3 ms·
> like in the 30s which is usually fatal but these patients were conscious and responsive. These meters are calibrated around the normal range of values. Once
by treis 7y ago
> like in the 30s which is usually fatal but these patients were conscious and responsive.
These meters are calibrated around the normal range of values. Once they get out of that they become very inaccurate. So a reading in the 30s is probably not actually an 02 sat in the 30s.
- tyingq 7y agoInteresting, because that would correlate with the high death rate. Sedation, intubation, respirator, is a low success path. Staving it off has value. And it feels like there is a path there.
- treis 7y agoThese lower level interventions don't make all that much of a difference. As the disease progresses your lung capacity reduces. If we put some made up numbers to it, it would look like: 0-50%: Can breathe on their own with increasing difficulty 50-55%: Can survive with O2, BiPap, CPAP, etc. 55-80%: Can survive with intubation 80%+: Dead Each individual patient will progress to a certain point and then either recover or die. The number that will progress to the O2, BiPap, CPAP, etc. level and then recover is relatively small since it's a pretty narrow band where it is effective. AFAIK, most places are skipping the O2, BiPap, CPAP stuff because they use pressurized air. That generates a lot of droplets/aerosols and poses a significant transmission risk. Since there's a relatively small chance that the patient will recover on those interventions they skip them and go straight to intubation.
- droopyEyelids 7y agoHere is a great explanation: https://www.youtube.com/watch?v=nO4xgcIaPeA https://www.youtube.com/watch?v=nO4xgcIaPeA There are three main causes of hypoxemia (low blood o2): 1) "V/Q" (volume/flowrate), where uneven flow of blood carries unoxegenated blood past alveoli faster than it can oxygenate, 2) "Shunt" where blood flows through the lungs without being able to exchange gasses at all 3) "Diffusion Abnormality" - usually seen in COPD, this is where the membrane between alveoli and the capillaries becomes thicker or different. CO2 can diffuse through a thicker membrane more easily than oxygen, so that can explain some of the findings other posters are discussing. Nothing peer reviewed on this yet, though we have techniques for analyzing exactly whats happening in the lungs by injecting inert gasses to the body and measuring how they leave.