Supplemental Oxygen induced Hypercapnia Question

[403710]

Did some research regarding a oxygen-induced hypercapnia in a patient with COPD exacerbation question in UW, and to quote Med-Bullets, 100% supplemental O2 would lead to:

• Increased dead space to tidal volume ratio
  • worsens V/Q matching because of loss of hypoxic vasoconstriction
  • most important contributing factor to worsening hypercapnia

How is it that the loss of hypoxic vasoconstriction increases physiologic deadspace? Wouldn't the vasodilation increase bloodflow to now hyperoxic alveoli? Thus reducing the physiologic deadspace?

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[yankees527]

I actually went over this for a while today

So normally there are areas in the lung which are poorly ventilated in COPD. Based on normal physiology, these undergo hypoxic vasoconstriction, which is good (we don't want to perfuse areas with no ventilation)

However, when you become hyperoxic, those same vessels which are normally constricted (based on mechanism above) vasodilate. This shunts blood AWAY from the other parts of the lung which do have adequate ventilation, and brings the blood TO those parts of the lung which are not ventilated

Therefore, in those ventilated areas where blood is shunted away, you create dead space (ventilation without perfusion)/increase v/q ratio

One step further in case you want to know, in those areas which are poorly ventilated, the increased perfusion will create a shunt(perfusion without ventilation)/decrease v/q. However, questions seem to point to the dead space fact rather than this.

It is a really confusing concept and I think the reason a lot of people don't explain it correctly is because they don't specify where things are happening exactly

Hope that helps

 

[Rahas]

Its basically a matter of perspective. I could tell you I scored 80% in an exam or dropped 20% questions, and its the exact same thing, except conventionally we would use 80%.

In COPD, in an effort to minimize V/Q mismatch, the lung is selectively vasoconstricted in areas of poor O2 flow.

When you give such a person high flow O2, it increases the O2 tension in all alveoli, which is what the vessels sense to mediate hypoxic vasoconstriction, but not necessarily the volume of air moving into diseased alveoli. This removes the state of vasoconstriction and redistributes blood away from aerated alveoli. For these alveoli, the V/Q ratio drops ie too much V for the Q they're getting - this is over-ventilation, or dead space. Meanwhile the alveoli with low V are now getting high Q, this drop in V/Q is an overperfused area ie a shunt. You could look at it from either perspective and its the exact same thing, but I guess the convention has become to use normally well aerated and well perfused alveoli as the starting point.