ahajournals.org/doi/pdf/10.116… This is an interesting theory as to why "silent hypoxemia" is a thing in #COVID19
Ordinarily, when not enough oxygen is getting to (parts of) the lung, due to lung damage (as from pneumonia), there's a thing called hypoxic pulmonary vasoconstriction. Arteries pumping blood to fucked-up alveoli become narrower, so more blood can pick up oxygen from good alveoli
This is called ventilation/perfusion (V/Q) matching. Failure is called V/Q mismatch. You have blood flow without oxygen, or oxygen without blood flow.
The sensor that triggers hypoxic pulmonary vasoconstriction is in the mitochondria and involves the NDUFS2 gene.
The theory here is that this sensing mechanism goes awry in COVID19. Pulmonary arteries don't constrict in response to poor oxygenation. Patients don't feel a sensation of breathlessness even though they're hypoxemic, because the usual responses to low O2 aren't working.
Why doesn't buildup of CO2 cause an increased respiratory drive though? Authors don't say. maybe it's obvious but I'm confused.
This article also has a model of what's going on that may clarify. ncbi.nlm.nih.gov/pmc/articles/P…
What do we see in COVID19 patients with "silent hypoxemia"?
1.) Normal lung elastance -- normal amount of gas gets into lungs.
1.) Normal lung elastance -- normal amount of gas gets into lungs.
2.) Low V/Q ratio: too much perfusion relative to ventilation, probably due to loss of hypoxic vasoconstriction.
3.) and 4.) low lung weight and recruitability: only a small amount of lung tissue is damaged (and thus filled with liquid or "recruitable" by forcing the alveoli open with ventilatory pressure).
So we only have a little bit of damage to the lung, but the circulatory system's not routing around it normally, so you have SUPER bad hypoxemia.
what this article says is that these "silent hypoxemic" patients DO have an increased respiratory drive; their breathing rate and minute volume (gas inhaled/exhaled per minute) is way up to compensate.
They're not feeling dyspnea due to CO2 buildup because they're not actually building up CO2; they're ventilating plenty via increased respiratory rate. And indeed they tend to have low measured blood CO2 levels.
V/Q mismatch impairs BOTH getting O2 in and getting CO2 out. But it usually results in low O2 and *normal*, not high, CO2, since any rise in CO2 results in more respiratory drive. (at least that's what Wikipedia says. en.wikipedia.org/wiki/Ventilati…)
(I'm new to all this stuff, bear with me.)
Why doesn't "silent hypoxemia" stay harmless? If I understand the article correctly, this is because you're breathing so much more that there's an increase in "inspiratory intrathoracic pressure", and this damages the lung, causing "P-SILI", or patient-self-inflicted lung injury.
If you make a sheep hyperventilate, it damages its lungs, for instance. link.springer.com/article/10.100…
Now patients who previously had a *little* bit of lung damage have a LOT of lung damage. And therefore it looks more like typical ARDS: low compliance, high lung weight, high recruitability, and much bigger lung lesions visible on a chest CT.
logically this implies: keep patients from hyperventilating while they're still in "silent hypoxemia" so they don't breathe so much they progress to full-blown severe ARDS.
how do you do this? it looks like it's a matter of debate right now. one thing I've seen in a couple papers is "use work of breathing to determine when to intubate". Patient can't breathe too hard if a machine's breathing for them!
The big conclusion the COVID19 paper draws about patients with low oxygen but no dyspnea is *give 'em lots of oxygen.* Tradeoffs are more ambiguous about PEEP.
The other conclusion is that you want to intubate when the inspiratory pressure swings are starting to get big, as controlling the breathing rate can *prevent* additional lung injury.
"As esophageal pressure swings increase from 5 to 10 cmH2O—which are generally well tolerated—to above 15 cmH2O, the risk of lung injury increases and therefore intubation should be performed as soon as possible."
Also, if we could figure out *how* COVID19 blocks hypoxic vasoconstriction, and find a way to make it *stop*, those "silent hypoxemic" patients could get their V/Q back to normal, and thus would no longer be hypoxemic (since they don't have much lung damage to begin with.)
