The respiratory problems that COVID-19 causes have some unusual characteristics. Here's a quote from https://www.hippoed.com/em/ercast/episode/tbd3/covid19weingart:
"One of the most astounding things about treating COVID-19 patients is how well they can look with extreme hypoxia. Patients with saturations of 50% (and consistent ABGs) can be talking, mentating normally, and have otherwise normal vital signs. Thus, this term: “the happy hypoxemic”. It is not well understood why these patients are able to tolerate such low sats without having compensatory measures, such as tachycardia." Clinicians are increasingly talking about these "happy hypoxemics" or "silent hypoxemics" with COVID-19. Not all patients, but a significant proportion fall into this category, at least temporarily. Here are my questions, for discussion:
Why can these patients tolerate such low oxygen saturations? Or can't they- are they on the edge of a crash, but don't know it? There are many stories of patients who thought they were doing ok at home, and sometimes even thought they were getting better, then declined suddenly and died at home or in the ambulance. The same thing is reported with people in the hospital who appear to be doing ok on just oxygen, but then they suddenly decline.
Why don't these patients have compensatory mechanisms, such as tachycardia, faster breathing, etc? Is it because they often have normal CO2 levels, or because of some other dysfunction in triggering compensatory mechanisms?
How can these patients have normal mental state with such low oxygen saturations? Or are their oxygen saturation readings not representative of their true condition, for some reason?
Does this mean no one with COVID-19 should be sent home without at least a pulse oximeter and instructions on when to seek help? Sending people home if they have less severe symptoms is standard in the US today. But people may not be able to tell when they need medical attention, especially if they can have very low oxygen levels without significant distress.
The following is a helpful discussion of the likely respiratory physiology going on with COVID patients. It proposes that natural variation among humans may be responsible for differences in responses to COVID-19- see the chart near the bottom:
https://threadreaderapp.com/thread/1247332371218628609.html
I would think the "happy hypoxemics" are actually the worst off in that chart, and that they would be likely to decline. And it might imply that if you could induce either better HPV, stronger ventilatory drive, or both, you could help these patients move into one of the other categories.
Would it be helpful to induce compensatory measures? During pregnancy, the body adapts to take in 40% more oxygen by changing the set point for CO2 and other changes. The body also adapts to handle the lower oxygen conditions at high altitude. For people who don't adapt well on their own, there are ways to speed acclimation by inducing compensatory measures (acetazolamide, for example). Could we mimic this for COVID-19?
Perhaps, one if the possible answers is connected with the relarively high intrapulmonary concentrations of ammonia generated due to the local urea hydrolysis by latent intrapulmonary urease-positive mycobacterium co-infection...
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Subject: A REVIEW OF IMPACT OF COVID-19 ON PSYCHO-ECONOMIC STATUS OF EMPLOYEES WORKING FROM HOME
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Hello DR Jiminez: Most of the queries you have raised in your question may find a response in the contents of this link:
https://emcrit.org/pulmcrit/happy-hypoxemia-physiology/
Regards--
Gudivada:
Is it possible to get a copy of your questionnaire emailed to me for personal use?
Dr Sha
PS: never received a copy of your questionnaire.
Theoritically it has been mentioned that hypoxia may not trigger respiratory drive from the higher centre if the PaCO2 level is lowered. This hypocapnia can be due to initial subconscious increase in ventilation as in high altitude physiology. But the problem here is lack of sufficient data of ABG on these cases. Also efficacy of acetazolamide can be discussed with the evidence only. More over, when they say the increase in coagulopathy associated with the consequence of stroke or infarction,, or new evidences suggesting the benefits of blood thinner .. remember the hypocapnia bringing alkaline condition of blood enhance coagulation.
I personally would like to thank for arising the question. And just that without the complete pictures of ABG,the answers would all be just the hypothesis.
Meanwhile if you have find some related data, it will be great to discuss..
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