4.2 Oxygen dissociation curve Flashcards

1
Q

Draw Oxygen dissociation curve - normal adult hb

What points Id w/ normal values

Why is it sigmoid

A

page 122
Hba one

Three main points -

Arterial point Po2 Sat O2 97.5 13.3kPa

Mix venous = 5.3

p50 3.5

Sigmoid - positive cooperativity

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2
Q

What is the mix venous point

A

Mix venous blood

Po2 here 40mmHg -
Hb sats 75%

Oxygen content - not specified without further info

Note mix venous point not like odc

increase poc2 and ph in mix venous means that mex venous point lies on a right shift ODC - bohr effect

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3
Q

What is meant by p50

What is it

What is it used for

why was point on curve chose

A

Reference oxygen dissoc curve - pp o2 - 50% sat carry protein

Normal p50 3.5

P50 - specify position oxygen on o2 dissoc curve - index of affinity of oxygen carrying protein

Most useful to specify curve positon becuase its on steepest point on curve most sneistive for detecting shif of curve

allows comparison position other curves under diff conditions

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4
Q

What does a right shift indicate

A

decrease oxygen affinity - p50 high for right hsift

Causes by 4 things

Tempertue

[H+]

pCO2

Red cell 2 3 DPG level

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5
Q

Superimpose curve HBf

Why is it that way

A

page 123

Left shifted - compared hba - cause lower binding 2 3 dpg by Hbf

Simgoid - similar to normal oDC but slightly left shift

lower by 2.3kpa

Lower p50 - hgiher oxygen affinity
reduced bind 2 3 dpg to feoteal hb

2 3 dpg binds best to beta chain adult hb - right shift decrease affinity

2 3 binds avdily to beta of deoxy

foeteal 2 alpha 2 gamma
no beta
- coneseq lower p50

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6
Q

Draw oxygen didsociaton curve with oxygen content on y axis

A

page 124

mls dlo

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7
Q

What is myoglobin

Draw oxygen dissoc for myoglobin

explain shape

whats the advantage of shape

A

Haem contain oxygen binding protein
present skeletal muscle - role oxygen store

page 125

Rectangular Hyperbolic shape
vlow p50 .36

Lies very left of sigmoid hb curve
high affinity

advantage
ptake oxygen from hb

load and unload of range po2 in cell
if p50 could never load oxygen

intracellular po2 - vary diff cells
typically low

ox phosp cease <1mmhg

myoglob with its low p50 well match intracellular needs muscle cell

load oxygen from hb

unload to cell as cytoplasmic po2 falls low

Chemical reason

different structure

myoglob single globin chain

dissoc curve rectang hyperobla

hb contain globin chain an doxygenation of each casues struct change w. increasing affinity of haem for reamins oxygen
subunit interaction positive cooperativity - increase oxygen affinity as load - causes sigmoid shape of curve

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8
Q

What is physiological signifcane of shape of oxy dissoc curve for adult hb

A

1 Flat upper part

act buffer -s ense po2 drop to about 10.6kpa yet hb remain saturate 96% with oxygen

keeps arterial oxygen conc high despiate impair sturation lung

keeps large pp diff b/w alveoli and capillary after most o2 transferred

2 Steep part curve
Tissue reqire more oxygen large amounts of oxygen can be removed wihtout much further drop in po2

Pressure grad for diffsuion from capillary to cell - welle mintainted despite increased oxygen extraction

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9
Q

Summary shpae odc

A

Double buffering because

flat upper part buffer hb sat against substatn drop in po2 - useful maintain art hb sat

steep part large o2 unloading and main o2 diffison graduiaton

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10
Q

How is saturation of hb definied

A

oxy sat = actual content of Hb x 100
_______________________________

Max oxygen content of hb

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11
Q

What is the effect of acute anaemia on ODV

A

Curve not alter if sat on y vs po2 on x

If drawn as oxygen cconent versus po2 - p2 halved - shape not alrered
in chronic anaemia 2 3 dpg rises and right shfits

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12
Q

What is affect of Carbon monoxide on ODC

A

1 Curve is LEFT shifted

2 o2 content reduced

Left shift - binding co conformational change in hb - increased affinity for oxygen in oher subunits

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13
Q

How is carboxyhb dissoc curve diff from two curve

draw curve

A

dissoc CO from HB - cruve dissoc of oxygen for Hb in presence of CO as modifiny

Diffrence -

axes - sat hb CO on yo

PP pCo on x

extremely high affinity for curve mean extreme left shift and rectangular hyperbola

Page 127

Oxygen diddosc curve for Hb in presence of carobxy

draw sat on y - o2 dissoc prsence of CO same shape left shift

reduction in o2 content not apparetn when o2 satus used on y

If drawn with o2 content of hb on Y odc in Carbom monoxide left shift and reduced in size

ex curve draw hb 15g 33% hb co 10g avail combo oxygen - max content is 2/3

Dissoc curve for Hbcvo diff curve
pp co on x and pcc50 very low

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14
Q

What is difference between function sat and fractional saturation? is it clin important

A

oxgen ssat - function sat

tradition way consider sa
sat cont x 100/capaity

sat hb - determ measure actual oxy coent and measure o2 of another sample after equib room air

but blood may contain 4 hb species

oxyhb
deoxy
methb
cohb
only one carries 

funct sat hbo2 x 1– / hbo2 + deoxy

Fraction sat

Hb o2 x 100/ total hb
total hb = hb deox met co

Clinically more useful consider fraction sat
large amt met co - function mislead

value displayed pulse oxy neither function or fract

depends on calibration used for brand - may be close to one or other
as a two wavelength limited measure two hb species hbo2 and deoxy

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15
Q

Carbon dioxide transport

Tell me about Co2 tport in blood

what is contribution diff forms tport Co2 carraige and AV difference Co2 content

What is the arterial Co2 Content

A

Carbon dioxide is carried in 3 forms

1 Dissolved Co2
2 Bic
3 Caarbamino compounds

Art blood contains 48 Co2/dl and mix ven 52

Percentage of and % contrib to AV difference

Dissovled 5 10

Bic 90 60

Carbamino 5 30

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16
Q

What are carbamino compounds

A

Formed Co2 reacting

1 terminal AA groups proteins

2 Amino groups in side chain arginine and lysine

Hb is more important plasma proteins in formation of carbamino because

1 More hb present 15 v 7

Hb teatremer 4 N terminal groups/molecule & alb has 1

Dormation of carbamino ncrease greatly as Hb becomes doexygenated

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17
Q

what are reactions occurring in systemic capillaries?

A

1 Unloading oxygen hb and diffusion into plasma

2 Loading and carriage of CO2 as bic and carbamino

3 exchange hco3 - and Cl- cross membrane - hamburger
cl bic tports band 3 protein capnophorin

Draw out from page 128 gas exhcnage in red cells

Oxygen unloading assists w/ co2 loading - Haldane
Co2 dix loading assists oxygen unloading from Hb bohr

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18
Q

What is haldane affect

Diagram

A

Increased ability o blood carry Co2 when Hb gives up O2

Art blood cotrain 48mls co2 and pco2 40

mix ven conitrains 52 at pco2 46

seen diagram - if position co2 dissoc curve not change when sat drop mix venous pco2 would rise to 55mmhg if same amount co2 carried

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19
Q

What factors are responsible for haldane effect

A

1 deoxy is 3.5 effective then oxy forming carbamino compounds - major factor accounts 70% haldane effect

Deoxy hb is better buffer than oxy
mops up more H+
produced when h2co3 dissoc
improve carriage CO2 as bic
accounts remaining 30% haldane
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20
Q

Does formation carbamino compound by deoxy hb account any increased buffering capcity of deoxy

A

No pka of carbinmo - so low fully dissoc plasma ph - net increase H+ conc

rather increasing buffering
more H requiring buffering produced

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21
Q

What groups Hb accoutn buffer capacity at phys ph

A

imidazole groups pka 6.8

in 38 histidine residue in Hb

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22
Q

Differences between base & apex of lung

A
Top
larger at end expiration
lower ventilation
lower perfusion
higher v/q (3.3 vs .63 in base)

Higher vq - diffrence gas compositon
higher Po2
Lower pco2 higher ph

difference oxygen uptake and Co2 output
higher exp exchange ratio at apex vs base RER 2 v .67

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23
Q

Why is there a vertical gradient v/q ratios in erect lung

A

Conseq vertical gradients in pulmonary perfusion & ventilation

Perfusion gradient direct conseq gracity on hydrostatic press in PAdifference hydrostaic pressure between top and bottom lung is 30cm h20

Ven gradient
indirect effect gravity lung

1 Intrapleural pressur egradient
weight lung cause gradient intraplur pressure top to bottom
-10 vs -2.5

2 Gradient alveolar size
apical alv large than basal more neg apical intrapleure P distenidng more

Vent grad
conseq gradient alveolar size at frc alveoli increase size diff amt inspiration on different part of compliance curve
smaller basal increase more w/ inspiration - receive more of TV cause of this
gradient ventilation top to bottom present

Vertical V/Q gradient exists - vertical gradient in perfusion is large than the gradient in vent

v/q calc high apex- 3.3 vs low base .63
imporant effect gas exchange

24
Q

How is sit diff at low lung volumes eg tidal breathing from just above RV

A

Change in distrib

Vent apex improves better than base
reverse typcal

IPP apex decrease -4 and IPP at bease decreaes +3.5
gradient same 7.5
as expected - weight alter

lower lung volume decrease size recoil forces

Apex is no on fave part compliance curve ventilates better

Positive IPP at base - airway closure and vent conseq reduced

breathing from RV - v/q mm and impaired Gexchange

25
Q

Volume pressure & flow during normal breathing

Draw 3 curves on page 131

Draw curve showing change intrapleural pressure during normal TV

Curve showing corresponding change in alveolar pressure

Gas flow in trachea

A

4.15 0 intrapleural during quiet breathing IPP v Time
-5 at start inspiration d.t elastic recoil lungs
fall in IPP during inspiration d/t increas elastic recoil and fall alveolar pressure

Alveolar P v time
decrease alveolar pressure est driving pressure
If no airway resstiance - alverolar pressure stay 00 thru-out inspiration
- Airway resistance is delta P between alveoli and mouth / flow
Major site resistant - medium sized bonrhci
most pressure drop occurs airways up to 7th gen
<20% d/t airways <2mm diameter

gas flow in trachea during quiet breathing

26
Q

Physiology of preoxygenation

A

Aim increase oxygen patient lung as a buffer against hypomaeia during apneoa
Aim displace N from FRC and replace O2
Denitrogenaiton
effective

oxygen in lung increased substatn
increase can occur rapidly

27
Q

Whats the max amt oxy after sev min preox

A

FRC supine 30mlkg
2.1l in 70kg adult
normal con 13% o2 = 270mls
little more than mins supply

if preoxy
al gas eqn pred max of about 660 
760-47 -40/.8
87% oxygen alveol and 1825 o2 at frc
7 mins oxygen at consump 250mls min
28
Q

Is hyperventilation safe during preoxy

A

Yes - hypervent 2 factors

1 rate wawshout N increase - signifcant effect speeds up

Condeq decrease alv PCo2 FRC sml amt addit oxygen pred alveolar g eqn

29
Q

What are the oxygen store in body and what are they increased with w/ preoxy

A
FRC
Blood
Dissolved in fluiod
myoglobi
VC inspir - increase

lungs 270-> 1825

Blood 820-> 910

tussye 45->50

Nyi gkib 200 -> 200 min cellular change

substant increase d/t lungs

total sotres breathing room air 1335 supine

increase ~~ 3l breathing 100%

30
Q

Which not increase much on 100%

A

Increase content blood d.t increase sat hb a+ v sides
increase dissovled .3 at 100mmhg -> 1.8 at 600mmhg

Only parts blood increase diss o2 - lheart and stem artery
veins not increase on 100%
extra dissolved in blood only 15mls

Incr ven po2 hb sat in veins high normal
increase carriage both art and venous side
70mls extra in veins and rheart
d/t igher sat hb

total increase oxygen store in blood 80-95ml
small compared increased stores in lung
tissue po2 mi alter little increase in o2 stores

myoglob low p50 sat little alter small icrease po2

31
Q

Dissobled oxygen improtnat?

A

vitally - present cell
participate rxn

dissovle o2 diffused capilary to cell across placenta

doesnt contrib to delivery bt has vital role in rxn cells

32
Q

Where is most o2 used cell

A

Mitochodn oxidative phospho - largest con ~90% total use

of o2 cell
oxy reacts w. H produce metabolic water in final step electron tpor tchain
catlysed cytochrome oxidsae

33
Q

What consequences of Co2 tport for intubation apnoea

A

Sit sm aponeic oxyugen
lungs full oxygen

airway opne - no vent
oxygen pulm cap blood cont normal no excretion co2
art pco2 rise rapidy as much 55mmhg

Reasons
1 wash thru mix venou blood
haldane effect - pco2 constant pco2 will rise - d/t rise in sats

Inevitable abrupt increase cbf - espec if difficult and prolonged
smyp stim -addit stress cbf and icp

34
Q

Breathing 100% oxygen

If a fit healthy adult at rest switches to 100% O2 what happens to alveolar and art Po2

A

Alveolar Po3 rises to high value - calc from alveolar gas equiaton

PaO2 = PiO2 - PaCO2/R

WHere R is reps exchange ratio
Pio2 is inpsired pp

Assuming paco2 is same value as art pco2

PiO2 = 760 -47 713 for oxyygen full sat wiht vapor 37

pao2 713 - 40/.8 = 663

sp wpi;d [redict value 663

arterial lower d/t venous admix (inlcude v/q mm)

Probably over 600 mmhg in health young adult

35
Q

What way is arterial PP of CO2 & nitrogen affected

A

PaCo2 - not be affected - value proportional tissue CO2 production and inversely proportional to alveolar venitlation - unaffected

pN2 - decrease as N2 being washed out of body
decrease low levels if breathing 100% oxygen continue

Nitrogen lungs washed out quickly - dentitrogenation

36
Q

What PP Co2 Nad o2 in mixed venous blood when breathing room air

A

O2 40mmhg - hb 75% sat

CO2 - 46

37
Q

Is mix venous PCo2 affected affected 100%

A

Pco2 is about 46mmHg rise in Po2 not sufficient to alter increase in deoxy

if po2 in venous blood was 100mmhg or more

  • hyperbaric oxyen
    then hb remain fully aR
    Pco2 rise to about 55mmHg - d/t absence haldane effect

As mix venous not much higher 100% oxygen - hldane imporant and mix venus pco2 not much affected

38
Q

In the person breathing 100% oxygen for time - what is po2 in mix venous blood

A

Po2 slightly eleavted 48->50

39
Q

If arterial PO2 >600mmhg in someone on 100% O2 - why isnt mix venous Po2 higher than sloght indication

A

Answer -appreciation difference oxygen content and oxygen partial pressure

Po2 600mhg in art blood - high partial pressure - oxygen content rise art blod small

As Hb almost fully sat at Po2 100mmHg
Increase PO2 >100 cannt add any more oxygen hb

AMount oxygen dissolved in blood directed related to PP
Amt oxygen dissolvedat 600 is x6 dissollved at 100mmhg

Amt O2 dissolved 100 at PO2 100 -
.003 x 100 = 3mls

amt 100mls at 600
.003 x 600 - 1.8
henrys law

Hb not start release oxygen until po2 <100mmHg because of shape of ODC

Oxygen released from hb but po2 not drop to 40 mix blood because signif contib dissolve oxygen

mix venous po2 48-50

40
Q

With an arterial Po2 >600mmhg will tissue be exposed to risk of normoabric oxygen toxicity

A

no
dissolved oxygen not suffficent supply needs of all the tissues
some dissociation of oxygen from Hb will laways occur

Mean capillary Po2 be only slightly elevated from normal not sufficient to cause toxic effect in periphery

Alveolar cells exposed to high Po2 with prolonged exporsure -s ome oxygen tox in lung

41
Q

If someones po2 is low on 100% what does this indicate

A

Major oxygenation problem

Must be d/t significant shunt

Other major cause hypoxaemia in ITU is V/Q mm
if this where the cause - vent 100% = high po2

arterial po2 should rise over 500mmhg if v/q mismatching presnet without coex shunt

rise art po2 slow - if many units with low v/qs

With 100% art po2 rise to high level in other 4 causes hypoxaemia

hypoventilation
low inspired o2
diffusion block
diffusion hypoxaemia (exercise at altitude)

42
Q

Resorption of PTX

A

Mech is diffusion gas down PP grad from gas pT into blood and pleural cap

Most cases ptx high Po2 than cap blood

o2 diff down into pleural cap blood

PTX decrease size
total pressure resmain same @1atm

Loss volume d/t xoygen absorption
concentrating effect on all gasses reamin

icnreasees gradient acouring resabso gases

oxygen PP increase by eefect reabson continue and size cont decrease

conc effect important till all gas reabsorbed

Key understand 3 point above

1 gas move down diffusion conc grad

Total pressure in ptx doesnt vary much beacuse voulme change
totral press ~~1atm

Becaume volume redcution and main constant pressure in PTx abso gas down conc grad has conc effect on remain gas
increase pp gases and maintain gradient
keeps process untull all reabasorb

PTTX may increase in size cert ciurm

room air to 70%N2o
NO DIFFUSION DOWN CONC INT ptx would increase size difference movemnt n2o and N
N2o diffusion fastr than N diffuse out
Increase size decreasePP grad other gases

Gas compostion of ptx vary on orignal source
if orig room air
pco2 low and grad cause entry co2 capillary
great reabs oxygen - decrease in vol and conc effect - conc effect increase PP of all gases present

43
Q

Actually theres one gas always present and whos pp remain thorugh reabs what and why

A

Water vapour
Ph20 remains 47mmh - and svp 37

Eliminate nitrogen cap glood grad fave reab N larger

Mixed venous po2 slightly increase breathing 100% not much affect in gradient facour oxygen reab offse effect dentropgenation

PTX reabsorb faster breathing 100% and this dt assos dentrogenation

44
Q

What is cyanosis

A

Blue discolouration sking d/t presence excess amt desat hb in blood

cyanosis detectable clinically when blood contains 5gdl of deoxy hb

45
Q

Why does cyanosis appear more rapidly with methb than hpyoxaemia

A

Cyanosis clin apprtly 1.5gdl meth-haem present in cap blood clinical significant lower than 5 g dl deoxy reqd

46
Q

what is methaem

A

Produced in hb when haem irons converted Ferrous Fe 2 -> Ferric Fe3

oxidation may be caused by some drugs or metabolites
eg metab of prilocaine prduces otoludine - which can oxidise haem iron

Met-haem doesnt bind oxygen

Redcells contain enzyme
methab reductase
which reduce ferric back o ferrous
requires NADH cytochrome b5 as cofacor

oxidation of ferrous ion in b occurs at 3% day

47
Q

WHat is hb auto oxidation

A

Iron in deoxyhb is in ferrous form

oxyhb is different - partial tfer electron from iron to oxygen

Oxy hb has a superoxyferrihaem Fe3O2

Unloading of oxygen restore the ferrous form

howerver rarely oxygen leaves as a superoxide radiacal o2
and the iron is left in the ferric stat - methhb

48
Q

Methylene blue is used as a therapeutic agent in Mehth hb how does it work

A

In additio to NADH meth hb redcuate

red cell contrain another enx can reduce hb

Enz is NADPH methhb reductase
under normal coniditon is responible few percent of daily methb reduction.

In presence of methylene blue - amt hb reduction d/t enzyme increase

enzyme directly reduces methylen blue - reduce form methylne blue non enzymatically reduce mehthb

49
Q

What affect anaemia have in cyanosi

A

Require 5gdl deoxy hb cap blood

person sever anmaei hb <5 - yanosis never be prseent

with less severe cyanosis require high level desat beofre present

50
Q

What is argyria

A

Salte grey blue discol skin - insoluble silver albuminate
occurs ingents silver salts long time

rare could be confused cyanosis

51
Q

Flow volume loop

What is the effort independent portion & why cant this part be breached

A

Page 138

Draw flow volume loop
flow is on y volme is on x
TLC start
rapidly increase flow towards 8l sec, then desending limb expiratory curve from onset closure to RV

Effor indep potion most descending part - occuring during expiration
-part descling lumb from onset airway closure down to RV

max poss flow rate at any particul volume on x defined by max expiratory curve
reason flow not exceed cause of dynamic airway compression

52
Q

Explain mechanism of dynamic airways compression

A

Consider forced expiration
increase intrapleral pressure - tmitted to alveoli -
alveolar pressure >mouth pressure (atm) - airway open
gas flows out lung thru airways down pressure gradient

Might be thouhgt - greater effort during expiration larger increase intrapleural pressure - greater rise in alveolar pressure - increase gradient alvoelar and mouht pressure increase expiratory flow rate

Happens to limit

particular max flow ossible depend lung volume at that instant - indicated on max exp flow vol loop
reason flow limitation related design chest
part airwys in thoracic cavity - like alveoli airways also exposed increaed intrapleural pressure

during forced expiration - larger pressure acts squeee alveoi - also acts compress airway

initiall held open airway pressure inside great than intrapleural
because resistance airway presure inside airway decrease preogressively further particular airway from alveoli

finally reach point airway pressure and intraplreal are equal

distal to equal pressure point airway collapse

Known as straling resistor

driving pressure flow differnece pressure alveolar and intrpleural rather pressure diff alveolus and mouth

dirivng foce - same even with incraed expiratory effort

Max flow constant each partic lung vol and decrease as lung vol decreases

53
Q

WHat factors make dynamic airway compression more pronounced

A

Increased airway resistance of intrapulmonary airways
-airway pressure drops rapidly

Increased compliance - results reduced driving pressure

Expiration from initla low volume - vecause reduced driving pressure - ie alveolar intrapleural press diffc decrease

forced expiration w/ emphysema - causes more ponounced dynamic airway compression
audible wheeze - may be presesnt during noraml TV
no wheze airway closed - no flow

54
Q

How would flow volume curve FVC different adult severe obstrctuin airway disease

A

TOtal lung voule high - chest over expand loop left shift

max flow rate reduced

total vol expire less fvc

descending limb - may be concanve

55
Q

Where else is the starling resistor meachnism imporntat

A

Intramyocardial pressurre limits perfusion lv during systele

Lung - alveolre pressure is external pressure - west zones

any organ has capule - oedema casues increase tissue pressure

pericaridal effsuion impar vr AND filling

icp - limits cbf

pregnant uterus contracts

vacval compression - supine hypotension pregn

muslce pump mech leg - promo vr

increase intraabdo pressure - bowel bladder emypty

tampomade pulm vessel during vaslavla

incrase IOP _ glaucoma

oedema muslce in CT ocompar

tight plaster cast - oedema tissue injury