Maybe I’m misunderstanding your query, but, in fact, a small amount of C02 is what triggers you to keep breathing. It’s why you can’t hold your breath until you die. The urge to breathe becomes so overpowering it is involuntary. It’s how drowning victims take in the first lungful of water.
Also, apparently, some divers of a particular stripe who prefer to hold their breath than to use SCUBA equipment (??) have managed to kill, or almost kill themselves, by teaching themselves to exhale so deeply, and hyperventilate so well, that they actually lose the urge to breathe, due to a lack of C02.
I’m puzzled why a surgeon would be seeing so many cases of asymptomatic or mild Covid-19 - seems like a patient referred for surgery would be rather severely affected.
Any severe pneumonia can potentially lead to scarring.
We’re still learning about long-term effects of Covid-19, but there are studies showing substantial improvement in lung function during recovery, including one detailed in this Medscape article (link not available) which reported no signs of progressive pulmonary fibrosis in their study cases.
"The vast majority of hospitalized COVID-19 patients show lung damage 6 weeks after discharge, but this proportion drops significantly after 12 weeks, suggesting that the lungs have a self-repair mechanism, researchers report.
“We know from other lung studies that lungs have the potential to recover from inflammation,” said investigator Sabina Sahanic, MD, a clinical PhD student at University Clinic in Innsbruck, Austria. “Specialists knew we’d have to wait some weeks to clarify this and estimate how good the resolution is. And we are very happy to see a good resolution…
Notably, CT scans at 6 weeks showed lung damage from inflammation and coronavirus-induced fluid accumulation — which shows up as “ground glass” patches — in 88% of patients. At 12 weeks, this measure dropped to 56%. The severity of overall lung damage dropped from 8 points on 6-week CT scans to 4 points on 12-week CT scans.”
Another study reported “preliminary evidence that hospitalized patients with mild-to-moderate forms of COVID-19 are not at risk of developing pulmonary fibrosis.”
My conclusion is that based on current knowledge, the story linked in the OP is unjustifiably hyping the risk of lung scarring post-Covid.
Yes, so normal CO2 indicates normal breathing, and normal breathing indicates normal CO2. @Tfletch1 has reported that breathing was slightly increased, indicating slightly higher CO2 along with low O2. @knobturner has reported normal breathing and normal CO2 along with low O2.
Either or neither or both could be right: I’m not interested in trying to start a debate.
An agreed observation is that in some patients, O2 perfusion does not match air ventilation. This matches many reports about COVID: the response to and requirement for ventilation is not exactly the same as what it is for other common respiratory conditions.
I think @RivkahChaya, @knobturner, and I are in agreement. @RivkahChaya is saying that under typical circumstances, high CO2 levels stimulates your breathing. If you have an obstruction (pneumonia, COPD) or exercised too vigorously, you will feel out of breath. Your response will be to increase your breathing rate will increase if you can’t breath very deeply. Your feeling of being out of breath is driven by high CO2, not low O2. Even if you can’t feel being out of breath, your breathing rate and depth (ventilation) will increase to get CO2 levels back to normal. That’s why CO2 levels are not so off for happy hypoxia covid patients.