Oxygenation worsening hypoxia

[iBS1972]

Can someone explain what it means to ventilate for me? My confusion stems from the idea that giving oxygen to areas of lung with low V/Q can worsen their respiratory status (increase hypoxemia) because it leads to increased perfusion to poorly ventilated areas of the lung and decreases perfusion to adequately ventilated areas of the lung. My question is why? Because if you’re providing/pushing oxygen to those poorly ventilated areas, aren’t you in effect ventilating them. ( in other words, aren’t you increasing the ventilation of those areas by you supplying constant (I’m guessing) oxygen there, in effect turning those areas into well ventilated areas, so increased perfusion to those areas should be beneficial?

Yes, perhaps you may worsen hypercapnea, but why does hypoxemia worsen (despite you providing continuous oxygen, even to areas that are poorly ventilated since the ventilaor is pushing oxygen into those areas?)

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[iBS1972]

Also, I'm reading for West's Pathophys: "The likelihood of atelectasis increases rapidly as the inspired oxygen concentration approaches 100%." Is this because there's less nitrogen, and usually most if not all of the inspired O2 is absorbed by the blood, thus the development of atelectasis and eventual shunt? (it's hard to believe that the blood can absorb all that oxygen being supplied by the ventilator).
I would highly appreciate any help. I'm at the end of my pulm rotation, and unfortunately just got to this part of the book.

 

[lymphocyte]

Also, I'm reading for West's Pathophys: "The likelihood of atelectasis increases rapidly as the inspired oxygen concentration approaches 100%." Is this because there's less nitrogen, and usually most if not all of the inspired O2 is absorbed by the blood, thus the development of atelectasis and eventual shunt? (it's hard to believe that the blood can absorb all that oxygen being supplied by the ventilator).
I would highly appreciate any help. I'm at the end of my pulm rotation, and unfortunately just got to this part of the book.

Nitrogen splints alveoli open because it has limited diffusion across the alveolar membrane so the partial pressure of nitrogen does not equilibrate. Remove the splint by cranking up the FiO2, and alveoli will start to collapse. This is called reabsorption atelectasis.

Of note, by the miricale of surfactant, you actually don't need that much nitrogen to splint aleveoli. I suspect the rate of atelectasis wouldn't be much different for a FiO2 of 30% vs 70%--but it be massively different for a Fi02 of 30% vs 100%.

 

[drmwvr]

Can someone explain what it means to ventilate for me? My confusion stems from the idea that giving oxygen to areas of lung with low V/Q can worsen their respiratory status (increase hypoxemia) because it leads to increased perfusion to poorly ventilated areas of the lung and decreases perfusion to adequately ventilated areas of the lung. My question is why? Because if you’re providing/pushing oxygen to those poorly ventilated areas, aren’t you in effect ventilating them. ( in other words, aren’t you increasing the ventilation of those areas by you supplying constant (I’m guessing) oxygen there, in effect turning those areas into well ventilated areas, so increased perfusion to those areas should be beneficial?

Yes, perhaps you may worsen hypercapnea, but why does hypoxemia worsen (despite you providing continuous oxygen, even to areas that are poorly ventilated since the ventilaor is pushing oxygen into those areas?)

Could you be conflating two different issues? Shunt leading to a fall in PO2 and increasing dead space ventilation leading to a rise in PCO2 are both possible when giving a high concentration of oxygen. Absorption atelectasis (and a rising shunt fraction) aside, a higher FiO2 can inhibit hpv in diseased alveoli thus stealing flow from healthy lung units. This relative change favors ventilation over perfusion in those units and causes a net increase in Vd. That causes a rise in PCO2 which, definition wise, means the patient is less well ventilated.

The blood moving to the diseased lung units might contribute to the shunt fraction and cause the patient to be less well oxygenated.