc curve increase vent - decrease co2 content blood - some area lung compensate increase co2 cotnent blood underventilated different situation oxygen flater upper part oxyhb mean increase cent not add adit oxygen compensate decrease content
43
Hypoxaemia vs hypoxia
Hypoxia - Presence tissue low enough adverse affect on tissue fxn hypomaemia - abnormally low Po2 in arterial blood
44
Classify hypoxia
Hypoxic hypoxia - gypoxia d/t low blood po2 Anaemic hypoxia D.t inadeq tissue delivery oxygen by hb w. anaemia of CO pois Circ hypxoia inadeq blood flow to tissue - critical fall in Po2 may affect whole body certain part - tonrinquet Histotoxic
45
Why does hypovent cause hypoxaemia Whats effect art pco2
Hypovent - less o2 deliver to and less co2 removed rise alverolar pco2 pred pco2 inversel relate to alv vent Fall alveolar Po2 - det use gas eqn PAO2 - Pi - PACO2 / R Eg - alv vent halved - doublin paco2 - inverse relationship 0.21 x 760-47 - 80.8 = 50 Art po2 lower - tissue po2 lower than that
46
Histotoxic hypoxia
Tissue are not able use oxygen normal cyanide pois binds inhib mito cytoo x ox cant react w/ H deliver from ETPch - oxy phosp halt Noted tissue po2 normal or elveated - impar oxy utilasation Opp other forms prime cause decerased o2 cell is decrease oxygen Doent fit defn revised Oxygen substrat cyto oxidase enz end etcp All tissue effects of hypoxia - lack avial energy form atp block ox phosphrylaton new defn hpyoxia oxidative phosprhylation stops d/t inadeq utilisation of oxygen crtil low cell po2 1-2mmHg level pasetru point very high oxygen affin for xyto oxidase rxn continue until nearly all o2 gone histotox hypica - ox phosp block - orimary effect on ETC
47
What phsyiological effect walk into room 100% N2 - close door
Hypoxaemia & anoxic hypxia cyanosed distressed death min initial affect art po2 drop - no oxygen in inspired gas po2 <50mmhg - peripher chemo repsond - vent progres increase increase washout of o2 lung frc major store other effect cerbral hypoxia - brain tisue lac admosis central chemo respond to stim resp centre cerenbgral hpyoxia - depression brai unconcuouss death circ effect autoreg - vasil near all tiuse increease flow vr and co vasocn - cerbral - overom hypocapnioa cbf incrase Carotid ody stim - severe brady - hypoxic brady increase RR - increase Symp stim - increase hr - masks direct brady HPV - rise in PApressure cerebral hypox - symp stim - rise arterial bp - cushing reflex Hypoxia - results depresion metaboims all cell high oxgen affinity cyto oxidase - mito ox phospho contin down to po2 of 1 - pasteru muscle internal small oxygen store omyoglobin many tissues can derive additonal energy anearobi meatob 0 intracell acidosis brain tissue most suecctile hypox and anox brain - coma death minutes
48
Shunt | What is the venous admixture
Term intechange shunt shunt - blood enter aterial system wihtout passing thru ventilated area lung ture shunt po2 blood diff po2 mix venous blood most cases po2 true shunt lower po2 blood - contrib depress art po2 Venous admix - amount mix venous blod added to pulm end capillary blood - produce obesreved drop art po2 from po2 in end capillary n
49
Normally healthy peorosn two main source blood
contribu venous admix - blood true shunt bronch benous blood - bronch circ blood thebesida - blood not mix venous blood not expect po2 same mix venous blood alveoli v/q <1 blood not fully oxygntead - passes poorly vent area lung not true shunt - passed some ventilation really v/q mm
50
Virtual shunt
Blood source - drop art po2 neither venous mdmix mixed venous blood amt venous admix calc shunt eqn value obtain - lable virtual shunt defined amount shunt present if shunt enitrely mix venous blood amt shunt fully accoutn drop art oxygen content ``` advantage estimate venous admix obtain - monitor patient clin usefu no easy way calc true shunt no alternat use virtual shunt ``` noted smome case ssunt will bbe mix venous blood mix ven blood shunt are lung not veniltaed this case venous admix - shunt will be same
51
How can shunt eqn be calulatied
Qs/Qt = (CC'O2 - CaO2)/(CC'O2-CvO2) eqn calc amt shunt of mix venous blood Actual blood shunt may diff comp value - not accurate in these esitn normal sitation shunt present bronchial circulation thebesian vessel - lv compositon diff mix venous blood Summary shunt eqn based assumption shunted blood has same com as mix venous blood gives measure amt mix venous blood if added to end cap blood produce observed epression in art Po2 - virtual or as if shunt - true shunt not measure by eqn
52
How is shunt eqn derived
Bloods that shunt mix venous blood CO Qt = sum of shunt blood flow Qs + blood flow thru lung Qt-Qs total oxygen delivery - to body is CO by art content Qt x CaO2 Must be equal sum of oxygen deliver from shunt and lung Hence Qt xCao2 = Qs CCvO2 + Qt-Qs X CCo2 Solvng yields shield eqn Draw page 155 must equal sum amt oxygen dleivery shunt from lung diagr page 155
53
PVR How does vascular resitance in Pulmonary circulation compare to systemic
General ft Pulm - low resistance circuit Pressure drop only 10mMhg - mean PA - 15 Mean LAP 5 Yet flow is same as systemic circuit - ie Whole Cardiac output Pul VR 1/10th SVR AS pressure drop in SVR 100 - 10x higher
54
What are major factors affecting PVR
1 Hypoxic pulmonary vascon 2 Lung volume 3 PA Pressure
55
What is HPV
Vasoconstrictive low alveolar Po2 - Alveolar Po2 - determins not art Po2 When Po2 falls in one part lung = decrease vent or atelac w/ mucus pplug - pulmonary vassels vasoconstrict - shunt pulmonary blood away - underdentialted area - better vent areas lung Match vent and perfusion advantrage - maint o2 uptake During early LVF _ congest and hypxia - cause hpv shunt to upper zone - pulmonary vascular redistrib
56
What circ HPV - interest anaetheitst
Effect volatile One lung anaesthsia
57
Relationsip PVR and lung volume
High and low lung vol - PVR increase PVR lowest - when lung vole close to FRC Low lung vol - extra alveolar vessels - small diamter high resistance as volume expands - wall pulled by elastic fibre in lung - and diameter increase resistance decreases As volume expands further increased stretching distort and decrease diam of pum capillary - alveolar vessels - causes increase PVR PVR higher at high and low lung vol - d/t different meachansms PVR is at FRC
58
how does PAP pressure affect PVR
Increase PA pressure signif decrease PVR Remark prop - how low PVR already Recruitment and dsitension of pulm capil
59
What are measure required to calculate PVR using swan
PVR = MEAN PAP =PCWP x 80 ____________________ CO Vas resistance = input P - output P/ blood flow Normal value 100 dynes sec
60
West zones
Zone 1: PA > Pa > Pv MAy be present at top - if drop in BP - Inc PA - 2' to IPPV - alveolar dead space Zone 2: Pa > PA > Pv Blow flow det diff b/w art & alveolar pressure - stralring resist mech - pulsatile Zone 3: Pa > Pv > PA FLow determ AV diffce Distenion Zone 4: Pa > Pi > Pv > PA alveoli (PA), in the arteries (Pa), in the veins (Pv) and the pulmonary interstitial pressure (Pi) :

Physiology Kerry (17 decks)

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