A few pulmonary physiology questions...

[cavitarynodule]

Hopefully someone can help a rising fellow with a few topics (some basic) that have come up and I haven't been able to get a good explanation for:

- How exactly does a CHF exacerbation cause hypercapneic respiratory failure? Pulmonary edema seems to be mainly a VQ mismatch issue and not increased dead space?

- How exactly does ARDS cause increased dead space? Again, it seems like blood is still flowing through the pulmonary vasculature and it's more of shunt physiology developing with blood going past collapsed or fluid filled alveoli, yet dead space fraction is high?

- Why is there not always auto-peep in PS modes if the expiration terminates at 25% of peak expiratory flow? In VC modes, expiratory flow not getting back to 0 raises concern for auto-peep, but in PS flow never returns to 0 but there do not seem to be issues with this.

- Why is bicarb gtt generally effective in improving acidosis in a patient with bad ARDS with a gas 7.15/80? Shouldn't the bicarb just get converted to more CO2 that can't be ventilated off in a patient with respiratory acidosis due to high dead space fraction?


I'd appreciate any explanations!

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[jdh71]

If you take enough alveoli out of the equation with pulmonary edema and especially if you have very high end diastolic pressures and capillary leak, then you will eventually not have enough ventilation to exchange CO2

What is "dead space" if not open areas in the lung that aren't participating in gas exchange? If the alveoli are full of junk in ARDS then they are simply the end of tubes. Might as well be the trachea.

Bicarb can help to a point in respiratory acidosis because it is increasing the amount of STRONG CATIONs to the equation which improves the pH, while adding back an anion that is basically neutral to acid base. Henderson-Hasselbalch is technically wrong when it comes to the physical chemistry of acid base, which is actually driven by strong ions and the bicarbonate plays actually no role when you do the math. Google: Stewart's strong ion acid base and read a bit. H-H equation gives you a good framework to try and wrap you mind around when you are within the usual or normal rages of human physiology.

I'm not sure I completely get your question about PS. Can you be a bit more detailed?

Hopefully someone can help a rising fellow with a few topics (some basic) that have come up and I haven't been able to get a good explanation for:

- How exactly does a CHF exacerbation cause hypercapneic respiratory failure? Pulmonary edema seems to be mainly a VQ mismatch issue and not increased dead space?

- How exactly does ARDS cause increased dead space? Again, it seems like blood is still flowing through the pulmonary vasculature and it's more of shunt physiology developing with blood going past collapsed or fluid filled alveoli, yet dead space fraction is high?

- Why is there not always auto-peep in PS modes if the expiration terminates at 25% of peak expiratory flow? In VC modes, expiratory flow not getting back to 0 raises concern for auto-peep, but in PS flow never returns to 0 but there do not seem to be issues with this.

- Why is bicarb gtt generally effective in improving acidosis in a patient with bad ARDS with a gas 7.15/80? Shouldn't the bicarb just get converted to more CO2 that can't be ventilated off in a patient with respiratory acidosis due to high dead space fraction?


I'd appreciate any explanations!

 

[cavitarynodule]

If you take enough alveoli out of the equation with pulmonary edema and especially if you have very high end diastolic pressures and capillary leak, then you will eventually not have enough ventilation to exchange CO2

What is "dead space" if not open areas in the lung that aren't participating in gas exchange? If the alveoli are full of junk in ARDS then they are simply the end of tubes. Might as well be the trachea.

But don't you still have blood flow going past these non-functioning alveoli so isn't that a shunt and not dead space? Or is there so much hypoxic vasoconstriction that no blood flow goes past those alveoli at all?

Regarding the PS question, I was confused about Esens and thought that referred to stopping exhalation and not inhalation so I think I understand it now.

 

[jdh71]

But don't you still have blood flow going past these non-functioning alveoli so isn't that a shunt and not dead space? Or is there so much hypoxic vasoconstriction that no blood flow goes past those alveoli at all?

Regarding the PS question, I was confused about Esens and thought that referred to stopping exhalation and not inhalation so I think I understand it now.

It’s a relative shunt *and* relative increased deadspace. It’s not an either or phenomena. Much in the lungs is just going to be some of both. Which is of the v or q is most contributing, yeah? The extreme situations that we get presented with only really exist in the minds of experimental physiologists.

 

[gutonc]

It’s a relative shunt *and* relative increased deadspace. It’s not an either or phenomena. Much in the lungs is just going to be some of both. Which is of the v or q is most contributing, yeah? The extreme situations that we get presented with only really exist in the minds of experimental physiologists.

...and USMLE question writers.

Which, now that I think about it, the Venn diagram of those 2 sets is probably just a circle.

 

[the argus]

- How exactly does ARDS cause increased dead space? Again, it seems like blood is still flowing through the pulmonary vasculature and it's more of shunt physiology developing with blood going past collapsed or fluid filled alveoli, yet dead space fraction is high?

But don't you still have blood flow going past these non-functioning alveoli so isn't that a shunt and not dead space? Or is there so much hypoxic vasoconstriction that no blood flow goes past those alveoli at all?

There is microvascular injury in ARDS due to inflammation which leads to capillary thrombosis. Some postulate this capillary thrombosis may actually be a protective mechanism, but ultimately microvascular blood flow is decreased and therefore you get increased dead space.

"Activated endothelial cells also assume a procoagulant phenotype to limit damage to lung microvasculature and localise infection. This is characterised by increased expression of platelet adhesion molecules, intra-alveolar and intravascular fibrin deposition, and release of activators of the extrinsic coagulation cascade, in particular nitric oxide. Moreover, upregulation and activation of tissue factor and loss of the ability to activate protein C and S results in capillary thrombosis and extravascular fibrin deposition, thereby contributing to the increased dead-space fraction that correlates with clinical outcomes."

The pulmonary endothelium in acute respiratory distress syndrome: insights and therapeutic opportunities | Thorax

 

[Hamhock]

Agree with all of the above. Good responses.

Additionally, I would add that the elevated pCO2 in pulmonary edema that I often see and that often confuses early trainees (too focused on the "books") is due to fatigue and hypoventilation in addition to effective dead space ventilation. As a "rising fellow", I understand you are unlikely to be missing that...but other trainees read here too.

Also, bicarb drips outside of AKI are useful to a point with respiratory acidosis (although I don't really use them for this), just like CRRTx is useful to a point [in one sense, a bicarb drip is the same as dialysis in the context of acidosis until anasarca]...the problem with either is that if you can't blow off enough CO2 (regardless of Stewart's strong ions; please note Stewart is essential) you will either die or need ECMO (there may be some inhaled general anesthesia options). Stewart and classical H-H blend at the extremes of physiology and iatrogenesis.

Finally, this is another post in the pulm-ccm forum (which I rarely visit) that would generate some great discussion in the CCM forum.

Future posters: I recommend considering if your post is so pulm-specific that is should be posted here to be seen by more pulmonologists and experienced internists -- or if it would be better posted in the CCM forum, where it will be seen by many multi-disciplinary CCM docs AND some reliable pulm-ccm docs too (@jdh71, @Hernandez, etc).

Mods: could this subforum be changed to pulm instead of pulm-ccm? would that not benefit the entire community?

HH