Lecture - Resp (Bevin Physiol 5 Gas Exchange #2) Flashcards
Once again, what are the two equations you need to know (for VA and PAO2) and what are their units?
All units are mmHg unless you’re talking about ventilation then it’s ml/min
There are 5 total mechanisms for arterial hypoxaemia but how many of those are gas exchange problems? (aka A-a gradient increased in these?)
- Reduced PB or FlO2
- Hypoventialtion (can tell by looking at PaCO2)
- Impaired diffusion
- Shunt
- V/Q mismatch
So the last three (diffusion, shunt and VQ) are all a result of impaired A-a gradient (so increased difference between the two)
- So how does impaired diffusion lead to arterial hypoxaemia?
- In which circumstances will imapired diffusion problem become apparant?
- Is there ever a problem with the diffusion of CO2?
- Will this problem respond to extra O2?
- So basically, you can have impaired diffusion because
- decrease surface area
- increased thickness of the barrier
- EXERCISE
- breathing low O2 mix (so not going to have that gradient driving it all)
All these will lead to some problem with the diffusion so will have increase A-a difference (they’re all part of Fick’s Law except exercise)
- Diffusion isnt much of a problem except when it comes to exercise - then the imapired diffusion will uncover. Usually the time spent in the pulmonary capiliaary by the rbc is more than enough for equilibration between alveolar gas and capillary blood. Even with imapired diffusion, the time spent by the rbc in the pul cap will still be enough for it to have completed the equilibration. But with exercise, the time spent by the rbc in the pul cap decreases significantly enough to not let the equilibriaiton to occur so will have reudction of PaO2 in exercise
- CO2 diffusion isnt really a peroblem because the dffusion constant for CO2 is 23 times greater than O2 and the equilibrium between alveolar and cap PCO2 also takes roughly the same time
- Yes, good response to extra O2 because you wil change the graidient in Fick’s Law even if the A or T are impaired
- How can a shunt lead to arterial hypoxameia? (Increased A-a gradeint)
- What’re the types of shunts?
- Can you give extra O2 to resolve this like with diffusion?
- Shunt means that the blood re-enters the arterial system without goig through the ventilated areas of the lung so venous blood is essentially ‘diluting’ the oxygenated arterial blood so this reduces the PaO2
- There are two types of shunts: anatomical or pathological. Anatomical are where you have a cardiac defect and venous blood from right heart goes into left heart without going to the lungs (like thebesian veins) or pathological eg in pneumonia where some alveoli are full of exudate (pus) so they arent ventilated - they willl be perfused but not ventialted so remain ‘venous’ and dilute out the arterial blood
- Shunt will respond poorly to oxygen because can’t get more O2 into the pus filled alveoli or cant change the anatomical shunt with extra O2
- How does V/Q mismatch lead to arterial hypoxaemia and increased A-a?
- Does this mismatch happen in normal lungs at all?
- What might cause:
- non-uniform distribution of alveolar ventilation
- non-uniform distribution of perfusion? - Will it respond to extra O2?
- So this is where you either have too little perfusion compared with ventilation or the other way around aka the ratio of V/Q is not This alters the gas exchange therefore increases A-a gradeint because you’ll have either wasted ventilation or wasted perfusion. So any disease tha alters ventilation and/or perfusion will increase V/Q mismatch and arterial blood will not be fully oxygenated
- This does happen in normal lungs due to gravitity. Functionally, the alveoli at the apex (the top) are relateively underperfused and overventilated whereas the alveoli at the base are relastively underventialted and overperfused so you naturally get variations in the ratio but we shouldnt increase this mismatch as this will lead to the arterial blood not being fully oxygenated
- Look at the image
- Yes, responsive to supplemantray O2 bc you can enrich the air in low ventialted alveoli so you dont have wasted perfusion
How can arterial hypoxemia be caused by the atmosphere?
If you have reduced PB or FlO2 then yuo will by hypoxic because if no O2 is in the air then how can you get it into your blood?