Nitrous oxide in the setting of pneumothorax...

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deleted9493

So this specific explanation of avoiding the use of nitrous oxide in conditions involving compliant, air-filled cavities (e.g. pneumothorax, intestinal obstruction, blebs etc.) has vexed me and I cannot come to the end of it.

If a higher blood:gas coefficient translates into higher concentrations of that gas in the blood, why is it that nitrous oxide causes a problem if it does in fact have a 34x greater blood:gas partition coefficient than nitrogen? It seems to me that Nitrogen (b:g of 0.014) would tend to remain in the cavity and Nitrous oxide (b:g of 0.46) would have a much smaller tendency for that space. Where am I going wrong in my thinking of this?


I appreciate the insight of all you gas sages here.

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Where are the big macho know-it-all guys now?

How come you are better at talking about CRNA's than at gas physics?
 
My understanding (lowly MS4 here) is that because of the 34x higher blood:gas coefficient, nitrous oxide is going to diffuse into the cavity 34x faster than nitrogen would. It's not an issue of what the equilibrium state is between alveolar gas, blood, and the air cavity, but the rate at which that equilibrium is approached.
 
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If a higher blood:gas coefficient translates into higher concentrations of that gas in the blood, why is it that nitrous oxide causes a problem if it does in fact have a 34x greater blood:gas partition coefficient than nitrogen? It seems to me that Nitrogen (b:g of 0.014) would tend to remain in the cavity and Nitrous oxide (b:g of 0.46) would have a much smaller tendency for that space. Where am I going wrong in my thinking of this?
.

In order to get into the cavity, the gas must first get into the bloodstream so it can be transported there. That is why N2O will fill up a pneumo or other badness faster. Nitrogen tends to stay in the alveolus where it does not cause problems.
 
In order to get into the cavity, the gas must first get into the bloodstream so it can be transported there. That is why N2O will fill up a pneumo or other badness faster. Nitrogen tends to stay in the alveolus where it does not cause problems.


I hear you, man and I definitely think that this is a spot on explanation for the expansion of a pneumothorax.

What of this explanation that Miller gives in Basics of Anesthesia that Nitrous has a 34x greater proclivity for the cavity than does Nitrogen? Based on the blood:gas coefficients, this explanation is entirely backwards. Even though it is a relatively insoluble anesthetic, Nitrous oxide is still much more soluble in blood than is Nitrogen. So I don't know how he arrives at that explanation.
 
In order to get into the cavity, the gas must first get into the bloodstream so it can be transported there. That is why N2O will fill up a pneumo or other badness faster. Nitrogen tends to stay in the alveolus where it does not cause problems.

Would you care to explain how come Desflurane, having almost the same blood:gas coefficient as nitrous, does not expand a pneumo? After you are done with that, explain how come Halothane, having a blood:gas coefficient much higher than nitrous, does not expand a pneumo.

Thanks!
 
Where are the big macho know-it-all guys now?

How come you are better at talking about CRNA's than at gas physics?

Really? The big boys know the facts about GAS as well:

British Journal of Aneasthesia Vol. 87 Number 6 pages 894-896
ACTA Anaesthesiol Scand 2004 August 48 (7) 894-898
Anesthesiology 2001 March; 94 (3) 475-7
LANDMARK STUDY: Anesthesiology 1965 Jan-Feb;26:61-6 (EGER)

There is more at play than just blood gas solubility as the British Journal article points out.
Please pull up these studies as they are avail. free via the web.

Blade
 
British Journal of Aneasthesia Vol. 87 Number 6 pages 894-896
ACTA Anaesthesiol Scand 2004 August 48 (7) 894-898
Anesthesiology 2001 March; 94 (3) 475-7

Good articles but they don't really answer the question at hand.
 
Would you care to explain how come Desflurane, having almost the same blood:gas coefficient as nitrous, does not expand a pneumo? After you are done with that, explain how come Halothane, having a blood:gas coefficient much higher than nitrous, does not expand a pneumo.

Thanks!

Eger looked at Halthane and Nitrous Oxide in 1965. Read the landmark article for his answer.
 
Eger looked at Halthane and Nitrous Oxide in 1965. Read the landmark article for his answer.

Eger's Answer:

It is obvious from figure 2 that they apply to any relatively SOLUBLE GAS used in concentrations exceeding 40 to 50%. Thus, ethylene or xenon should produce (see my other studies for proof that they do) the above phenomena while the more POTENT ANESTHETICS requiring less concentrations such as halothane,.... should not. It also may be predicted according to figure 2 that at concentrations exceeding 80% the phenomenon of gas pocket expansion is markedly exaggerated.


Blade
 
Eger's Answer:

It is obvious from figure 2 that they apply to any relatively SOLUBLE GAS used in concentrations exceeding 40 to 50%. Thus, ethylene or xenon should produce (see my other studies for proof that they do) the above phenomena while the more POTENT ANESTHETICS requiring less concentrations such as halothane,.... should not. It also may be predicted according to figure 2 that at concentrations exceeding 80% the phenomenon of gas pocket expansion is markedly exaggerated.

He is just assuming from nitrous' chart, how halothane's chart would be. That does not seem very scientific. I would like hard evidence.
 
He is just assuming from nitrous' chart, how halothane's chart would be. That does not seem very scientific. I would like hard evidence.

Urge,

I am not sure why you want to continue this any further. Eger in 1965 combined with the other studies I listed pretty much answered the original poster's question. I attempted to answer yours as well. Here is another ancient study where they looked at N20 vs. Halothane at gut expansion.

Canad. Anesth Soc. journal, Vol. 22 No. 2 March 1975 200-202

This study found that the gut expanded a lot with N20 and very little with Halothane. Do you want more evidence? Why?

Blade
 
http://web.squ.edu.om/med-Lib/MED_CD/E_CDs/anesthesia/site/content/v02/020075r00.HTM

These spaces normally contain nitrogen (from air), a gas whose low solubility (blood/gas partition coefficient, 0.015) limits its removal by blood. Thus, the entrance of nitrous oxide (whose solubility permits it to be carried by blood in substantial quantities) is not countered by an equal loss, and the result is an increase in volume.
 
It seems to me that Nitrogen (b:g of 0.014) would tend to remain in the cavity and Nitrous oxide (b:g of 0.46) would have a much smaller tendency for that space. Where am I going wrong in my thinking of this?

This of it in terms of osmotic pressures. You have a container with a partition. On side A you pump in 50% Nitrogen; on the other side, B, you pump in 50% N2O. Assume the partition is 34x more soluble for N20. The nitrous will attempt to have equal concentration on both sides: solutes are driven by equalization of concentrations as well as pressures. The nitrogen will attempt to do the same. However, because of the greater ease the nitrous moves across the membrane cavity, side A with the nitrogen will swell with nitrous. The nitrous will try to mimic the 50% concentration of side B on side A, and will do this by doubling the volume.

(equal Volume of N20)/(stuff in A + equal volume N20) = 1vol/(1vol + 1vol) = 50% Concentration of N20,

where the volume of the stuff in A = volume of pure N20

Side B will by unchanged if the membrane does not allow the nitrogen to come across with any ease. While Desflurane has a similar blood:gas coefficient, such low concentration are used that there is no significant volume-filling effect.
 
the real world answer is to not use Nitrous in the first place. It causes PONV, suppresses immune system function, impairs wound healing, and supresses bone marrow.
 
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