So why are you talking about kidneys?
8 out of 10 isn’t close to 10 out of 10?
Useful information - thanks!
I was replying to your comment? I’m just pointing out that some internal organs, like lungs and the liver, do have good repair capacity.
When I was in AIT (advanced military training), I came down with what they call “walking pneumonia.” I felt like I had a cold, and not a particularly bad one, it had just been lingering for a while, and I decided to go to sick call to make sure it wasn’t bacterial, and I wasn’t shaking it because I needed an antibiotic.
I had a temp, which was the first thing they noticed that I hadn’t been aware of, because they take your temp first thing on sick call, and since it’s full of people who had three hours sleep, and just really couldn’t do PT that morning, and that’s all, so when I had a temp over 101°F, the aide taking the temps startled, and said “Hey! We got one that’s actually sick!”
I wasn’t coughing, and for as congested as my nose was, was breathing pretty well. I’d taken OTC decongestants, and also some Benadryl the night before, and had slept fairly well (they worked us HARD, and I’d hit my bunk at 7pm).
I’d been running PT perfectly fine the morning before, but the medic sent me for x-rays.
I don’t think “severe” was the word used, but they said something like “nearly complete” on one side, but “just beginning” on the other. So basically, I was mostly breathing on only one side, but that side was pretty normal. I could run to miles, and march with the 6’4 men like that.
I didn’t feel great, I felt sick, but like I had a cold– I’d have expected much worse from pneumonia.
I don’t recall whether it was viral or bacterial, but I was put on antibiotics. Sometimes that’s a precaution, though.
A year later, my home unit requested that I go for follow-up x-rays, and sent me on a drill weekend for them to a local lab. They were clear. The tech even commented that he could see I’d never smoked, and he was guessing my parents hadn’t either. (Not in my lifetime, anyway.) If he could tell that, they must have been pretty darned clear.
I had chest x-rays again about 3 years later when the doctor who was scheduling me for a tonsillectomy wanted them. I don’t know if they were a regular part of tonsillectomy pre-op, or just people who’d previously had pneumonia, or pneumonia in the past n years. But as no one ever said anything to me, I assume they were fine.
A couple of related, and equally compelling, articles:
If you start with two healthy lungs you have a certain amount of lung capability above and beyond that needed for mere survival. My guess would be that someone could have “severe viral pneumonia” but still have enough functional lung that they might not notice if they weren’t exerting themselves.
But I’m not a doctor and that’s just a guess.
A chest X-ray is standard preoperative work for any procedure that may require inhalation anesthesia or supplemental oxygenation. It is always the surgeon’s call. Some are more cautious or risk adverse, they may order X-rays more often.
I guess anesthesia for an adult tonsillectomy is complicated-- and it was a tonsillectomy, adenoidectomy. Giving someone GA for throat surgery is difficult, is my understanding. I suppose that meant the doctor would have wanted to be pretty sure about potential problems.
You got it in one.
And wanted to be sure the lungs could oxygenate well in case they were needed as a problem solver.
If their C02 levels are “normal” with low oxygen levels, doesn’t that mean that the C02 is not leaving the lungs at normal rate? Because if it was, it would be at a level comparable to the hypoxia.
IANA medical anything, but from my reading the CO2 exchange system and the oxygen exchange system are essentially independent.
They have some common dependencies, like if your blood isn’t circulating or your chest isn’t going up and down they both fail. And if your total lung interior surface area becomes too small or too fouled they’ll each eventually become insufficient. But not necessarily at the same point. There’s lots of other chemistry & biology that are more or less independent processes. Each separately regulated to achieve their target blood levels of O2 & CO2.
The idea that breathing is pretty much a one-for-one exchange of oxygen vs CO2 is one of those simplifications for laypeople.
Disclaimer: I’m not a medical doctor, but here goes…
In “happy hypoxia” patients, their CO2 levels are normal because of increased breath rate and deeper breaths. This is enough to expel enough CO2 from healthy parts of the lungs to keep blood CO2 levels normal. People don’t necessarily know that they are breathing faster or deeper, so they don’t feel “shortness of breath” (dyspnea). In other words, ventilation (breathing), appears to be unhindered.
The problem with Covid-19 patients with happy hypoxemia is that there is a problem with perfusion (circulation and gas exchange within the lungs) due to clots and damage to alveoli. Unlike CO2, increasing breathing rate isn’t enough to compensate. However, humans are only aware of increasing CO2 levels due to ventilation or external issues. Low O2 cues are much more subtle and not always felt by the patient.
I’m a radiologist and have seen chest x-rays from many of those, both in and out patients. with COVID-19. I have seen a 3 or 4 cases out of hundreds where the disease has caused significant scaring. A number of those with the worse acute infiltrates never make it to follow up x-rays, so I cannot guess on how many were potentially going to be scared but the number is nowhere close to 75%. A few percent tops, but I have not kept count and cannot give actual numbers.
Thanks. So the article in the OP is utter bullshit. I mean, it kind of had to be, right? It’s not as though 100% of symptomatic and 75% of apparently asymptomatic infections leading to severely scarred lungs would have gone unnoticed except by one Texas trauma surgeon.
Yes, it’s rather in the “crazy if true” category. It reminds me how a Vox explainer article contained:
Take that to the one end. If 88% of covid patients suffered symptoms for months, it wouldn’t be called “long covid”. It’d be normal covid.
Apparently, increased respiration and deeper breaths are not observed in the “happy” hypoxic patients?
In normal people, increased breath rate and deeper breaths leads to low levels of C02 – hyperventilation can lower your C02 levels enough to depress automatic breathing demand. In the happy hypoxic, there are no signs of depressed breathing or exaggerated breathing because C02 levels are “normal”.
?But low levels of oxygen in the blood would also lead to low levels of C02 in the blood?
?So the existence of “normal” C02 levels in the happy hypoxic suggests that C02 respiration, like oxygen respiration, is not normal?
Under normal circumstances, hyperventilation reduces your blood CO2 levels and your blood pH increases. What I’m describing is increased ventilation in happy hypoxia patients to compensate for reduction in perfusion (gas exchange with blood) due to damaged tissue and/or blood clots in the lungs.
The increased ventilation is enough to get rid of the CO2 but not enough to increase O2 in the blood. I’m not sure why, but maybe it has to do with the fact that the difference in CO2 levels throughout the body is not as large as oxygen. In the blood, the partial pressure of CO2 moving toward the alveoli is 46 mmHg and is reduced to 40 mmHg after exchange with air in the alveolar space. The partial pressure of O2 is 40 mmHg moving toward the alveoli and increases to 102 mmHg after exchange with air in the alveolar space.
I don’t think that there is increased ventilation in happy hypoxia patients. I’m willing to be educated.
So C02 is normal for some other reason: either perfusion is unaffected, or low oxygen levels lead to (low C02 increased to normal by poor perfusion).
I’m particularly interested because (it’s been brought to my attention) I know nothing about perfusion. But I have to be convinced that there is increased ventilation: I’m not seeing a description or a mechanism?
I’m no expert so I could be wrong. The Covid patients have what’s known as a V/Q mismatch (ventilation/perfusion).
In the paper I posted, they did say that ventilation (breathing) increases. I take that to mean that the patient is unknowingly breathing faster and deeper (hyperpnea or hyperventilation).They are hyperventilating to compensate for increased CO2 levels due to reduced perfusion. (The kidneys can also compensate, to some extent, for low blood pH caused by high CO2.) They don’t have regular pneumonia; so their passageways are not obstructed mucus or constriction. Since they are not aware of it, they don’t feel out of breath (dyspnea).Therefore, they’re happy.
Perfusion is definitely reduced in Covid lungs. Since circulation, in general, is reduced, it has to affect both O2 and CO2 exchange since they both happen in the capillaries at the alveoli. Both gases passively move across a single layer of cells lining the alveoli, then a layer in the capillaries. I’ve always assumed they both diffuse across these layers at the same rate.
The paper goes on to discuss why oxygen levels are low but all of them involve issues that should effect both O2 and CO2 gas exchange. The only thing that would affect O2 more than CO2 is changes in O2 binding to hemoglobin.