two resp questions

[aashkab]

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Hi -

1) Why does destruction of "lung parenchyma" in COPD lead to pulmonary hypertension? The way I am envisioning it, is that there is simply less tissue so the blood vessels have less resistance and should therefore NOT lead to hypertension. Perhaps you can paint a better picture for me.

2) Shunting increases the A-a gradient as mentioned in First Aid. I wanted to clarify and confirm with yall that they are talking about BLOOD SHUNTING (aka R to L shunt, specifically as seen in the table below on p506) but VENTILATION OBSTRUCTION SHUNTING does NOT affect the A-a gradient?

Its taken me so long to figure out (not even sure about if i have it right) how shunts work. Your help is appreciated!

 

[PokerDoc]

I'll take a shot

1) remember, the lung's are the only organs whose blood vessels CONSTRICT when in hypoxic conditions.. thus, vessels are being vasoconstricted to divert blood away from areas that are no longer being perfused. So I would assume that as this occurs more widespread, you get more vasoconstriction of the pulmonary vasculature and thus leading to pulmonary hypertension

2) Yes you are correct.. the A-a gradient occurs with blood shunting only.. If there were an upper airway obstruction, A and a would both decrease proportionally so the A-a gradient would not change.




(these are my assumptions, I dont declare myself an authority on this, im actually a bit weak on resp myself)

 

[MoscowAbe]

Hi -

1) Why does destruction of "lung parenchyma" in COPD lead to pulmonary hypertension? The way I am envisioning it, is that there is simply less tissue so the blood vessels have less resistance and should therefore NOT lead to hypertension. Perhaps you can paint a better picture for me.

2) Shunting increases the A-a gradient as mentioned in First Aid. I wanted to clarify and confirm with yall that they are talking about BLOOD SHUNTING (aka R to L shunt, specifically as seen in the table below on p506) but VENTILATION OBSTRUCTION SHUNTING does NOT affect the A-a gradient?

Its taken me so long to figure out (not even sure about if i have it right) how shunts work. Your help is appreciated!

Shunt is basically an area with low ventilation but high perfusion. No exchange of gases occurs in a shunt. On the other hand low perfusion is dead space. Think physiological dead space were ventilation occurs with no perfusion.

 

[Vikingwizardguy]

Shunt is basically an area with low ventilation but high perfusion. No exchange of gases occurs in a shunt. On the other hand low perfusion is dead space. Think physiological dead space were ventilation occurs with no perfusion.

p.507 of FA 2010 has a nice little image of this.

 

[MoscowAbe]

p.507 of FA 2010 has a nice little image of this.

That's what I call FA under your finger tips.

 

[NRAI2001]

I'll take a shot

1) remember, the lung's are the only organs whose blood vessels CONSTRICT when in hypoxic conditions.. thus, vessels are being vasoconstricted to divert blood away from areas that are no longer being perfused. So I would assume that as this occurs more widespread, you get more vasoconstriction of the pulmonary vasculature and thus leading to pulmonary hypertension

2) Yes you are correct.. the A-a gradient occurs with blood shunting only.. If there were an upper airway obstruction, A and a would both decrease proportionally so the A-a gradient would not change.




(these are my assumptions, I dont declare myself an authority on this, im actually a bit weak on resp myself)

1) I think when it comes to "destruction of lung parenchyma" as is seen with emphysema its partly bc of the hypoxia but I was under the impression it is more so of the fact that Resistance goes up as you take BVs out of parallel.. there are less BloodVessels so overall resistance goes up and Pulm HTN eventually developes.

Please correct me if I m wrong..👍

 

[PokerDoc]

yeah i dunno man, its over my head to be honest.. but the blood vessels arent in the parenchyma itself, its just passing by along, so I'm not sure I follow your logic.. the way i see it is that its just hypoxic vasoconstriction.. its not like the blood vessel is inside the parenchyma thats getting destroyed. I guess if you explained to me why there are less blood vessels I would follow you better.

 

[NRAI2001]

yeah i dunno man, its over my head to be honest.. but the blood vessels arent in the parenchyma itself, its just passing by along, so I'm not sure I follow your logic.. the way i see it is that its just hypoxic vasoconstriction.. its not like the blood vessel is inside the parenchyma thats getting destroyed. I guess if you explained to me why there are less blood vessels I would follow you better.

Its been a really long while since I ve reviewed physio myself... but I thought the parenchyma is made of lung tissue + BVs..etc. So there is a loss of BVs with any parenchymal destruction?? If it was just COPD without destruction then hypoxic vasconstriction would be the main reason for the increase in pulmonary BP..?

I definitely need to review lung physio again 👍

 

[PokerDoc]

Its been a really long while since I ve reviewed physio myself... but I thought the parenchyma is made of lung tissue + BVs..etc. So there is a loss of BVs with any parenchymal destruction?? If it was just COPD without destruction then hypoxic vasconstriction would be the main reason for the increase in pulmonary BP..?

I definitely need to review lung physio again 👍

im imagining something like this

the vessel comes right up to the lung alveoli and is like hey how you doing they shake hands and go there own ways, they never actually join, thats why its a 'diffusion' process. And when you destroy lung tissue youre just increasing physiologic deadspace. But i really have no idea now

 

[NRAI2001]

im imagining something like this

the vessel comes right up to the lung alveoli and is like hey how you doing they shake hands and go there own ways, they never actually join, thats why its a 'diffusion' process. And when you destroy lung tissue youre just increasing physiologic deadspace. But i really have no idea now

So the question is if there is loss of BVs with any destruction of lung parenchyma... I dont have my physio book with me.

 

[MoscowAbe]

This is how I understand it:

In COPD there is constant hypoxia which causes chronic vasoconstriction. This chronic vasoconstriction leads to vessel wall remodeling and sclerosis which in the end increases vascular resistance and subsequently increased RV afterload.

 

[NRAI2001]

This is how I understand it:

In COPD there is constant hypoxia which causes chronic vasoconstriction. This chronic vasoconstriction leads to vessel wall remodeling and sclerosis which in the end increases vascular resistance and subsequently increased RV afterload.

Thats true... I guess our question is when there is destruction of lung parenchyma was is the mechanism?

 

[MoscowAbe]

Thats true... I guess our question is when there is destruction of lung parenchyma was is the mechanism?

I'm assuming if there is destruction of the parenchyma than there is a V/Q mismatch.

 

[theivgirl]

I'll take a shot

1) remember, the lung's are the only organs whose blood vessels CONSTRICT when in hypoxic conditions.. thus, vessels are being vasoconstricted to divert blood away from areas that are no longer being perfused. So I would assume that as this occurs more widespread, you get more vasoconstriction of the pulmonary vasculature and thus leading to pulmonary hypertension

2) Yes you are correct.. the A-a gradient occurs with blood shunting only.. If there were an upper airway obstruction, A and a would both decrease proportionally so the A-a gradient would not change.




(these are my assumptions, I dont declare myself an authority on this, im actually a bit weak on resp myself)

you mean "areas that are no longer being ventilated"