4.2 Oxygen dissociation curve Flashcards
Draw Oxygen dissociation curve - normal adult hb
What points Id w/ normal values
Why is it sigmoid
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
What is the mix venous point
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
What is meant by p50
What is it
What is it used for
why was point on curve chose
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
What does a right shift indicate
decrease oxygen affinity - p50 high for right hsift
Causes by 4 things
Tempertue
[H+]
pCO2
Red cell 2 3 DPG level
Superimpose curve HBf
Why is it that way
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
Draw oxygen didsociaton curve with oxygen content on y axis
page 124
mls dlo
What is myoglobin
Draw oxygen dissoc for myoglobin
explain shape
whats the advantage of shape
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
What is physiological signifcane of shape of oxy dissoc curve for adult hb
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
Summary shpae odc
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
How is saturation of hb definied
oxy sat = actual content of Hb x 100
_______________________________
Max oxygen content of hb
What is the effect of acute anaemia on ODV
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
What is affect of Carbon monoxide on ODC
1 Curve is LEFT shifted
2 o2 content reduced
Left shift - binding co conformational change in hb - increased affinity for oxygen in oher subunits
How is carboxyhb dissoc curve diff from two curve
draw curve
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
What is difference between function sat and fractional saturation? is it clin important
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
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
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
What are carbamino compounds
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
what are reactions occurring in systemic capillaries?
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
What is haldane affect
Diagram
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
What factors are responsible for haldane effect
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
Does formation carbamino compound by deoxy hb account any increased buffering capcity of deoxy
No pka of carbinmo - so low fully dissoc plasma ph - net increase H+ conc
rather increasing buffering
more H requiring buffering produced
What groups Hb accoutn buffer capacity at phys ph
imidazole groups pka 6.8
in 38 histidine residue in Hb
Differences between base & apex of lung
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
Why is there a vertical gradient v/q ratios in erect lung
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
How is sit diff at low lung volumes eg tidal breathing from just above RV
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
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
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
Physiology of preoxygenation
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
Whats the max amt oxy after sev min preox
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
Is hyperventilation safe during preoxy
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
What are the oxygen store in body and what are they increased with w/ preoxy
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%
Which not increase much on 100%
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
Dissobled oxygen improtnat?
vitally - present cell
participate rxn
dissovle o2 diffused capilary to cell across placenta
doesnt contrib to delivery bt has vital role in rxn cells
Where is most o2 used cell
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
What consequences of Co2 tport for intubation apnoea
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
Breathing 100% oxygen
If a fit healthy adult at rest switches to 100% O2 what happens to alveolar and art Po2
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
What way is arterial PP of CO2 & nitrogen affected
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
What PP Co2 Nad o2 in mixed venous blood when breathing room air
O2 40mmhg - hb 75% sat
CO2 - 46
Is mix venous PCo2 affected affected 100%
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
In the person breathing 100% oxygen for time - what is po2 in mix venous blood
Po2 slightly eleavted 48->50
If arterial PO2 >600mmhg in someone on 100% O2 - why isnt mix venous Po2 higher than sloght indication
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
With an arterial Po2 >600mmhg will tissue be exposed to risk of normoabric oxygen toxicity
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
If someones po2 is low on 100% what does this indicate
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)
Resorption of PTX
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
Actually theres one gas always present and whos pp remain thorugh reabs what and why
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
What is cyanosis
Blue discolouration sking d/t presence excess amt desat hb in blood
cyanosis detectable clinically when blood contains 5gdl of deoxy hb
Why does cyanosis appear more rapidly with methb than hpyoxaemia
Cyanosis clin apprtly 1.5gdl meth-haem present in cap blood clinical significant lower than 5 g dl deoxy reqd
what is methaem
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
WHat is hb auto oxidation
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
Methylene blue is used as a therapeutic agent in Mehth hb how does it work
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
What affect anaemia have in cyanosi
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
What is argyria
Salte grey blue discol skin - insoluble silver albuminate
occurs ingents silver salts long time
rare could be confused cyanosis
Flow volume loop
What is the effort independent portion & why cant this part be breached
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
Explain mechanism of dynamic airways compression
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
WHat factors make dynamic airway compression more pronounced
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
How would flow volume curve FVC different adult severe obstrctuin airway disease
TOtal lung voule high - chest over expand loop left shift
max flow rate reduced
total vol expire less fvc
descending limb - may be concanve
Where else is the starling resistor meachnism imporntat
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
