Giving Oxygen

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Kluver_Bucy

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What would be the effect of giving oxygen to a patient with ARDS, Pulmonary Shunt, Emphysema, Fibrosis, and Pleural Effusion. Which conditions would increase oxygen saturation in a patient?

Thanks for your help 😍
 
Diffusion across a membrane is directly proportional to the surface area and gradient, but inversely proportional to the membrane thickness. Giving oxygen increases the O2 gradient, so any condition characterized by a diffusion problem would be helped. ARDS and fibrosis are characterized by increased diffusion distance, while emphysema has a reduced diffusion surface area. Cranking up the O2 gradient would help counteract these problems.

Giving O2 to someone with a shunt will not help, as oxygen is not going to get to the shunted blood no matter what you do.

Not sure about the effusion, but I'd guess that since an effusion compresses the lung, it would reduce the surface area available for O2 diffusion, so perhaps additional O2 would help. I'd need confirmation from someone else though, as I'm not sure.


Kluver_Bucy said:
What would be the effect of giving oxygen to a patient with ARDS, Pulmonary Shunt, Emphysema, Fibrosis, and Pleural Effusion. Which conditions would increase oxygen saturation in a patient?

Thanks for your help 😍
 
Kluver_Bucy said:
What would be the effect of giving oxygen to a patient with ARDS, Pulmonary Shunt, Emphysema, Fibrosis, and Pleural Effusion. Which conditions would increase oxygen saturation in a patient?

Thanks for your help 😍
You should categorize these.
1. Diffusion defect: CHF, interstitial fibrosis, pulm edema, etc. In these people, there is increased thicknes btwn alveoli and capillaries. However, giving them O2 increases the gradient, and therefore, they respond to increase in O2. A-a gradient decreases as a result.
2. Pulm shunt: atelectasis (ARDS), congenital R-->L shunts. Here, there is another story. Arterial PaO2 is going to be less than PAO2 (in addition to the normal minor decrs). In the case of atelectasis, alveoli are compressed. Remember, when alveloi are compressed, you get hypoxic vasoconstriction shunting the blood away from these collapsed alveoli. Basically, there is no alveoli to perfuse these vessels, so you have deoxygenated blood comming back to the left heart. Likewise, in R--L shunts, same scenario. And, giving these people O2 will not increase in the PO2 significantly (this is usually how u can differentiate a diffusion deefct vs. shunt, because in the latter you won't see an increase in PaO2 after giving O2). And, again, this is because you have collapsed alveoli, no matter how much O2 you give, it won't make a difference.
3. Perfusion defect - dead space: PE, etc. Think of this as acting like the "apex" (ventilation > perfusion, so you get better gas exchange-->increased O2, decreased CO2-->resp alk)--so these people have increase V/Q with a small thrombus (unless of course there is a saddle embolus or something, where there is complete loss of blood flow). But, usually, there are other capillaries that can compensate. So, here, giving O2 will increase PaO2.
4. Emphysema (COPD): think of this as the "apex" as well. Here the alveoli are dilated (ventilation>>perfusion, despite ventilation being decrs), but this produces different acid base distrubances because, despite having dilated alveoli, and increased ventilation compared to the little blood flow, you have increases in C02 and decrease in O2, becuase you are not able to expel the CO2 out. And, pt will respond with O2. And, that's simply because their ventilation is decreased (not able to expel CO2 and exchange for O2).

Hope this helps.
 
Also just another little random factoid... when you give O2 to someone who has chronic hypercapnia (i.e emphysema) you reduce their ventilatory drive by increasing the PAO2---this is bad, very, very bad. So you wouldn't do this in real life
 
Doc Ivy said:
Also just another little random factoid... when you give O2 to someone who has chronic hypercapnia (i.e emphysema) you reduce their ventilatory drive by increasing the PAO2---this is bad, very, very bad. So you wouldn't do this in real life
Really? I mean the theory makes sense, but this happens very frequently I believe, at least during my IM rotation. I mean, they come in with a pretty severe COPD exacerbation...but they get put on 02, albeit, just acutely to get them out of the exacerbation.
 
HiddenTruth said:
Really? I mean the theory makes sense, but this happens very frequently I believe, at least during my IM rotation. I mean, they come in with a pretty severe COPD exacerbation...but they get put on 02, albeit, just acutely to get them out of the exacerbation.

I mean I'm sure it's ok acutely, but you really have to watch that you don't throw them into respiratory depression. You just can't give O2 and then leave them alone. At least this is what was drilled into my head when I spent last summer at Mayo.
 
Doc Ivy said:
I mean I'm sure it's ok acutely, but you really have to watch that you don't throw them into respiratory depression. You just can't give O2 and then leave them alone. At least this is what was drilled into my head when I spent last summer at Mayo.

These patients are also in a hospital - they can always be put on a respirator.

ANother factoid: 24h O2 therapy has been proven to extend lives in COPDers whose PO2 is below 55
 
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