Exam 3 - Lecture 4 Flashcards
In order to find O2, you need 3 things
PO2, Hgb, and Hgb sat
How is CO2 different than O2 when it comes to solubility in water?
CO2 doesn’t want to escape water like O2 does.
when CO2 binds to terminal amine groups on proteins, what results for the protons?
The protons are liberated and will hang around in solution (blood)
the ones that aren’t buffered are the reason for drop in pH (acidosis)
In comparison to arterial, venous blood has more or less protons, bicarb and carbamino CO2?
venous blood has more protons and carbamino CO2, but less bicarb.
CO2 is ___ more soluble than O2, and is ____ more diffusivity
24x; 20x
Carbamino CO2 formation mostly occurs on ______, because it has more capacity.
deoxygenated hemoglobin
Haldane effect: Deoxy-Hb favors ____
CO2 binding (increased carbamino/H+ buffering)
How is bicarbonate formed?
via carbonic anhydrase: CO2 + H2O → H2CO3 → H+ + HCO3-
After CO2 becomes bicarb in the RBC, what happens? (shifts) Why?
Bicarb exits and chloride enters to maintain charge balance
Proton buffering occurs mostly by ______
proteins like hemoglobin, especailly when deoxygenated.
What type of blood has more protons?
Venous blood
What is the CO2 content %’s in the venous blood by type? why does it change?
30% carbamino, 60% bicarb, 10% dissolved
there is more deoxygenated Hb in the venous blood, which results in more carbamino compounds being formed.
A right shift on the O2 curve indicates what for Hb affinity and oxygen loading/unloading?
Lower Hb affinity
Easy to offload oxygen into tissues, but harder to LOAD oxygen in the lungs
A left shift on the O2 curve indicates what for Hb affinity and oxygen loading/unloading?
Higher Hb affinity
Harder to offload into tissues, easier to load in the lungs.
The CO2 dissociation curve is ____ and ______ steep than O2.
why?
linear; less steep than O2’s
offloading occurs over a small pressure change, and shifts with Hgb oxygenation level.
What is the total CO2 content of arterial blood?
48 mL/CO2/dL @ 40mmHg
What is the total CO2 content of venous blood?
52.5 mL/CO2/dL @ 45mmHg
Why does CO2 content increase more with a small pressure change in comparison to O2?
High solubility + haldane effect
Deoxyhemoglobin better buffers H+, which will promote more
HCO3- formation
How much CO2 do the lungs offload per dL of solution?
4.5mL/CO2/dL
Venous CO2 curve is shifted how?
Up and to the left, because it has more content at a given pressure (more CO2 can fit on Hb that is deoxygenated)
When tissue produces CO2, where does most of it diffuse into?
Into plasma with largest portion heading to RBCs
Where does carbonic anhydrase ONLY live? What does this drive?
In RBCs
Drives CO2 to combine with water to form carbonic acid which will then dissociate into bicarb and H+, all in the RBC
In the tissues, after bicarb is produced in the RBC, where does it go?
Exits via Cl-/HCO3- exchanger
What does chloride do in the RBC after it enters/exchanges with bicarb?
Hangs out inside RBC until it gets back to the lungs in order to maintain electric neutrality.
What happens to chloride once the RBC gets to the lungs?
O2 binds to Hb, which makes it more acidic and releases H+. The RBC needs HCO3- in order to bind with H+ to form carbonic acid and then obviously dissociate into CO2 and H2O to be exhaled. So to do this, HCO3- re-enters the RBC from the plasma, exchanging with Cl-
This is how the body can efficiently carry CO2 as bicarb through the plasma and then reclaim it in the lungs for exhalation.
Chloride shift direction in tissues:
Chloride shift direction in lungs:
Tissues: Cl- in, HCO3- out
Lungs: Cl out, HCO3- in
In the RBC, the H+ that was generated with bicarb will what?
Most will be buffered by proteins in the RBC, mainly deoxyhemoglobin. Deoxy-Hb accepts H+ better than oxygenated-Hb because its a weaker acid.
Having more protons around will do what to Hgb affinity for oxygen?
Decreases; helps with O2 unloading.
What creates the diffusion gradient in the lung to “extract” CO2 from blood?
The alveolar lung air has a PCO2 of 40 and the blood is 45, so this gradient is what causes the extraction.
The CO2 that extracts into the alveoli, where does it come from?
MOSTLY RBCs, but some comes from plasma as well. But RBCs are the primary site of CO2 release due to storage as bicarb and carbamino compounds.
The primary reservoir for bicarb is _____, but the primary site for CO2 release into the lungs is ____.
plasma;RBC’s
Bicarb stored in plasma, but once in lungs, it moves into RBCs to be exhaled as CO2
What triggers the HCO3-/Cl- exchanger in the lungs?
O2 binds to hemoglobin, and since oxyhemoglobin is a stronger acid than deoxyhemoglobin, this causes the Hgb to release H+ ions.
Once excess H+ ions are in the RBC, the HCO3-/Cl- exchanger allows bicarb to bind with H+ to form carbonic acid and dissociate into CO2 to be exhaled.
How long does gas exchange in capillaries normally take?
0.25 seconds under normal conditions
How long does it take for blood in the pulmonary capillaries to go from a PO2 of 40, to 100mmHg?
0.25 seconds
what could cause venous blood to be lower than 40mmHg?
Exercise or under stress
How much time does blood spend in alveolar capillaries at rest? What does that mean for a “buffer”?
0.75 seconds
since gas exchange only takes 0.25 seconds, that gives us a 0.5 second protective buffer in case of diffusion impairment and is why we can tolerate a little bit of edema without being symptomatic.
What does blood time spent in capillary drop to during exercise or increase in cardiac output?
0.25 seconds, which is still sufficient for gas exchange UNLESS diffusion problem is present.
Diffusion problems can be asymptomatic if not severe until
working out or increasing cardiac output, then they will show.
Severe diffusion problems can appear at rest.
under normal conditions, O2 exchange is _____-limited.
perfusion
In disease states such as pulmonary fibrosis or edema, or during exercise, O2 may become _____-limited
diffusion
What does perfusion limited mean?
O2 reaches equilibrium with alveolar PO2 quickly, so the only way to increase O2 uptake is by increasing perfusion (blood flow)
Obviously we aren’t discussing increasing FiO2, this is for normal atmospheric oxygen
What does diffusion limited mean?
For O2 to become diffusion limited, equilibration doesn’t happen before the blood leaves the capillary (0.75 seconds). This is a result of pulmonary edema, fibrosis, etc. Membrane is fluid filled or thickened, impairing diffusion.
What limitation is “normal” for most gases?
Perfusion limited. Most gases don’t have issues diffusing across with healthy membranes.
What is the solubility order of Oxygen, CO2, nitrogen, and nitrous oxide ACCORDING TO SCHMIDT, but NOT ALL OTHER LAWS OF SCIENCE?
CO2 > O2> N2O > N2
Look up literally any other source, and it will say: CO2 > N2O > O2 > N2. N2O is actually 360x more soluble than O2 according to outside sources
Nitrous oxide onset and blood solubility?
Fast onset and low blood solubility
How is carbon monoxide different than other gases?
Does not equilibrate and is diffusion limited
What gas is used to test lung diffusion capacity?
CO. It has similar weight and diffusivity, making a great surrogate for O2 that diffuses without being influenced by perfusion.
CO binds to hemoglobin with ____ affinity compared to O2.
Schmidt didn’t explicitly say this, but the purpose of this card is to fully emphasize how much more affinity it has
250x more affinity
Why doesn’t CO equilibrate?
It’s pulled out of plasma so fast with such a strong affinity for Hb that there’s no back pressure to stop diffusion.
What are causes for carboxyhemoglobin in the lungs according to Schmidt?
Hanging out in a drive thru, changing oil, smoking
What should CO levels be in non-smokers?
zero.
This is why its ideal to use CO to measure diffusion capacity.
Pulmonary edema can cause what fraction of normal diffusing capacity?
This was on a graph and not explicitly stated
1/4th - 1/8th normal diffusing capacity
One last CO question that is similar and pretty much summarizes previous cards:
Why is CO ideal for DLCO?
-High Hgb affinity which its uptake will reflect barrier performance ONLY
-Unaffected by perfusion
-Very little to zero CO in non-smokers, so should have a clean baseline.
According to ficks law, what factors affect diffusion?
Thickness, surface area, pressure gradient, and diffusivity
How does thickness, surface area, and pressure gradient affect diffusion?
Thickness (↑ thickness = ↓ diffusion)
Surface area (↑ area = ↑ diffusion)
Pressure gradient (↑ gradient = ↑ diffusion)
What is diffusivity?
Depends on solubility and molecular weight
Solubility divided by square root of molecular weight
CO2 is ___ more soluble than O2
24x
How much faster does CO2 diffuse than CO2, and why is it different than the “diffusible” number?
This also means “How much more diffusivity is CO2 vs O2?”
20x
CO2 is heavier than O2, but so much more soluble that it still wins. Factoring in molecular weight decreases it from 24x to 20x since its heavier.
What molecule is faster, CO2 or O2?
O2, its smaller.
What is a normal V/Q ratio?
0.8 to 0.85
(4.2L/min of air divided by 5L/min of blood is 0.84 technically)
What does a V/Q ratio of <0.8 indicate?
Reduced ventilation but normal perfusion (Partial obstruction)
OR normal ventilation with increased perfusion, technically…
What does a V/Q ratio of > 0.8 indicate?
Perfusion problem such as PE
Normal ventilation but decreased perfusion.
What is the limit for a high V/Q ratio?
infinity.
What V/Q ratio would a shunt be?
0 (NO ventilation)
What V/Q ratio would COPD have?
<0.8 d/t poor ventilation
What V/Q ratio would a PE have?
> 0.8 d/t poor perfusion
In comparison to the average of the entire lung, the base of the lung has ____ ventilation and perfusion.
Which one (V or Q) has more than the other and what ratio does it end up with?
High ventilation and perfusion, but Q > V. Both rise, but perfusion rises more than ventilation does.
Ends up with a V/Q of <0.8 since perfusion is greater than ventilation.
In comparison to the average of the entire lung, the apex of the lung has ____ ventilation and perfusion.
Which one (V or Q) has more than the other and what ratio does it end up with?
Lower ventilation and perfusion; but perfusion drops MORE than ventilation drops, which results in a V/Q ratio of > 1.
What is the PO2 and PCO2 of the base of the lung?
90 and 40
What is the PO2 and PCO2 of the apex of the lung?
130 and 30
Mixed expired air reflects all lung regions, but skews slightly toward the ____. Why?
Base. The base has a greater contribution from well-perfused alveoli.
Where does the crossover for perfect V/Q occur, per the chart?
around rib 3
this is the sweet spot where ventilation matches perfusion for optimal oxygen exchange.
What are the effects of general anesthesia on ventilation?
Decreased ventilation, increased alveolar deadspace which results in alveolar collapse (atelectasis)
What is the onset of GA effects on ventilation after induction? Which populations are more at risk?
Rapid onset post-induction.
More pronounced in older or compromised patients
What can be used to prevent atelectasis during GA?
PEEP
matching of ventilation/perfusion worsens with ______. (2 things)
Age and anesthesia
Why does aging cause ventilation distribution to become uneven?
Lower lung units under-ventilate due to loss of elastic recoil, while perfusion remains the same
What is Laplace’s Law? What is the formula for both big and small?
Predicts that air from small alveoli would move to larger ones, because they are more full with less pressure, until it’s 100% full.
P1 = T/r
P2 = T/2r (2r = diameter)
P1 is smaller, P2 is larger
Pressure = tension / radius
Does Laplace’s Law apply to healthy alveoli? Why or why not?
No. Surfactant counteracts this law. When the alveoli is less full, surfactant is MORE CONCENTRATED, which will balance out the pressure and allows air to go into less full alveoli.
Surfactant concentration is _____ related to alveolar volume
inversely related
e.g. surfactant is more concentrated in small alveoli, and dilutes as alveoli expands.
Surfactant deficiency results in ______ ventilation.
uneven
Leads to alveolar collapse and creates regions of low or zero ventilation
What is the famous Dr Schmidt quote about every pulmonary disease ever studied?
“Every lung disease ever studied has surfactant deficiency”
If lungs stay collapsed too long, _____ will eat up _____.
Macrophages: surfactant
Harder to reopen
Anatomic dead space can be estimated using
1mL/lb of IBW
3 things that increase alveolar dead space are
age, anesthesia, disease
What’s the equation we use with mixed expired gases to estimate physiological dead space?
Vd/Vt = (PaCO₂ – PeCO₂) / PaCO₂
Dead space will have ___ O2 and ____ CO2
High O2; zero CO2
Alveolar air has a PO2 of ___ and PCO2 of ____
100; 40
What is the PO2 and PCO2 of mixed expired air in levitskyz example? why does it change from alveolar and deadspace air?
~120 and ~27
Increased PO2 and decreased PCO2 from alveolar air due to mixing alveolar air with dead space air
General anesthesia can unmask dead space how?
Creates regions of ventilation that doesn’t have perfusion.
Deadspace has a PO2 of
150mmHg (has water vapor)
How do you calculate total CO2 of mixed expired air under normal conditions? (This is the easier way)
150mL of dead space @ 0mmHg, 350mL alveolar air @40mmHg
(350 x 40) + (150 x 0) = 14,000
14,000 divided by 500 (total mL of breath) = 28mmHg
What is Schmidts way of finding total mixed expired CO2 under normal conditions, which is way more complicated then the other way just displayed?
PPgas/PTOT
40/760 = 5.3%
if 350mL is VA and 500mL is VT, then:
350mL x 5.3% = 18.42mL of CO2
Take 18.42mL and divided by 500mL = total mixed concentration is 3.7%
3.7% x 760mmHg = 28mmHg
A 70-kg patient is breathing a tidal volume of 500 mL. They are switched to 100% oxygen for a nitrogen washout test.
You are given the following:
PACO₂ = 40 mmHg
Total pressure = 760 mmHg
Mixed expired PCO₂ = 28 mmHg
Question:
Using this data, estimate the patient’s anatomical dead space.
PeCO2 = (PACO2 x alveolar volume) / VT
28 (given) = (40 x ?) / 500mL
500 x 28 = 40 x ?
14,000/40 = 350mL
Now that we have alveolar volume, we just subtract that from tidal volume
500 - 350 = 150mL
A 160-lb patient is breathing a tidal volume of 500 mL.
They are intubated and on 100% oxygen for a test of ventilation efficiency.
You are told:
Anatomic dead space = 150 mL
Alveolar dead space = 50 mL
PACO₂ = 40 mmHg
Mixed expired PCO₂ = ???
Question:
Estimate the mixed expired PCO₂ (PeCO₂) for this patient.
PeCO2 = (40 x 300) / 500
PeCO2 = 24mmHg
A 70-kg patient is undergoing a ventilation efficiency test.
You are told:
Tidal volume = 500 mL
Anatomic dead space = 150 mL
Alveolar dead space = 50 mL
Mixed expired PCO₂ = 28 mmHg
PACO₂ = ??? (not given)
Question:
Estimate PACO₂ using the available data.
28 = (? x 300) / 500
28 x 500 = 300 x ?
14,000/300 = 46.7mmHg
Partial pressure = ___ x ____
concentration x total pressure
e.g. 5.3% x 760 = 40mmHg PCO2
CO is the exact opposite of
N2O
After doing a DLCO test, it was determined that a patient had slower CO uptake. What does this indicate?
Impaired diffusion, could represent edema or fibrosis.
DLCO uses CO to measure ______.
CO-oximetry uses CO to measure _______.
diffusion
carboxyhemoglobin saturation
In summary, if PCO2 of mixed expired gas is <28mmHg, this means what?
more dead space
