https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.120.047915 … This is an interesting theory as to why "silent hypoxemia" is a thing in #COVID19
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The sensor that triggers hypoxic pulmonary vasoconstriction is in the mitochondria and involves the NDUFS2 gene.
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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.
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Why doesn't buildup of CO2 cause an increased respiratory drive though? Authors don't say. maybe it's obvious but I'm confused.
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This article also has a model of what's going on that may clarify.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7154064/ …
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What do we see in COVID19 patients with "silent hypoxemia"? 1.) Normal lung elastance -- normal amount of gas gets into lungs.
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2.) Low V/Q ratio: too much perfusion relative to ventilation, probably due to loss of hypoxic vasoconstriction.
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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).
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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.
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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.
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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.
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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. https://en.wikipedia.org/wiki/Ventilation/perfusion_ratio …)
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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.
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If you make a sheep hyperventilate, it damages its lungs, for instance.https://link.springer.com/article/10.1007/BF00255628 …
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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.
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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.
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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!
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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.
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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.
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"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."
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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.)
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