Alveolar gas exchange Flashcards
how does airway resistance affect blood flow?
high= airlfow slows and takes more muscels to produce effort
low= airflow fast and easy
what controls airway resistance?
mostly radius of vessel! because its easiest to change
R=8nL/r4
does this thru smooth muscle of airways
why do we want to control airway resistance?
we want to send blood to right places- usually means to alveoli (that have good blood supply and O2)
what is alveolar ventialtion?
how is it calculated?
what is average value?
rate of volume of air reaching alveoli
VA(dot)= VA* F
4 air L/min
what is perfusion?
what is normal value?
blood flow into alveolar capillaris from right ventricle
5 L blood/min
what is the point of the lungs?
to bring together ventilation and perfusion to the alveoli for gas exchange
what is the equation for diffusoin of gases?
J= (SA)*D*(P1-P2)/ distance
J= diffusion rate
D= diffusion coefficient
(P1-P2)= pressure gradianet acroos alveolar membrane
SA= surface area for diffusion
distance= thickness of alveolar barrier
equation solved individually for each gas
what are the normal values of J at rest?
250 mL O2 and 200 mL CO2
not equal!!
what two factors depend directly on structure of alveolus?
SA and distance
what factor depends on # of alveoli in lungs?
SA- millions of alveoli that take up 70 sq m!
also depends on # of open pulmonary caps (greatky increases with demand/exercise)
why do patients with COPD have a hard time getting enough oxygen?
destruction of alveoli causes SA to decrease–> decreases J (directly proportional)
what all does the alveolar barrier consist of?
- fluid layer
- alveolar epithelium
- interstitial space
- blood vessel wall
average: 0.6 microns
why does J decrease in patients with interstitual lung disease?
deposition of collagen on the alveolar barrier–>
increases diffusion distance—> decreases J (inversely proportional)
what does D depend on for each gas?
- solubility of gas in water- greater solubility means easier to diffuse
- molecular weight of gas- heavier means less likely to diffuse
(O2 or CO2) is more soluble in water
CO2
(O2 or CO2) weighs more
CO2
(O2 or CO2) more readily diffuses
CO2 (20x more likely than O2!!)
*its solubility compensates for its size
how do you find pressure gradient (P1-P2) and which direction gases are moving in?
PAO2 (O2 in alveola)- PVO2 (O2 in venous blood)
- before gas exxchange occurs, PAO2 should be a lot greater (104 mm Hg)
- PVO2 is around 40 mmHg normally
- pressure gradient should be about 60 mmHg
PACO2 (CO2 in alveola)- PVCO2 (CO2 in venous blood)
- at rest, PVCO2 should be higher (45 mm Hg)
- PACO2 should be about 40 mmHg
- gradient should be -5mmHg
how long does it take for blood to travel in pulmonary cap?
how long for equilibrium of O2 to be reached?
what is the purpose of this?
- 75 sec
- 25 sec (40 mmHg–> 100mmHg)
to give us a safety net on the amount of time RBCs spend in cap to ensure that blood get fully oxygenated
why is it that person with lung diease first notices sx during exercise?
blood travels a lot faster thru pulmonary cap during exercise (0.25 sec vs 0.75) which leaves jsut enough time for diffusion of O2—>
causes diffusion factors to be critical in our ability to get O2 and people with lung disease have problms with those?
what is diffusion capactiy (DLO2)?
what is the normal diffusion capactiy (DLO2) for a person at rest?
what do we use to measure this? why? how?
what is then calculated?
how much O2 the lungs take up can actually be diffused into the blood
about 21 mL O2
use carbon monoxide! (CO)
O2 binds too easily to plasma so not all of it is binding to Hb, but CO binds only to Hb (Paco= 0mmHg)
have patient inhale a little bit of CO
DLO2= 1.23* DLCO
what diseases does it suggest if DLCO is lower than normal?
- pulmonary hypertension
- anemia
- carboxyhemoglobinemia
O2 is diffusing suggesting a lung or blood flow problem
why does a person with lung disease not show increase CO2 retention for a long time?
CO2 is so soluble that it reaches equilibrium immediately(45–> 40mmHg) (in pulmonary cap a fraction of the time that O2 is)–>
even if diffusion is crappy it has an even bigger safety net of time that it can leave cap
what are some diseases involving diffusion limitation?
- interstitial lung disease
- pulmonary arterial hypertension
what will premature infant present with if surfectant has not been produced?
- bradycardia
- occasional gasping for air
- cyanotic
most likley will have acute respiratory distress syndrome (ARDS)
what is the the significiance of the air/water interface?
the water layer covering the alveoli do not want to associate with the air in the alveoli—>
causes air to pull away from it—>
causes layer to become thinner—>
increases surface tension—>
increases collapsing pressure of alveoli
what is LaPlace’s law?
(collapsing pressure)= 2T/r
T= surface tension (think of as surfectant)
what is the relative (collapsing) pressure in large alveoli?
low (P and r are inversely proportional)
what is the relative P in small alveoli?
high
why is it a problem that all of the alveoli are different sizes along with being connected to one another?
what problem does this cause (that will of course be solved in healthy indiviuals)?
pressure tries to move from high to low gradient–>
as air flows into big alveoli they will get even bigger while small alveoli lose their air and surface tension causes them to collapse—> is bad for SA
how does surfectant work and what does it utlimately do?
sufectant decreases surface tension (T) in the smaller alveoli more than large—>
decreasing T decrease (collapsing) P—>
this abolishes the pressure gradient—>
stops collapse of small alveoli
and allow little and big alveoli to coexist peacefully <3
in equation form, what does sufectant do?
P= 2 (decrease) T/ (decrease) r
what produces surfecant?
what is it composed of?
how is it stored?
where is it secreted?
type II pneumocytes
phospholipids, dipalmitoylphospatidylcholine, multiple proteins (SPA, *SPB, SPC, *SPD)
intracellular lamellar bodies
into alveoli
** SPB and SPD important for immune functions
