Ventilation and Perfusion Defects - Why one gets 100% O2?

[automan2]

---

Members don't see this ad.

Alright, I have listened to goljan a thousand times, veltillation defects do NOT improve with 100% O2, but perfusion defects DO improve (increase PaO2) with 100% O2.

I have racked my brain and I can't figure out why, unless the ventillation defect is a total blockage, but then the person would be dead.

Both result in a decrease in gas exchange, and an increase in the A-a gradient. Both have extra areas of the lung that are functioning ok, so why does giving 100% O2 to a perfusion defect work to increase the PaO2, but not to the ventilation defect.

I understand the the ventillation defect means none of the 100% O2 would get to the problem area, but how is this different from 100% O2 getting to an area of absolutely zero perfusion? In both cases, there is no gas exchange.

Can someone please clear this up for me? Thanks a bunch.

 

[SkylineMD]

from my understanding of this, if you have a ventilation defect, your body will adjust for the difference in the A-a gradient by shunting blood to other parts of the lung that are ventilated. Normally, there are various zones which are more perfused than others. In a V-Q mismatch, you can shunt blood to the normally underperfused areas (by vasodilation)......and since diffusion of O2 is perfusion-limited AND the fact that it usually equalibriates prior to the end of the vessel (i think theres a graph in BRS physio that shows this --- perfusion vs diffusion limited exchange), there is enough time for the blood to equilibriate its oxygen concentration.

Another point is that room air is 21% oxygen so by giving 100% oxygen, you allow for greater perfusion-limited diffusion and thus will resolve the hypoxemia.

 

[lord_jeebus]

I understand the the ventillation defect means none of the 100% O2 would get to the problem area, but how is this different from 100% O2 getting to an area of absolutely zero perfusion? In both cases, there is no gas exchange.

In the ventilation defect, there are alveoli with blood but no gas. This blood thus passes through the lungs without getting well oxygenated. This part you understand already.

In a pure perfusion defect, there are alveoli with gas but no blood. Hence all the blood is going to other places, that are well perfused. With 100% O2, all the blood is getting exposed to a high O2 concentration. There is no low-O2 blood that gets mixed.

 

[automan2]

In the ventilation defect, there are alveoli with blood but no gas. This blood thus passes through the lungs without getting well oxygenated. This part you understand already.

In a pure perfusion defect, there are alveoli with gas but no blood. Hence all the blood is going to other places, that are well perfused. With 100% O2, all the blood is getting exposed to a high O2 concentration. There is no low-O2 blood that gets mixed.

We are getting closer, but I still don't get it. I like the phrase "ALL the blood is going to other places" but wouldn't this occur in the ventilation defect as well. No gas = low PaO2 = vasoconstriction and thus all the blood is going to the area that is ventilated with the 100% O2. (Yes, it's not a 100% stop in flow, and some blood would flow past alveoli that aren't ventillated, but is this enough to create a big difference when the majority of the other parts of your lung are getting bombarded with 100%02?

Would this vasoconstriction even occur?

Is it the arterioles or the venules that constrict? if it is the arterioles, how can they tell their specific area has no ventilation, as they are before the cappillary and each arteriole in the entire lungs would be getting the same blood, were is the specificity? Are there post-capillary receptors that send a signal to the arterioles?

Here is how I am thinking, say your right lower lobe gets a marble stuck in it producing an obstruction (aka: ventilation defect). How is this any different from an emboli (aka: perfusion defect) that gets stuck in the major artery supplying your right lower lobe?

One has blood but no gas, and the other has gas but no blood. Both = a non-functioning right lower lobe, but you still have the rest of your lungs to fill with 100% O2. And the hypoxemia induced vasoconstriction in the ventilation defect would shunt all the blood to the well ventilated area minimizing the mixing of poorly oxygenated blood with the rest of the pulmonary flow.

 

[SOUNDMAN]

Here is how I am thinking, say your right lower lobe gets a marble stuck in it producing an obstruction (aka: ventilation defect). How is this any different from an emboli (aka: perfusion defect) that gets stuck in the major artery supplying your right lower lobe?

Ok so you've plugged the lobe causing a ventilation defect. You aren't getting O2 to that area. No matter how much O2 you give it's not going to change is it?

 

[lord_jeebus]

Would this vasoconstriction even occur?

Yes, but it's not going to cut off all flow.

 

[fakin' the funk]

I understand the the ventillation defect means none of the 100% O2 would get to the problem area, but how is this different from 100% O2 getting to an area of absolutely zero perfusion? In both cases, there is no gas exchange.
Can someone please clear this up for me? Thanks a bunch.

The difference is, in one situation there is shunting, in the other, there is not. Shunting = bad.

In a ventilation defect there can potentially be a crapload of shunting. Imagine a mainstem bronchus occlusion.

In a perfusion defect there is not a whole lot of shunting. All the blood that does enter the lung is being oxygenated, albeit by a proportionally smaller # of alveoli. So bump up the oxygen to compensate.

Of course, it's late, and I might be wrong.😴

 

[automan2]

Sounds good to me, shunting is bad because it causes mixed blood, and there is more shunting in ventilation defects. Giving 100% 02 helps a perfusion defect more. (I still think it would help a ventillation defect though)

Thanks for the help. At least I will remember this.

 

[WhoisJohnGalt]

Sounds good to me, shunting is bad because it causes mixed blood, and there is more shunting in ventilation defects. Giving 100% 02 helps a perfusion defect more. (I still think it would help a ventillation defect though)

Thanks for the help. At least I will remember this.

Our professors told us it was an academic distinction and not a practical one. We're supposed to know academically that giving 100% O2 won't help that much, but practically speaking, they're going to give the O2 in either case. It definitely won't help AS MUCH, but your gut instinct is right-- it will help a little. For the boards though, don't give O2.

 

[Pepsy]

🙂

 

[lord_jeebus]

lets see how i can bring it down..

its a matter of size.. practically..

ventilation defect.. chances are you get clogged up with a nice lil steak up in the airway.. its a huge shunt. even if you give 02, the airway is still at large clogged up. most parts of the lungs arent gonna get much of that 02 neway.

perfusion defect.. its not like there's this huge artery thats embolized and 02 is not getting through to most part. it probably jus occludes a small part of the lung. So increasing the 02 by giving 100% 02 would be better absorbed by other parts of the lung which are unaffected.

so its all practical.

If we are to get technical and for theory sake say a steak works its way down to a small bronchi (ventilation defect still), only some part of the lung would struggle to get 02, and giving 100% 02 in this case will be effective because 02 would be absorbed by the other unaffected parts of lung.

This reasoning is mostly incorrect and I recommend rereading the other posts on this thread.

Even a small ventilation defect could have a significant impact on response to 100% O2. Think about why.

 

[Pepsy]

i thought about the post and i figured i should do some reading up on it.. and saw how the post i made is incorrect indeed.you beat me to it before changing it up jeebus.

 

[Hashmeister]

10 years later and I'm still shady about the topic haha.

 

[Pepe18]

.