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277 Cards in this Set

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what is the PvO2 entering Ratria? PvCO2?
PvO2: 40
PvCO2: 46
What is the PaO2 leaving Left atria? PaCO2?
PaO2: 100
PaCO2: 40
what happens to the diaphragm when you inhale?
contracts and shortens expanding the volume of the thorax
what structure separates the 2 lungs?
mediastinum thus they can behave differently: one can collapse while the other doesn't
where does gas exchange take place?
only in the last 4 generations: the alveolar ducts and the alveoli
what components of the airway make up the conducting zone?
trachea
bronchi
bronchioles
terminal bronchioles
what components of the airway make up the transitional and repiratory zones?
respiratory bronchioles
alveolar ducts
alveolar scs
shape of individual alveoli?
hexagonal
what makes up the alveolar wall?
capillaries and air space on either side of the capillaries
*think of alveolar wall as a mesh of cap segments (spaghetti)
features of the diffusion distance in alveoli?
less than 1 micron distance for gas to diffuse from alveoli to capillary therefore rapid, efficient exchange
alveolar type 2 cells make what?
surfactant
the unit of pressure is?
1 mmHg = 1 Torr
The atm is a mixture of what gases? what is the pressure exerted by these gases combined?
mixture of O2 and N2 that exerts a pressure of 760 mmHg (this is Pb, barometric pressure)
what percent of Pb is exerted by O2? N2?
21% by O2
79% by N2
what is the pressure exerted by O2? N2?
O2 = 160mmHg
N2 = 600mmHg
what is the partial pressure of any gas? (eqn)
Pgas = Fgas * Ptot
the product of its mole fraction and the total pressure exerted by all the gases ex: O2: (760) * (.21)
when do the partial pressures of O2 and N2 change?
when room air is moved into aiways
compare Po2 and Pn2 in room air vs airways
P02 room = 160
PN2 room= 600
P02 airway = 150
PN2 airway = 563
what is added when room air is drawn into the airways ?
water vapor
at body temp, what is the partial pressure of water vapor? what does this do to the Pb?
47mmHg
Pb becomes: 760-47 = 713
what happens to Po2 and PN2 as it enters the airways?
both decrease b/c of water vapor
the vapor pressure of water is a fxn of what?
tempertature
at 37.5 C = 47torr
which is more soluble, Co2 or O2?
CO2 (20 times more soluble)
how do gases dissolve in fluids?
by moving down a partial prssure gradient rather than a concentration gradient
gases move down _____?
partial pressure gradients (gas phase to liquid phase until reach equilibrium..want PO2 in gas = PO2 in blood)
what is the difference b/n partial pressures of O2 in gas phase and liquid phase at equilibrium?
nothing.they are the same b/c at equilibrium fluxes are equal
what are teh factors taht determine how good a gas exchanger is?
1. partial prssure differences
2. thickness of membrane
3. surface area b/n gas compartments and blood
compartments
4. solubility of gas in membrane
5. degree of matching of gas and blood (ventilation = perfusion)
in a perfect exchanger, what will be true?
both the expired gas and the arterial blood wil have equal Po2
PAO2= PaO2
the bigger the A-a difference, the ____
poorer the exchange
as you increase the surface area, what thappens to gas exchange?
increases
if you decrease the thickness of membrane, what happens?
the thinner it is, the more gas is exchanged
what happens to gas exchange as you change solubility?
the greater the solubility, the better the gas exchange
what does PaO2 refer to?
mixed pulmonary venous blood as it leaves the lung (same as PO2 in pulm systemic arterial blood)
what does it mean when ventilation and perfusion are perfectly mismatched?
the lung is both ventilated and perfused, but NO gas exchange is taking place bc the gas is pumped to locations that have no blood flow. the blood is pumped to places that hve no ventilation
in a perfectly mismatched exhchanger, what happens in the presence of occluded airway?
occluded airway like in COPD, perfusion is taking place, but no ventilation
in a perfectly mismatched exchanger, what happens with an occluded blood vessel?
ex: pulmonary embolus
ventilation but no perfusion
"dead space" wasted ventilation
what is the local response to an occulded airway?
vasoconstrict causing R-L shunt
all the blood that passes through will not undergo gas exchange. now the unoxygenated blood passing through the shunt gets mixed in w/ other oxy blood lowering the partial pressure of O2 and riasing the PCO2 in the mixed blood leaving the lung
what is a shunt? what does it result in?
a vascular pathway through the lung in which there is NO gas exchange (COPD pts)
*results in lowering PaO2 and raising PaCO2 (mixed venous blood leaving lungs)
b/c of an occluded airway what happens to PAO2 and PaO2?
PAO2 coming out the mouth is normal
PaO2 is low b/c was never oxygenated creating shunt
what is dead space in lung?
parts of the lungs where gases are pumped, but where no gas exchange takes place
*wasted ventilation
what is the affect of an occluded blood vessel on PaO2 and PAO2?
PaO2: normal
PAO2: higher than normal b/c a component of the gases coming out of the mouth consitutes room air b/c no gas exchange could take place
do you have ventilation or perfusion with an occluded blood vssl?
ventilation with NO perfusion creating dead space=wasted ventilation
what happens to the cross sectional area of the airway tree when it bifurcates? what effect does this have on resistance?
increases- almost doubles
the flow resistance at each bifurcation now decreases
where is the airway tree smallest in cross section?
larger upper airways therefore the flow rate during respiration is always greatest there
as you increase the flow rate, you have a greater chance of what?
greater collapsing prssure casued by Bernoulli effect: thus the large airways have solid, cartilaginous rings to prevent collapse
where is resistance to flow greatets? smallest?
greatest in large upper airway
smallest in alveolar sacs
(bc resistance to flow decreases with each bifurcation)
lung unit w/ Q but no V =
right - left shunt
lung unit w/ V but no Q =
dead space
characteristics of chest wall?
muscular organ that lung is coupled to: as chest wall expands, lung follows it
what do the P-V curves for lung and chest wall represent?
relaxation pressures
how are relaxation pressures measured?
by taking the structure of interest, blowing it up to some volume, plugging its orifice, and then measuring how much pressure it exerts at its orifice
the slope of the lung P-V curve represents what?
softness or compliance of the lung
at zero prssure in the lung, do you have zero volume?
no, you can't get all air out of it
how is the chest wall relaxation curve different than the lung relaxation curve?
b/c the chest wall is rigid, you can suck the air out of it and it will exert a negative relaxation prssure
how do you collapse the chest wall?
by sucking all the air out of it; it is rigid, bony, muscular
diff b/n hydrostatic pressures and partial prssures of gases?
gas partial pressurs are always referred to using absolute pressure, expresed in mmHg
Hydrostatic pressures are expressed relative to barometric pressure, which is always zero
at sea level, room air has a hydrostatic presssure of what? and PO2 of what?
hydrostatic prssure of 0cmH20
PO2=160 mmHg
what does negative pressure imply?
negative means subatmospheric
ex: to say that pressure of pleural cavity is -10 means it is 10 cmH20 below atmospheric prss (750mmHg)
where is the energy needed to pump gases in and out of lungs come from? why?
lungs are totally pssive so energy comes from chest wall
how can you inflate the lungs?
1. by blowing them up like balloon
2. by putting them in a space with negative pressure like in a thorax
*in both situations, Pin is greater than Pout and keeps the lungs inflated
in reality, what prssure keeps lungs inflated?
transmural pressure in pleural cavity that is subatmospheric
what pressure holds the lungs inflated?
transmural prssure: pleural prssure that is subatmospheric
what are the 2 components of the chest wall?
1. diaphragm, made of muscle
2. rib cage, made of bone
in the natural state, what is the state of the chest wall?
large volume, diaphrahm flat
somewhat collapsed; its elastic recoil force acts to expand it
in the natural state, what is the state of teh lungs?
inflated in the thorax
its elastic recoil force acts to collapse it
when the lungs are not in the thorax what state are thye in?
deflated, b/c dont have opposing elastic force of chest wall to keep inflated
when the air is sucked out of the pleural space, what happsn to the lungs and chest wall?
lung is inflated
diaphrahm is pulled up
chest wall and lung have same volume
pleural spce vol decreases and fluid exerts neg prssure
what is the elastic recoil force of lung? chest wall?
lung=collapse
chest wall= expand
why does the fluid in pleural space have neg prssure?
b/c of opps elastic forces of lungs adn chest wall
what is the fxnl residual capacity FRC?
the equilibrium situation, where the elastic recoil forces of lung and chest wall are equl and opp. this is the amt of gas prseent in lungs when you mouth is open and your resp. mm are relaxed
what happens in the event of pneumothorax?
lung recoils in diretion of getting smaller (collapse) and chest wall recoils in the direction of getting bigger
lung elastic recoil arises from what?
surface tension and tissue elastic recoil
why does the lung have tissue elastic recoil?
when inflated the polymer molecules that make up the physical lung become deformed and exert a restorative (recoil)force
when comparing volume to relaxation pressure, what happens when lungs are filled with air?
tissue elastic forces + surface tenstion forces come into play and you need a high pressure to inflate lungs b/c you have to overcome the recoil and surface T
when comparing volume to relaxation pressure, what happens when lungs are saline filled?
no surface tension forces b/c lack air/water interface therefore you only have to overcome the recoil
you now need less pressure than when lungs arefilled with air to inflate
why is there suface tension forces when lungs are filled with air?
b/c each alveolus is basically a water-lined compartment so the water exerts surface tension forces that act to reduce teh size of the surface (collapse the lung)
what is the main contributer to lung recoil?
surface tension
explain where the lung elatic recoil forces come from.
recoil forces are resolved into 2 components: one component is parallel to surface and the second is inwardly directed. the suface parallel forces are equal and opp and they cancel out. the inward forces sum together and act on every particle in the lung:they exert a pressure on any gas inside
what type of forces b/n liquid molecules are responsible for surface tension?
strong intermolecular attractive forces b/n liquid molecules
how is surface tension different w/n fluid and at surface?
w/n fluid: the forces acting on molecule are all balanced
at surface: they are unbalanced b/c downward forces w/o upward forces resulting in downward force w/ tension
what is the affect of surface tension on alveolus?
alveolus is spherical, so at surface the particles are all pulled downward which tends to collapse alveolus
what would happen to the alveoli of lung according to LaPlaces law?
if one alveolus was smaller, it would empty into larger
P = T/R
P1=T/R1
P2=T/R2
T same in both
R2 > R1 then P1 > P2 causing shunt
*lungs would still be perfused but not ventilated (collapsed alveoli don't get V)
the smaller the radius of the compartment, the greater that what?
inwardly directed force
P=T/R the bigger R is, the smaller P is (bigger balloon, smaller pressure)
what is surfactant?
phospholipid secreted by type II alveolar cells that inserts its way in b/n water molecules along the surface lowering surface tension
what does surfactant do to intermolecular forces b/n water molecules?
replaced by cohesive forces b/n water molecules and surfactant lowering the tension in the surface film
what happens in premies?
absence of surfactant
lung recoil forces are very high and the forces rqd to inflate the lungs are greater than the infant can manage (infant resp distress syndrome)-increased difficulty in breathing
is surfactant more concentrated in larger alveoli or smaller?
smaller therefore net surface tension is smaller in smaller alveoli and the prssure in large alveoli is greater
is surfactant hydrophobic or philic?
mostly phobic and so poorly soluble in water so it sits on surface
the bigger the alveoli, the ____ the surface tension?
higher
when a unit is expanded, its surface area increases as the _____ of the radius?
square of the radius so if the unit is double in radius, the surface cocentration of surf is 1/4 the concentration of that in smaller alveoli
if you double R what happens to T?
P=T/R increase T by 4
what is FRC?
at rest, the volume of air in lungs *the inward recoil of lungs exactly matches the outward recoil of chest wall
affect of surfacant on compliance?
increases the compliance and decreases the surface tension
explain the pressures in pneumothorax?
pleural P = 0 (bc you have opened it to room air and it is no longer neg)
alveolar P = 0
no elastic recoil
explain what happens to prssures when you inhale and exhale
you are always going to be at Pin=0 b/c mouth open, but to get air into lungs the pressure in the lungs will become negative until enough air has entered then it is 0 again. To exhale, the Pin becomes positive
inhaling is a ____ process
exhalaing is a ____ process
ihale: active
exhale: passive
mm involved in inhalation?
main mover is diaphragm
external intercostal mm: lift the ribs when they contract
explin the pressures in a person on a ventilator
they are completely the opp of a normal person (inhalation)
inhalation: Ppleural + Pin +
exhalation: Ppleural + Pin +
explain the breathing of an emphysema pt.
always use forced exhalation b/c decrease elastic recoil that is needed for passive exhalation
what happens to the airway during forced exhalation?
airway collapses as pressure inside gradualy becomes less than the pressure outside the airway.
do large or small airways tend to collapse?
small airways b/c large airways have cartilaginous rings
how does normal exhalation occur?
the diaphragm relaxes and the elastic recoil force of the lung makes alveolar pressure positive driving the gas out of the lung
how does the alveolar pressure become positive for exhalation to occur?
the diagphram relaxes and the elastic recoil force of the lung makes alveolar pressure pos
how do you forcefully exhale?
contract internal intercostals
contract abdominal mm to raise the intra-abdominal pressure to push the guts up into the diaphragm
*used during exercise or hyperventilation
action of internal intercostals
for forced exhalation push the ribs down and back
explain what is occuring at the beginning of inhalation
the diaphragm contracts and lowers. this increases Pleural volume and lowers Ppleural. Now the elastic recoil forces arean't balanced across lung so lung expands
how does the lung expand during inhalation?
when the diaph. contracted it increased the pleural volume which decreasd the pressure (making it more neg). now the elestic recoil forces of the lung were unequal so the lung expands lowering the pressure inside the alveoli (-2) pressure at the mouth is now greater than the pressure in the alveoli so airflow happens
explain what is happening to pressures during exhalation.
when you relax the diaphragm it makes pleural pressure less negative which unbalances the recoil forces; lung recoil force is greater than the transmural pressure diff therefore teh lung gets smaller, and the pressure in the lung rises ; airflow happens
when is pleural pressure negative?
always during normal breathing
what is true about transmural forces during both inspiration and exhalation?
transumural forces are always EXPANSILE to the airway therefore pleural pressure always holds the airways open during normal breathing
airway resistance is determined by what eqn?
poisuille eqn : R ~ 1/r^4 therefore if radius increases, resistance decreases
lung compliance is determined how?
slope of P-V curve
C = V/P
lung + chest wall using relaxation pressures
@ FRC, Ppleural becomes more ___? Palveolar becomes ___
Ppleural: more -
Palveolar: -
Ppleural and Palveolar during forced exhalation?
Ppleural: +
Palveolar: +
what device meausures compliance? how?
spirometer tube with known resistance in which you breath into and it measures the pressure. since Q=P/R R is a constant and by measuring P you can find Q which you can then use to determine volume
explain what the P-V curve wold look like in an emphysema pt?
steep slope due to increased compliance
relaxation prssurs measure what?
P-V relationship of the lung + chest wall together
units of pulmonary compliance?
liter/cm H20
shape of P-V curve?
not linear
specific compliance =
Compliance/ TLC
C = V/P
greater compliance means?
less elastic recoil forces and easier to inflate
in which respirtory diseases do we see a decrease in compliance? effect on P-V curve? TLC?
intersitial lung diseases (fibrosis-PV curve shifts to right and TLC is reduced)
Loss of surfactant
PV curve shifts how in emphysema? TLC?
curve shifts Left
TLC increased b/c less elastic recoil making lung easier to inflate
relaxation pressures reflect what?
the elastic recoil forces of the chest wall and lung
FRC in emphysema pt?
larger than normal b/c the lung is softer but the area for gas transfer is diminished
how do you normalize the change in volume to the size of the person?
divide the volume by TLC this will show you that even though a small child has a smaller compliance, both subjects are actually normal in relation to their TLC
during normal exhalation, what are the transmural forces along the airway?
positive inside and negative outside thus the airway is held open: during normal passive exhalation, the airway is subjected to expansile forces along its length
what type of transmural forces exist in forced exhalation?
at some point the pressure outside the airway is greater than the pressure inside. from that point on, the airway is subjected to collapsing transmural forces
if you reduce the airway dimater by 1/2, what happens to the resistance?
R~ 1/r^4 therefore the resistance increases by 16
what does the Bernoilli effect state?
the faster the airflow the lower the pressure exerted on the inside of the walls of the airway; promotes collapse
the faster the airflow, the ____ is the force holding the airway open
smaller
the greater the tendency of airways to collapse
why do the large airways have cartilaginous rings?
b/c the flow rate is greatest in the larger airways causing a decrease in the pressure exerted on the walls of the airways promoting collapse. the rings keep them from collapsing
which disease states is the Bernouli effect most impt?
emphysema because they used forced exhalatin which promotes the collapse on top of the bernoulli effect
asthma causes airway constriction
in terms of energy, what does the bernoulli eqn state?
when air moves faster, you convert potential energy (pressure) to a kinetic energy (moving gas). when the airway closes the flow rate goes to zero and the kinetic energy is converted to potential energy and the process repeats
when is a forced exhalation a good thing?
when coughing b/c turbulent flow created drags mucus in the airway towards the mouth
what factors keep airways open?
tethering
pursed lip breathing
PEEP
what is tethering?
tethering of alveoli refers to them being attached to their neighbors promoting the stability of the airway. If they are all connected, a particular alveolus will have a hard time collapsing but loss of interconnextions means an alveolus can collapse
what always holds airways open?
expansile transmural prssurs
what does PEEP stand for?
positive end expiratory pressure in ventilators *always maintain pos pressure in airways
action of both pursed lip breathing and PEEP?
keep pressure inside airways greater than the pressure outside teh airway so collapse is avoided
reason for pursed lip breathing?
make small hole in mouth for air to flow through. the smaller radius increases the R to airflow increasing the intrathoracic prssure in the airways. this incresaed intrathoracic prssure will keep the airways open
what is the downside to pursed lip breathing?
the R to expiratory flow is high and the pt has to do a lot of extra work to exhale
a partially obstructed airway will have what problem ?
underventilated but lung units with high airway resistance are not well ventilated, but it will continue to be perfused creating a low V/Q unit (shunt)
what are the 2 reason for pressure gradient from top to bottome of lung?
1. lung has finite density
2. gravity
both affect ventilation in the lungs
Ppleural at top of lung? bottom?
Ppleural top is more negative
Ppleural bottom less neg
what happens to lung with no gravity?
uniform negative Ppleural and space
the neg pleural P evently inflates the lung to fill the chest cavity
what are the 2 reasons that inspired air is not evently distibuted in the lungs?
1. the gradient of Ppleural
2. the non-linear compliance curve of the lungs
how are alveoli throughout the lungs in terms of size?
because of the gradient of pleural pressure, alveoli at differnt locations are inflated to different sizes: alveoli near the bottom of the lung are more ventilated upon inhalation
describe the PV curve for lung units.
it is not linear
alveoli at top of the lung are further along the PV curve than those at the bottom
*more RV at top
why is the lower part of the lung ventilated more than uppermost?
because when inhaling the Ppleural becomes more negative. this increases the change in volume of the lung units. The unit with the greatest change in volume are the lung units near the bottom
the differential distribution of ventilation is caused by the action of what?
gravity
will a low compliance lung unit be more or less ventilated?
less ventilated such as in interstial diseases (fibrotic diseases) where the distibution of the disease is uneven throughout the lung "patchy"
are fibrotic areas ventilated and perfused?
they are not ventilated b/c low compliance, but they are still perfused: low V/Q unit creating a shunt
what is He dilution spirometry?
at FRC you want to determine exactly what FRC is so you have them breathe into a helium mixture bag and determine how much the pt. dilutes teh helium in a known sample. measure the concentratin and use it to determine the unknown FRC
what is the single most valuble pulmonary fxn test you can do?
evalute airway resistance by determining forced expiratory volume in 1 sec (FEV1.0) by having the pt do a maximal forced exhalation from TLC and measure it for 1 sec
FEV1.0 is a measure of what?
airway resistance b/c maximum expiratory flow rates are largely effort-independent
the bigger the FEV1.0, the ___ the R is
lower the R
abnormally low FEV1.0 is highly diagnositic of pt with what?
obstructive pulmonary disease
explain the axis of Flow-Volume loop
x axis: volume that has volume increasing from right to left
y axis: inspiration as negative flow (downward from 0) and exhalation as positive flow (upwards)
**no time on graph
effect of emphysema on FV loops?
shifted to left towards larger volumes as a result of high compliance
low expiratory flow rates from airway collapse
RV larger than normal from trapped gases and high compliance lung tissue
effect of airway blockage (asthma) on FV loop?
no effect on volumes (same as normal)
limitation of flow everywhere* (depressed curve)
effect of resistrictive disease on FV loop?
loop shifted to R towards smaller volumes as a result of low compliance
flow rats normal b/c airways not particulary effected
TLC less than normal
what does surfactant indirectly affect?
pressure by affecting suface Tension
decrease surface tension in smaller alveoli therefore decreaes pressure
why/how does a ventilator keep airways open upon exhalation?
keeps Palveolar + so that Pout will not cause collapse (we don't require this normally becase the Ppleural is -, in a ventilator situation Ppleural is +)
in a pneumothorax, why does the lung collapse?
b/c there is no pressure diffrence and elastic recoil of lungs pulls lungs in
Ppleural = 0
PA=O
why is the TLC increased in emphysema?
b/c incresaed compliance therefore easier to inflate and higher TLC
hard to exhale bc decreased elastic recoil forces
what do relaxation pressures reflect?
the elastic recoil forces of the chest wall and lung
why are alveoli at base of lung more ventilated?
b/c the alveoli at top during FRC are more inflated thus when you inhale, Ppleural drops even more and you fill the alveoli. the alveoli at the top can only fill a little more while the alveoli at the base can fill a lot more. thus they get more ventilated
diseases in which you have decreased compliance means what for ventilation?
less ventilation bc harder to inflate
not soft= rigid
what is the standard amt of room air that you can pump into alveoli every minute? How much O2 do you extract per minute from gas in your alveoli? How much CO2 do you put into alveoli?
3600ml
Vo2 = 250ml
VCO2 = 200 ml
what is teh Po2 in alveoli? PCO2?
102 PO2
40 PCO2
Vexpired =?
Vexpired = Vd+Va
How doe you estimate alveolar ventilation?
it is the Va (not inluding Vd)
when is it necesary to determine what fractio of total ventilation goes to anatomical dead space vs actual exchangign areas of lung?
when a pt is connectd to a ventilator that adds dead space to the pts airways
PaCO2 is proportional to what?
PaCO2 ~ Vco2/VA
this says that as you incrased the amt of gas delivered to alveolus, the PCO2 decreases
if you double the VA, what happens to PaCO2? if you double VCO2 what happens?
halve because PaCO2 ~ VCO2/VA
double Vco2 doube PaCO2
PaCO2 is determined by what?
the amt of CO2 production and the amt of ventilation
if you are hyperventilating, what happens to CO2 production? PaCO2?
CO2 production is constant
PaCO2 halved b/c PaCO2 ~ VCO2/VA
if you are hypventilating, what hapens to CO2 production? PaCO2?
CO2 production is constant
PaCO2 doubles
in exercise, what happesn to PaCO2?
both ventilation and CO2 production incrases therefore PaCO2 is constant
what eqn do you use to estimate the partial pressure of O2 in Alveoli?
PAO2 = PIO2 -PaCO2/R
it says that PAO2 is incrased if you inhale gas with a high PO2. PAO2 is decrsaed if you raise your PCO2
effect of hyperventilation on O2 and CO2?
PAO2 incresae PaCO2 decreases
affect of altitude on PAO2?
decrease PIO2 therefore decrased PAO2
How do you measure PaO2 and PAO2?
PaO2 is measured from arterial blood sample
only estimate PAO2 using eqn: PAO2 = PIO2-PaCO2/R
R=0.8
if you hyperventilate, what happens to PIO2?
doesnt change
PaCO2 is halved
what are the 2 kinds of dead space?
1. anatomical dead space: the large airways
2. physiological dead space: includes alveoli that are ventilated but not perfused like in pulm embolism
compare PCO2 in dead space and alveolar space?
in dead space, PCO2 =0
in alveolar space: PCO2=PaCO2
PO2 at room air? airways? alveoli?
room air: PO2=160
airways: 150
alveoli: 100
the amt of O2 dissolved in blood is a fxn of?
the partial pressure of the gas
solubility of the gas in the liquid
for blood in lungs, whre teh PO2 = 100 torr, what is the amount of O2 dissolved?
0.3ml/dl
what are the 2 ways in which O2 is carried in blood?
dissolved in plasma and bound to Hb but O2 is poorly soluble in water therefore the fraction that is dissolved is a very small fraction of total O2 held in blood
binding of O2 to Hb shows what type of kinetics?
saturation kinetics
the avidity with which O2 binds to Hb is strongly influenced by what?
tertiary structure of the Hb molecule: has 4 heme groups, each heme can bind 1 molecule of O2
explain the shape of Hb/PO2 curve.
on x axis: PO2
on y axis: % saturation of Hb or O2 content
**not linear, sigmoidal
Normal Hb is 100% saturated at PO2 = ?
100mmHg
if all Hb sites are saturated, blood contains ___ml O2/100ml?
20.1 mlO2/100ml or @ 100%=20 vol% O2
if each 10%of Hb saturation, what is the vol % O2?
2 vol %
1 vol % means 1 ml O2 contained in 100ml of blood
what happens to the Hb-O2 curve vs O2 content-O2 curve in anemia?
in anemia, Hb is 50% of normal
in the Hb-O2 curve, the curve will look the same however, in the O2content-O2 curve, it will be depressed b/c now when fully saturated (100%)=10 vol% O2 (when fully saturated with O2, this blood can transport and deliver only half the normal amt of O2
even though the amt of O2 dissolved is small compared to the amt carried by Hb, why must we still consider it?
b/c dissolved is how O2 is tranferred in and out of blood (to tissues)
when O2 is delievered to a tissue, it is the dissolved gas that moves out. this lowers the Po2 in plasma and causes Hb to release O2
explain how O2 moves from red cell to tissues.
O2 moves down partial pressure gradients by diffusion
it dissociates fro mHb and goes into soln in plasma
the dissolved gas then diffuses down a partial prssure gradient into intersitital space
why does O2 have to be dissovled in order to move into tissues?
b/c while in RBC, the O2 bound doesn't exert a partial pressure until it is dissolved
what is the effect of the eqn: O2 + Hb = HbO2?
it is an equlibruim eqn that minimizes swings in PO2 that might be caused by adding O2 to or removing O2 from the blood
**Hb acts as a buffer for O2
what are the 3 ways in which CO2 is transported in blood?
1. dissolved in plasma (H2CO3)
2. as bicarb (HCO3) **
3. bound to Hb (HbCO2)
why is it that more CO2 can be transported dissolved than O2?
CO2 is 20X more soluble than O2
*still only 10% of total CO2 is transported as dissolved
what vol % of CO2 is dissolved at 40torr?
at 40 torr, 2.4vol% CO2
what happens when dissolved CO2 moves by diffusion into RBC?
it reacts with water catalyzed by carbonic anhydrase to form H+ and HCO3
what happens to the H+ produced when CO2 + H20 with carbonic anhydrase?
it is buffered by Hb b/c in the systemic capillaries, Hb is deoxy and thus can buffer H+
what happens to the HCO3 that is produced in RBC when CO2 + H20?
the HCO3 diffuses down its conc gradient out of the RBC replaced by inward flux of Cl-
waht is the main transporter of CO2?
bicarb 85%
what happens in the lungs in terms of O2 displacing H+?
in thelungs Hb gains O2 displacing the H+ that was buffered, this drives H+ and HCO3 back to H20 and CO2. the CO2 leaves RBCs and capillaries by diffusion
when is CO2 held as carbamino?
when it is deoxy (venous blood) thus if looking at the CO2 content-CO2 curve, at a higher CO2 content, this is the CO2 in venous blood (venousblood line is above the arterial line)
describe the CO2 content-CO2 curve.
the main point is that it is linear and shows NO saturation kinetics
the top of the line indicates venous blood PCO2 46 and the bottom of the line is arterial blood PCO2 40
when you mix blood samples that have different PO2s, what is the PO2 of the resulting mix?
you have to avg the O2 content (from table) of the blood samples and determine the PO2 of the mix from its content
when 2 blood samples have different PCO2s, how do you determine the PCO2 of the mix ?
simply avg the PCO2s of the 2 samples b/c of the linar relationsship b/n PCO2 and CO2 content
affinity of Hb for O2 is determined how?
take the slope: % saturation/PO2
slope=affinity
what is P50?
the PO2 at which Hb is 50% saturated with O2 apprx 27mmHg
what happens as you increase P50 to affinity?
Incrsae P50, decrease affinity
what are the 3 short term regulators of affinity of Hb for O2?
H+ ion conc
temp
PCO2
increasing H+ conc. does what to the affinity of Hb for O2?
lowers
increasign temp does what to the affinity of Hb for O2?
lowers
increasing PCO2 does what to the affinity of Hb forO2?
at high PCO2, HbCO2 is higher thus reducing the amt of Hb sites available for O2 binding
how does the O2 content-PO2 curve change in tissues?
in tissues/muscle, H+ is high, CO2 is high and temp is high thus curve is shifted RIGHT to unload O2 by decreasing the affinity of Hb for O2
how does the affinity of Hb for O2 change as blood moves through circulatory system?
in tissues: curve is shifted R to unload O2
in lungs: curve is shifted L to load O2 (increase affinity of Hb for O2)
what is the cooperative effect ?
when one gas is removed from blood, it enhances the uptake of the other:
in lungs: removal of CO2 promotes O2 uptake by lowring H+ conc which raises affinity of Hb for O2
while the addition of O2 promotes CO2 delivery
the affinity of Hb for O2 is regulated by what?
2,3 DPG that is present in RBC in molar conc equal to that of Hb
2,3 DPG does what?
associates with Hb lowering its affinity for O2; otherwise the extremely high affinity of Hb for O2 would be incompatible with life
*shifts curve to R
what is a long term regulator of Hb affinity?
2,3 DPG: it modulates the affinity of Hb for O2
increasign 2,3 DPG LOWERS affinity of Hb for O2
how does 2,3 DPG change in persistant hypoxia?
results in increases in 2,3 DPG which lowers Hb affinity
*impt compensatory mech to receive more O2 unloading
persistent elevation of PO2 results in _____ 2,3 DPG levels?
lowering to increse the affinity of Hb for O2
wht happens to 2,3 DPG in stored blood?
amt decreases therefore teh affinity of Hb for O2 increases and infusing a pt with blood containing high affnity Hb is dangerous-
how long does it take in hyoxia situations to increase amts of 2,3 DPG? (think mountainclimbing at high elevations)
days
in order to determine how well gas transport/delivery system is fxning, what do you do?
need to determine the PO2 in a solid organ: PO2 in venous blood from a metabolizing organ is an estimate of the PO2 inside the organ
how is it possible to determine the PO2 in some solid organ or tissue?
if you know the PO2 of venous blood coming from some organ, then you have a good estimte of wht the PO2 is in that organ (PvO2)
mixed, systemic venous blood will give you incorrect answers
PvO2 from a metabolizing organ is an estimate of what?
the PO2 in that organ- this will tell us how well gases are being transported
in a typical human, O2 is consumed at what rate? CO in that human is?
O2 consumed at 250ml/min
CO= 5L/min
therefore each 100ml of blood delivers 5ml O2/min
if arterial blood contains 20vol%, what does venous blood contain?
15 vol% bc each 100ml of blood delivers 5ml O2/min
thus to estimate what is going on in tissues, look at venous blood
for the case of normal blood, when extraction is 5 vol%, the PvO2 will be what?
40
anemia=
low RBC count therefore low Hb content
what will happen to the tissue PO2s in anemia?
b/c you have ~40% O2 content of normal blood (~12 vol%)O2content-PO2 curve is lowered
when you extract 5 vol% venous blood contains 7 vol% which is indicative of PO2 of 30 (lower PvO2 than normal=40)
what is the stimulus in anemia to produce more 2,3 DPG?
the PvO2 is lower than normal b/c RBC content is decreased
what happens when outdated blood is tranfused in a pt?
the blood will have a low 2,3 DPG content and thus will not increase the tissue PvO2 as it would normally in for example anemia pts.
what happens to PvO2 in athletes that blood dope?
polycythemia
will show an increase in PvO2 thus very advantagous for an athlete
wht does CO do to Hb?
occupies some O2 sites while increasing the affinity of others
affinity of Hb for CO?
very high! decreases the amt of available sites for O2 also changes the affinity of other O2 binding sites on Hb
curve is shifted to the L and is flatter (decreased saturation)
effect of CO on PvO2?
shifts curve to left giving a very low PvO2 b/c Hb has a very high affinity for CO
what does it mean that CO rasies the affinity of the remaining O2 binding sites for O2?
the remanining sites have a much higher affinity for O2. this means that the unloading of O2 can only happen when PO2 is lowered to very low levels
what limits the uptake of O2 in pulm capillaries?
perfusion limitation: when a gas diffuses thru the membrane and equlibrates quickly. the amt of gas taken up is determined by how much blood you pump through this capillary
on avg, blood is fully saturated O2 when?
by the time it is 1/3 of the way down a pulmonary capillary therefore if you want to deliver more O2 to the body, you have to pump more blood through the lung
the amt of O2 taken up into the blood is determined by waht?
rate of perfusion of pulmonary capillaries
Ex: exercise you get more O2 into blood by increasign CO
What happens to saturation when you triple the flow along a pulm capillary?
the blood will still be fully saturated so O2 uptake is perfusion limited
what limits CO uptake?
the ability of the membrane to transfer CO as CO is transferred to blood as it runs along the capillary b/c of the high affinity of Hb for CO
is there diffusion limitation for O2 like there is for CO?
only at very high altitudes where the driving force for O2 (PO2) is so low that blood doesnt saturate by the time it exits the pulm capillary
what does the pulse oximeter measure?
the saturation of Hb by shining photons of 2 wavelenghts (650 and 900) into a structure and measuring the amt of each light that is reflected
in the pulse oximeter, Hb alone will reflect what color? Hb bound by CO or O2?
Hb alone: blue
Hb bound: red
with the pulse oximeter, how can you determine the relative proportions of Hb and HbO2?
by looking at the ratio of reflectance at 650 and 900 nm
*pulse oximeter constantly measures the relftance ratio
will the reflectance ratio for O2 saturated Hb be high or lwo?
the ratio 650/900=large number/small number therefore a high ratio
will the reflectance ratio for an unsaturated Hb by high or low?
the ratio 650/900 = small number /large number therefore low ratio
wht is the only thing to change the reflectance ratio?
a cardiac systole which pumps some fresh oxy blood into the structure you are recording from. thus the change in ratio will tell you the saturation of the incoming (arterial) blood
the pulse oximeter is not affected by what?
things that might change the absolute level of light from the 2 sensors: black skin, white skin, earlobe, fingertip
***the ratio of reflectance of the 2 wavelenghts is indepent of the absolute amt of light
what is the one thing that the pulse oximeter tells you?
the saturation of whatever Hb is under the sensor
DOES NOT tell you how much Hb is there: anemia will have normal saturation
DOES NOT tell you what Hb is saturated with: CO poisoning will have normal saturation
what are the 2 controlled variables in respiration?
[H] in blood*
[H] in brain interstitium
what are the 2 sets of chemosensors in respiration?
peripheral: carotid bodies that respond to *plasma [H]low PO2 in plasma, and plasma PCO2
central: brainstem respond to [H]/CO2 in brain
what is/are considered the effector of respiration?
the mm that control ventilation: diaphragm and intercostal mm
carotid bodies respond to what?
peripheral chemoR's
plasma [H]
plasma PCO2 (b/c changing PCO2 causes changes in [H])
plasma PO2 (only when lower than 60torr)
where are the central chemoR's located?
in brainstem
when is the response of carotid bodies to PO2 observed?
only at rather low levels of PO2 (less than 60mmHg)
when CO2/H increases in the brainstem region, what do the central chemoR's do?
effect on increase in ventilation
activity in chemoR's is referred to as what? sensation assoicated with this?
respiratory drive: increase ventilation through interaction of chemoR's with respiratory mm Ex: raising PCO2 increases ventilation. We say that increasing pCO2 increases respiratory drive
resulting sensation is "air hunger"
what is the difference in response of carotid and aortic bodies?
they both respond to [H], only carotid bodies respond to low PO2
describe the blood flow in periphearl chemoR's?
high blood flow
neurons activated by a change in [H] blood
are the peripheral chemoRs responding to PCO2 or to the resulting change in pH?
they are sensitive to [H], not PCO2
this is the same for central also: they are driven by H in blood and in the brain interstitial fluid
what can cross the BBB to activate central chemoR's?
H+ cannot cross
HCO3 crosses slowly
CO2 can cross b/c solulbe and interact with H20 to form H+ and HCO3
this [H] is what the chemosensitive cells are sensitive to in the brain interstitium
describe the graph of ventilation vs plasma [H]
ventilation on yaxis
plasma [H] on x axis
as you increse plasma [H], ventilation increases linearly** it also decreases linearly
hypoxic ventilation is mediated by what chemoR's?
peripheral
when does PO2 cuase an increase in ventilation?
there must be moderatly severe hypoxia: less than 60mmHg otherwise the PO2 has little effect on resp drive
how does hypercapnia affect hypoxia?
it amplifies the effects of hypoxia which is exclusively mediated by the peripheral chemoR's
does hypoxia adapt?
NO! no matter how long you stay at high altitude, or suffer from lung disease, hypoxia will always have the same excitatory effect