Resp physio Question: ventilation C02 exchange.

[RxBoy]

---

Members do not see this ad.

Question:

Why is there no CO2 exchange through the anatomical dead space from alveoli to atmospheric air without the expiratory recoil of alveoli?

Apenic oxygenation can occur as long as there is unobstructed flow of high FiO2 to non collapsed alveoli (gradient between PAO2 and PaO2 allows diffusion to hemoglobin molecules). However, the gradient between paCO2 and PACO2 will equaliberate between the alveolar capillary membrane, but even if there is no ventilation it seems logistical that CO2 should simply diffuse out of the lungs because there is a gradient between atmospheric and PACO2. I know its not the case because a non breathing patient on SV with CPAP added will result in no EtCO2. However if CPAP is increased to say 30 using the pop off then released back to 0 (creating an artificial breath) you see the normal capnogram with EtCO2. So why does CO2 have to be "pushed" out of the alvoeli as opposed to just being diffused out? (I figure it has something to do with turbulent resistance but still don't quite understand)

With that said, if a patient is on the vent with a pressure control of 30, will the addition of PEEP decrease the amount of CO2 exchanged?

 

[sevoflurane]

With that said, if a patient is on the vent with a pressure control of 30, will the addition of PEEP decrease the amount of CO2 exchanged?

It can... depends where you are on the compliance curve. If you are recruiting atelectatic alveoli, then you may optimize V/Q match and therefore C02 x-change.

However, over-distending non-atelectatic (or any alveoli) to the point where you are transmitting that pressure to the surrounding alveolar capillaries which now become compressed = DEAD SPACE and a decrease in your V/Q matching/ C02 x-change.

Optimal/Best Peep is the pressure you are looking for = the pressure (mmhg) at which you pop alveoli open without over-distention.

 

[PMPMD]

Apneic oxygenation works because more O2 is absorbed from alveoli to blood than CO2 is released. This creates a pressure gradient from atmosphere to alveoli. PaCO2 and PACO2 will equilibrate. PEEP would help facilitate oxygenation, since patent airways are a prerequisite for apneic oxygenation. It wouldn't have any effect on CO2 because there is no ventilation in AO. CO2 will continue to rise (~6 mmHg the first minute, ~3 mmHg/min thereafter.).

 

[RxBoy]

Apneic oxygenation works because more O2 is absorbed from alveoli to blood than CO2 is released. This creates a pressure gradient from atmosphere to alveoli. PaCO2 and PACO2 will equilibrate. PEEP would help facilitate oxygenation, since patent airways are a prerequisite for apneic oxygenation. It wouldn't have any effect on CO2 because there is no ventilation in AO.

My question was why isn't the reverse true. I understand you have to ventilate to expel CO2 but my original question is why.... But I found the answer. I was thinking too deep into it... Its actually much more simple then I thought:

"Air Flow: Air will flow from an area of higher pressure to one of lower pressure; during inspiration, the pressure in the alveoli must be less than the pressure at the mouth for air to flow in, and during expiration, the reverse is true."

In apneic oxygenation you are creating a prolonged and sustained inspiration by providing a high inflow pressure which traps CO2 from going in the opposite direction, even though there is a CO2 gradient from alveoli to atmospheric air. I guess the reverse of apneic oxygenation would be hooking up suction (vacuum) to an ET tube which would result in apenic CO2 elimination but obviously this would eventually collapse the alveoli in which there be no gas exchange. THat is of course if hypoxia doesn't kill the patient first.


Sevo thanks for the PEEP explanation makes sense.

 

[proman]

My question was why isn't the reverse true. I understand you have to ventilate to expel CO2 but my original question is why.... But I found the answer. I was thinking too deep into it... Its actually much more simple then I thought:

"Air Flow: Air will flow from an area of higher pressure to one of lower pressure; during inspiration, the pressure in the alveoli must be less than the pressure at the mouth for air to flow in, and during expiration, the reverse is true."

In apneic oxygenation you are creating a prolonged and sustained inspiration by providing a high inflow pressure which traps CO2 from going in the opposite direction, even though there is a CO2 gradient from alveoli to atmospheric air. I guess the reverse of apneic oxygenation would be hooking up suction (vacuum) to an ET tube which would result in apenic CO2 elimination but obviously this would eventually collapse the alveoli in which there be no gas exchange. THat is of course if hypoxia doesn't kill the patient first.


Sevo thanks for the PEEP explanation makes sense.

Despite what the thoracic surgeons think, suction to a non ventilated lung doesn't cause atelactasis faster than simple isolation. The reason is because the small airways collapse under the negative pressure within a minute and obstruct active removal by the suction catheter. 100% oxygen or high concentration of nitrous are faster.

 

[nap$ter]

Question:

Why is there no CO2 exchange through the anatomical dead space from alveoli to atmospheric air without the expiratory recoil of alveoli?

--- there is co2 exchange during apnea. recoil has nothing to do with it. you are assuming that all co2 exchange is measured by etco2 - but this is not so. at high flows during apnea you may not see etco2 - but co2 is being exchanged and removed.

whether this "ventilation" is sufficient - that is the question. depends on peep, flow, CO, co2 production, etc. 2nd question is how to monitor adequacy of ventilation in the absence of reliable etco2 measurements. there is no continuous measurement of paCO2, yet.

continuous flow apneic oxygenation (CFAO) is well described in the anesthesia literature.

continuous flow apneic ventilation (CFAV) is better described in the physiology literature - the paper below is a good starting point.

Anesthesiology. 1986 Oct;65(4):399-404.
Continuous-flow apneic ventilation during thoracotomy.

Babinski MF, Smith RB, Bunegin L.

 

[nap$ter]

Apneic oxygenation works because more O2 is absorbed from alveoli to blood than CO2 is released. This creates a pressure gradient from atmosphere to alveoli. PaCO2 and PACO2 will equilibrate. PEEP would help facilitate oxygenation, since patent airways are a prerequisite for apneic oxygenation. It wouldn't have any effect on CO2 because there is no ventilation in AO. CO2 will continue to rise (~6 mmHg the first minute, ~3 mmHg/min thereafter.).

this is not quite correct. there is "ventilation" during AO - the "ventilation" (elimination of co2) depends (slightly) on the amount of flow. the anesthesiologist's definition of ventilation (RR x TV) is too simplistic. the physiologist's definition is a bit better - elimination of CO2..

ie during apnea in a paralyzed patient if you clamp the ett co2 will rise more quickly then in the same patient with a flow of 10L/min.

 

[RxBoy]

continuous flow apneic ventilation (CFAV) is better described in the physiology literature - the paper below is a good starting point.

Anesthesiology. 1986 Oct;65(4):399-404.
Continuous-flow apneic ventilation during thoracotomy.

Babinski MF, Smith RB, Bunegin L.

Wow. I had a hunch that CO2 must be able to diffuse out whether recoil occurred or not. According to this paper its only possible with endobronchial intubation because there needs to be high turbulance/flow that reaches deep peripheral lung tissue + possibly cardiac oscillations to assist in dead space mixing (like a natural mini High Frequency Oscillatory Ventilator). Natural CO2 elimination, at least to a clinical extent does not seem possible with simple endotracheal intubations.

What still boggles my mind is how does the CO2 diffuse out after leaving the alveoli? The ET tube that held the 2 bronchial tubes was even cuffed. Maybe CO2 diffuses around the cuff (as the cuff is designed to prevent liquid and tube movement not total gas trapping on the molecular level) and this is why EtCO2 monitor is unable to process it. Or maybe it actually diffuses against the incoming flow itself like you said and these high flows mask the CO2 diffusion by EtCO2 monitoring. Seeing as I am not a physicist, I don't know enough about molecular diffusion (http://en.wikipedia.org/wiki/Molecular_diffusion).

In any case, that was a great article. Goes against everything we're taught about "ventilation" but makes much more sense.