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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Draw oxygen didsociaton curve with oxygen content on y axis

A

page 124

mls dlo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is saturation of hb definied

A

oxy sat = actual content of Hb x 100
_______________________________

Max oxygen content of hb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What groups Hb accoutn buffer capacity at phys ph

A

imidazole groups pka 6.8

in 38 histidine residue in Hb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
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
26
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
27
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 ```
28
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
29
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%
30
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
31
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
32
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
33
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
34
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
35
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
36
What PP Co2 Nad o2 in mixed venous blood when breathing room air
O2 40mmhg - hb 75% sat CO2 - 46
37
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
38
In the person breathing 100% oxygen for time - what is po2 in mix venous blood
Po2 slightly eleavted 48->50
39
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
40
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
41
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)
42
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
43
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
44
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
45
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
46
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
47
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
48
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
49
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
50
What is argyria
Salte grey blue discol skin - insoluble silver albuminate occurs ingents silver salts long time rare could be confused cyanosis
51
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
52
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
53
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
54
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
55
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