FRC in Obstructive Lung Disease

[Ronin786]

I'm having a bit trouble grasping the change in FRC in Obstructive Lung Disease. I always assumed that it would be increased given the air trapping that occurs in the lungs. But according to SUTS2 it is markedly decreased.

Is this because while the RV increases, the ERV decreases even more? Or is there some other reason?

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[sevoflurane]

I'm having a bit trouble grasping the change in FRC in Obstructive Lung Disease. I always assumed that it would be increased given the air trapping that occurs in the lungs. But according to SUTS2 it is markedly decreased.

Is this because while the RV increases, the ERV decreases even more? Or is there some other reason?

FRC is increased in obstructive diseases... as is RV. Remember, ERV usually stays the same but RV increaes and since FRC is a capacity it is composed of 2 volumes: ERV + RV... since RV goes up, so does FRC.

An important take home message is that of closing capacity/volume... this is the volume at which small airways start to collapse. In severe COPD, closing volume approximate that of normal tidal volume breathing giving you atelectasis and small airway collapse at rest.

Been a while since I've thought about lung capacities, but I think I have this right.

Hope it helps.

 

[Ronin786]

Thank you very much. It definitely helps. I'll have to annotate that in.

 

[fakin' the funk]

Remember that FRC is determined by the balance of two opposing forces:
-- the elastic recoil of the chest (trying to "spring" outward)
-- the tendency of the lung parenchyma to collapse inward

In COPD, emphysema in particular, the lung's collapsive forces are reduced due to the reduced alveolar airspaces and connective tissue destruction. So the chest's elastic recoil predominates and FRC is higher than normal. Hence, barrel chest.

 

[Ronin786]

Makes sense. Didn't connect the two till you mentioned it though lol.

On a slightly related note, can someone explain why PaCO2 doesnt increase in cases of pulmonary shunting? For example, with pulmonary edema, if the alveoli are filled with fluid, then there won't be any gas exchange taking place and the CO2 should increase, no? And wouldn't the same apply with a V/Q mismatch?

 

[ssmallz]

Co2 has such a high capacity for diffusion that mild pulmonary shunt doesn't increase the CO2....it same reason you get a normal CO2 level w/an endobronchial intubation

 

[WashMe]

I'm having a bit trouble grasping the change in FRC in Obstructive Lung Disease. I always assumed that it would be increased given the air trapping that occurs in the lungs. But according to SUTS2 it is markedly decreased.

Is this because while the RV increases, the ERV decreases even more? Or is there some other reason?

well, ignore SUTS2 then this is a good example of how review books can screw up basic concepts with typos. Trust your instincts; it all comes back to basic physics when talking about any respiratory or cardiovascular diseases.

 

[StumpC28]

Makes sense. Didn't connect the two till you mentioned it though lol.

On a slightly related note, can someone explain why PaCO2 doesnt increase in cases of pulmonary shunting? For example, with pulmonary edema, if the alveoli are filled with fluid, then there won't be any gas exchange taking place and the CO2 should increase, no? And wouldn't the same apply with a V/Q mismatch?

PaCo2 doesn't rise with a shunt until your shunt fraction reaches 50%. You can drop your PaCO2 in well ventilated portions of the lung (hyperventilating) compensating for the non-ventilated portions. Well ventilated portions of the lung will contribute blood w/ PaCO2 of <40 mmhg (say 32mm hg) while non-ventilated portions contribute blood with a PaCO2 of 46 mm hg. In small shunts your PaCO2 will actually be low (<40mm hg).

 

[Ronin786]

Thanks for the help guys. I'm studying for Step 2 and some of these concepts were unclear for me.

 

[navigator]

So I get why FRV would increase during emphysema. But in my notes it says that IRV also decreases. Why is this? TLV doesn't stay the same - it increases because of the unopposed, outward movement of the chest ("barrel chest").

 

[vector2]

So I get why FRV would increase during emphysema. But in my notes it says that IRV also decreases. Why is this? TLV doesn't stay the same - it increases because of the unopposed, outward movement of the chest ("barrel chest").

it's all about the proportion of the change in each of the lung volumes