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83 Cards in this Set

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  • Back
what is tidal volume?
volume normally inspired/expired during quiet breathing
how can Functional Residual capacity be measured
1) helium dilution method. Person breathes in a known concentration of He, and vol calculated by dilution of he in end expiration. CON: gases trapped behind obsstruction do not equilibrate.

2) body plethysmograph: instrument is in a sealed cabinet where subject sits...etc...
what is inspiratory reserve volume?
volume above tidal inspiratory volume that lundg can inflate actively
what is inspiratory capacity?
volume above tidal end expiratory volume that lung can inflate
What is vital capacity?
total lung capacity minus expiratory reserve volume
what is FRC?
tidal volume at end expiration
what is residual volume
volume of lung after forced expiration
Definitionof ERV (better)
amount of air that can be forcibly expired after normal expiration)
better definition of inspiratory reserve volume
max V that can be inhaled following a normal inspiration
what happens to TLC in chronic obstruction?
It can actually increase: years of high flow resistance causse increased expanseive forces and a physical remodling of the chest wall. Also, lung elastic recoil is reduced, allowing increases in FRC and RV.
what is minute ventilation?
volume of air excanged per minute, expressed either as volume inspired or expired
How do you calculate minute ventilation?
Vt (tidal volume) * f (resp. freq.)
what is normal tidal volume?
500 mL
what is normal minute ventilation
6 Lpm
what is the physiologically relevant measure of ventilation?
alveolar ventilation, which subtracts out the 30% of tidal volume that is "dead space" (not participating in gas exchange)
how do you calculate alveolar ventilation?
Vdot(A) = f (Vt - Vds)
what is normal minute alveolar vent rate
4.2 lpm
what makes up physioloical dead space?
Total wasted ventilation: anatomic dead space (conducting airways) + alveolar dead space (alveoli that get no blood space)
compare lungn compliance when filled w/saline v. air
compliance is higher when lung is filled with saline,, because there is no surface tension at the alveolar air/liquid interface.

ALSO: air inflated lung has higher compliance in inflation rather than deflation.
what 2 factors determine lung compliance
surface tension
elastic recoil
why do we need surfactant in alveoli
otherwise liquid in alveolus creates surface tension, and the small radius of the alveoli mens that there musst be a high internal pressure to keep the alveolus open. without surfactant, alveolus woiuld collapse at end expiration
Why does alveolar surface tension change as the size changes in respiratory cycle?
during expiration the film of surfactant is compressed and surface tension therefore decreases.

so surfactant has its maximal impact at end expiration
compliance in emphysymatic lung?
compliance in fibrotic lung?
chest compliance equation
1/compliance (total) = 1/compliance(chest) + 1/compliance(lung)
what is the distiction between resistance of individual airways and resistance in the aggregate?
With each division, resistance in each individua airway increass. but because of the exponential increase in aggregate cross-sectional area, the AGGREGATE resistance declines was the divisions prceed
where is the most resistance to airflow in the luns found?
first few segmental bronchi
why do people breathe off the top of their lungs?
airway resistance to airflow is minimized by breathing at high lung volumes, because the airways are dilated
What is the essentially explanation of dynamic compression?
The small airways coollapse during the effort-independent phase of a forced expiration, thereby increasing their resistance and reducing airway pressure essentially to zero. Airflow becomes independennt of effort following small airways collapse because during this phase it is driven solely by elastic recoil.
if you increase expiratory effort, which way does the equal pressure point migrate?
Toward the mouth. Airway pressure is elevated, so it stays higher than intrapleural pressure longer (but doesn't intrapleural pressure also go up?)
describe obstructive disease flow rate expiration curve
1) lower peak flow rate
2) scooped out portion of effrt independent phase of forced expiration--becaue airways lose elastic recoil, less alveolar iterdependence, and dynamic compression occurs earlier.
Restrictive lung disease flow volume curve
1) low peak flow
2) low peak lung volume.
3) Overal lung compliance s low.
What is FEV1? What is it good for
forced expiratory volume--volume of air expelled in first second after maximal inspiration.

You calculate ratio of FEV1 per forced vital cappacity.

>.8 in normal patients. Much less with obstructed lungs
What is forced mid-expiratory flow rate?
slope of line drawn between points on curve of 75 and 25% of FVC.
Why is FEV1/FVC elevated over normal in restrictive lung disease
indicates reduced lung compliance--harder to fill (low FVC), but easy to empty.
How does the introduction of water vapor into inhaled air affect the partial ppressure of 02
decreases it, as well as that of other gasses.
A v. a
What is the alveolar ventilation equation?
VdotA = 863 (VdotCO2 / PACO2)
what is relationship of alveolar vent and alveolar PCO2
As ventilation rate goes up, PACO2 goes down (and PaCO2 goes down, and pH of blood goes up)
why dooees the body not regulate ventilation based on PA02
if you increase ventilation, you can only increase PA02 to the PO2 of the dry air, no more. Tying ventilation control to CO2 is better because the body can produce variable and lots of CO2, and increased ventilation can get rid of it....
What is hyperpnea
Increase in alveolar vent is proportional to increase in metabolism (production of CO2), so the PaCO2 is UNCHANGED.
What is hyperventilation
Alveolar ventilation rises more (proportionally) than any rise in metabolism. Lung is "clearing" more CO2 than comes in from blood, so PaCO2 goes down, and pH goes up.
What is hypoventilation
Vent is less than needed for metabolism. PACO2 and PaCO2 goes up, pH drops.
what is the Respiratory quotient?
Ratio of CO2 production to O2 consumption. Usually aroung .8.
describe relationship of paCO2 and pACO2
it is alwas in equilibrium in the alveoli
What is the alveolar gas eq
PA02 (predicted) = PIO2 - (PACO2/R)

where PIo2 is always around 147, and R (resp qu) is always around .8. (rate of CO2 production per O2 consumption)
Which region of the lung gets most ventilation?
Reasons why lower lung gets more ventilation
1) gravity pulls down on lung and keeps upper alveoli forced open more, so they cant get as much Gas out on expiration

2) there is more intrapleural pressure at the top because of suction created by lung sliding down, so alveoli held open more...

3) the therefore smaller alveooli are at the bottom. They are more compliant since they start out smaller...they have a greater change in volume...more respiration
describe effects of raising arterial and venous pressure on pulmonary vascular resistance
In either case it decreases resistance.

In either case, increased pressure increases flow and increases cap diameters which decreases resistance.

2d, higher pressures recruit quiescent capilaries, which increases overall cross sectional area and decreases resistance
What is the distribution of blood flow in the lung?
Low in upper lobes (like ventilation)

1) perfusioon pressure lower up top
2) also, because of the low pressure up higher, there is low flow and susceptibility toarterial collapse
why is diffusion of CO2 across membrane greater than that of O2
CO2 is more soluble in h2O, and it will partition between the gas and liq phases much more readily.
describe relationships of CO2 and O2 gradients and diffusion times
1) O2 gradient is much more than CO2 gradient. But CO2 is much more permeable in the membrane than O2. So both eqilibrate approximately equally.
Describe the role of O2-Hb reaction rates
the binding of molecular O2 to Hb takes about as much time as the O2 takes to get from the alveolus to the RBC. So it is an important factor.
Descrone how fibrosis might affect oxygenation
Fibrosis might thicken the blood gas barrier and increase time it takes for O2 to equilibrate. It now might take .75 sec--which still means it has time to equilibrate while in the lung--but if VELOCITY of flow increases (exercise), then the time available for equilibration decreases, and patient becomes hypoxemic.
How are diffusion impediments measured?
how much of your O2 is in the form of dissolved gas?
at what pt on the o2-hb dissociation curve is hb essentially saturated?
as low as 70 mmHg o2
what affect does decreased pH have on the dissociation curve?
shifts it right. dissociation occurs quicker,.
waht does 2,3 dpg do to dissociation curve
shift it right
how is most CO2 carried from the tissue
Enters erythrocyte
Becomes carbonic acid via carbonic anhydrase
Excreted from RBC in exchange for CL. In the alveolus, thhere is low Cl-, CL- flows out in exchange for HCO3-, reverse process occurs from HCO3 to form CO2
What is a volatile acid? Give an example
H2CO3 is volatile b/c reactions in the lung normally eliminate CO2 from the body at a rate equal to its rate of production
What is a volatile acid? Give an example
H2CO3 is volatile b/c reactions in the lung normally eliminate CO2 from the body at a rate equal to its rate of production
where are nonvolatile acids eliminated?
what makes a good buffer
weak acid and its conjugate base, or

weak base and its conjugate acid.

Usually effective a range of 1 pH unit on either side of its KA.
WHAT is the Henderson hasslenbback equation?
pH = PKz + log [conjugate base] / [acid]
why is bicarbonate a good buffer, even tho its pKa is 6.1?
1) abundant.
2) in the body, its effective pKa is greater than 6.1, since it is an open system.
3) bicarbonate and PCO2 are regulated independently: kidney regulates HCO3 and lungs regulate PCO2 (numerator and denominator of HH
where are volatile acid and base loads buffered?
almost entirely intracellularly
Where are fixed acids and bases buffered?
intracellularyly and extracellularly
which is faster: repiratory or renal correctgion of acid balance?
Respiratory. renal doesn't kick in for 6-12 hours
Describe what a davensport diagram looks like
pH on X
HCO3- on Y

rising PCO2 isobars, increasing from R to L
what contributes to the A-a difference? what is normal?
Normal: 97-95, or 2.

Contributing factors:

1) diffusion barrier
2) anatomical shunts
3) ventilation-perfusion inequality
diffusion barrier contribution
Generally a rare contributing factor. Fibrosis may cause a larger A-a difference due to thickening of the alveolar capillaries
what effect of giving supplemental O2 to patient with a large shunt
minimal. If most of the blood is not even getting to the pulmonary circuit, then it doesn't matter if plenty of o2 is available in the lungs. you likely already have more than enough o2 to saturate the blood taht does get there. You might be able to dissolve a bit more O2 in the plasma.
describe the respiratory rate of someoone wiht a large shunt
Their PaCO2 is rising because it is not getting expelled in the lungs. This triggeres increased ventilation rate, which does effecctively get rid of PCO2 (how) and make pCO2 near normal.
how does the ventilation/perfusion ratio chane regionally?
Is decreases exponentially from the top of the lung (or increases exponentially from the bottom.

Bottom: vent/perfusion is less than 1
Top: Vent/perfusion is way over 1.

See fig 50, p 74
describe ventilation/perfusion in emphysema lung?
Most alveoli are well ventilated and poorly perfused, because the alveoli break down into larger sacs that don't have good perfusion
describe perfusion/venntialtion with bronchitis lung
Many alveoli have good perfffusion but are unventilated due to lung obstruction.

this is a physiological shunt--blood again is essentially "bypassing" ventilated areas, because the areas it goes to are not ventialted (even though you are in the lung)
what is Vent/perf rate ratio at rest?
.8 because it is working inefficiently in upper and lower regions
what happens to vent/perf during exercise
Can rise to around 4.0. But in effect, the lung is working more generally at a 1.0 ratio as compared to .8, and the overage is just the excess reserve of the reseppiratory system.
what is the most common respiratory cause of hypoxemia?
Vent/perf mismatch (one or the other drops)

accounts fo 90% of the cases
what are the features of generalized hypoventilation
1) total ventilation is depressed
2) PaO2 goes down
3) PaCO2 goes way up, because vent is down and there isn't any respiratory compensation/hyperventilation
4) NORMAL A-a difference: PaO2 is low, but PAO2 is LOW AS WELL because vent is depressed
5) Pa02 INCREASES when you give more inspiratory O2. UNLIKE SHUNT.
is A-a difference affected in anemia or CO posining/
no, but I don't know why
which decreases faster from bottom of lung to top: perfusion or ventilation
perfusion/blood flow is higher than ventilation int he bottom of the lung, but it decreases more rapidly than ventilation from bottom to top.

Thus, at the bottom, ventilation/perfusion is less than 1, wehreas at the top it is greater than 1