pulmonary question

[forbes270]

guys could someone explain how preoxygenation with 100% oxygen before induction and during induction of anesthesia causes atelectasis??

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[Noyac]

guys could someone explain how preoxygenation with 100% oxygen before induction and during induction of anesthesia causes atelectasis??

100% O2 means no nitrogen. The O2 gets completely absorbed and therefore the alveoli collapses since there is no N to keep it open.

 

[veetz]

guys could someone explain how preoxygenation with 100% oxygen before induction and during induction of anesthesia causes atelectasis??

Nitrogen is highly insoluble in blood and therefore tends to reside in high concentration in the alveoli, thereby helping to keep them open. 100% O2, which is readily taken up in the blood, washes out (i.e. decreases) nitrogen in the alveoli and can accelerate collapse of alveoli. There are other factors that contribute to atelectasis with general anesthesia, but high inspired O2 concentrations tend to exacerbate formation of atelectasis.

http://www.anesthesia-analgesia.org/cgi/content/full/95/6/1777

 

[cchoukal]

What the others have said, but not quite said, is that the alveoli need to be filled with gas in order to stay open. Oxygen in an alveolus is taken up into the pulmonary circulation, but nitrogen, being insoluble, is not. Ergo, if all the gas in the alveolus is oxygen (as in the case of a high fraction of inspired oxygen), all of the gas will be taken up, leaving the alveolus empty and, therefore, collapsed.

 

[pgg]

One thing to keep in mind is that for absorption atelectasis to occur, those alveoli need to be distal to small airways that are closed. Anesthesia, the supine position, obesity, and other factors can decrease FRC while increasing closing volume. To minimize the impact of these factors, there are a couple things you can do while preoxygenating.

- don't go completely supine to preO2, elevate the back a little (or a lot)

- set the APL to 5 or so, a bit of CPAP is not uncomfortable for the patient and it will improve FRC/CV

Also worth clarifying that atelectasis can occur with low FiO2 also. N2 will also be absorbed if those alveoli are isolated by closed small airways. O2 is just a lot mor soluble so it happens faster.

 

[pgg]

http://www.anesthesia-analgesia.org/cgi/content/full/95/6/1777

This study addresses slightly different circumstances - postoperative atelectasis after extubation on 100% O2. In this case the patient doesn't have any ventilatory support, and atelectasis (with or without 100% O2) is likely to occur fast enough to be seen in the PACU, if you look for it. Most of these patients, 100% O2 or not, are going to develop atelectasis postop anyway ... just a bit slower if they're on room air.

Intraop, with PPV and appropriate PEEP (or CPAP in the spontaneously breathing patient), absorption atelectasis is typically not going to occur.

100% O2 doesn't cause atelectasis, it just hastens it in patients who are set up to get it anyway. This may be clinically significant in the PACU where patients still have some residual anesthesia to contend with. Intraop lots of us use high FiO2s routinely and we just don't see problems with atelectasis (with appropriate vent settings).

 

[militarymd]

hmm...

we consume about 200 ml of oxygen a minute...probably less under GA...

our lungs are what? 5 liters in volume...

and we ventilate....ie push air into and out of the lungs at 5 liters a minute....

Hard for me to imagine that 4% absorption of volume is going to cause any appreciable atelectasis.

 

[Planktonmd]

Obviously you don't understand the physiology here! (no surprise)
Under anesthesia and in the supine position there are areas of the lungs that simply do not get any ventialtion because of decreased FRC and increased closing volume.
The alveoli in these non ventilated areas could remain open if they contained nitorogen since that nitrogen will not get absorbed, but if you remove the nitrogen and replace it with 100 % oxygen during preoxygenation (while these areas were still getting ventilated), then these alveoli are going to collapse and create atelectasis later when they are no longer ventilated, because 100% of their gas content is going to get absorbed.
Makes sense now genius?

hmm...

we consume about 200 ml of oxygen a minute...probably less under GA...

our lungs are what? 5 liters in volume...

and we ventilate....ie push air into and out of the lungs at 5 liters a minute....

Hard for me to imagine that 4% absorption of volume is going to cause any appreciable atelectasis.

 

[militarymd]

hmm...

we consume about 200 ml of oxygen a minute...probably less under GA...

our lungs are what? 5 liters in volume...

and we ventilate....ie push air into and out of the lungs at 5 liters a minute....

Hard for me to imagine that 4% absorption of volume is going to cause any appreciable atelectasis.

and don't forget about the respiratory quotient....between 1.2 and 0.8...

meaning for every molecule of oxygen absorbed....we are releasing between 1.2 to 0.8 molecules of carbon dioxide into the lungs....



A good cough at the wrong time during emergence will collapse a BIG pulmonary segment....

give a stick of propofol...and all the posterior segments collapse....

Some myths just go on and on and on.....

 

[Planktonmd]

You still don't get it do you?
To keep the non ventialted alveoli open they need to be filled with a gas that can not be easilly absorbed into the circulation.
Oxygen and CO2 both are highly absorbable.

and don't forget about the respiratory quotient....between 1.2 and 0.8...

meaning for every molecule of oxygen absorbed....we are releasing between 1.2 to 0.8 molecules of carbon dioxide into the lungs....



A good cough at the wrong time during emergence will collapse a BIG pulmonary segment....

give a stick of propofol...and all the posterior segments collapse....

Some myths just go on and on and on.....

 

[cfdavid]

Good question OP. Also, thanks to the contributors. I need to start thinking about basic physio again....

cf

 

[pgg]

The alveoli in these non ventilated areas could remain open if they contained nitorogen since that nitrogen will not get absorbed

Nitrogen will be absorbed from isolated alveoli ... just not as quickly as oxygen. Think back to the last time you suffered through a surgical ward month. Every single one of those postop patients breathing room air had some degree of atelectasis on POD 1.

 

[pgg]

and don't forget about the respiratory quotient....between 1.2 and 0.8...

meaning for every molecule of oxygen absorbed....we are releasing between 1.2 to 0.8 molecules of carbon dioxide into the lungs....

I don't think that's really relevant here, for the same reason that people who are mainstemmed get hypoxic before they get hypercarbic. CO2 is so much more soluble than either O2 or N2 that it's not going to accumulate in isolated alveoli, it'll just get back in the blood and be expired elsewhere in the lung.

But I agree with your basic point that absorption atelectasis is clinically irrelevant unless you do something to really ask for it.

 

[militarymd]

I don't think that's really relevant here, for the same reason that people who are mainstemmed get hypoxic before they get hypercarbic. CO2 is so much more soluble than either O2 or N2 that it's not going to accumulate in isolated alveoli, it'll just get back in the blood and be expired elsewhere in the lung.

But I agree with your basic point that absorption atelectasis is clinically irrelevant unless you do something to really ask for it.

Gases don't dissolve AGAINST a partial pressure gradient.

venous CO2 partial pressure is 50 to 60 mmHg

arterial CO2 partial pressure is 35 to 45 mmHg

What that means...is that in any particular alveoli...carbon dioxide will only be absorbed until the partial pressure of CO2 in the alveoli drops to, at the lowest 35 mmhg...

same applies to oxygen...you can't absorb oxygen until the partial pressure is ZERO....which is what everyone is implying with "collapse"...the LOWEST possible is what ever pO2 is...usually around 100 mmHg + 40 mmHg of CO2.....plus water vapor.....so AT the minimum....around 200 mHg of gas pressures in the alveoli....or around 25% of initial volume....IF nothing else was going on.l.....ie ventilation...

Collapse occurs..but it's not from the so called absorption atelectasis....

 

[Planktonmd]

True, Nitorgen gets absorbed slower (much slower).
And if these alveoli by the end of the anesthetic are still "isolated" because the FRC is still low and the closing volume is still high because of postop pain and splinting then sure these alveoli are going to collapse regardless of what gas they contain.
But we still need to understand the physiology and do our best to minimize these atelectasis.

Nitrogen will be absorbed from isolated alveoli ... just not as quickly as oxygen. Think back to the last time you suffered through a surgical ward month. Every single one of those postop patients breathing room air had some degree of atelectasis on POD 1.

 

[Planktonmd]

Alveoli are like bubbles, they remain open as long as the pressure inside equals the surface tension that is trying to collapse them.
Surfactant helps in maintaining this balance.
So you don't need the gas content to go down to ZERO for the alveoli to collapse, all you need is for that gas pressure inside to decrease under the surface tension.
Got it?

you can't absorb oxygen until the partial pressure is ZERO....which is what everyone is implying with "collapse"...the LOWEST possible is what ever pO2 is...usually around 100 mmHg + 40 mmHg of CO2.....plus water vapor.....so AT the minimum....around 200 mHg of gas pressures in the alveoli....or around 25% of initial volume....IF nothing else was going on.l.....ie ventilation...

Collapse occurs..but it's not from the so called absorption atelectasis....

 

[pgg]

same applies to oxygen...you can't absorb oxygen until the partial pressure is ZERO....which is what everyone is implying with "collapse"...

With absorption atelectasis, the partial pressure of oxygen in the alveoli is minimally change, at least initially. The volume of the alveolus decreases as O2 is absorbed.

Consider a cluster of alveoli have a combined volume of 1 mL and you fill them with 100% oxygen at 730 mmHg ... with maybe 30 of water vapor. There is an A-a gradient here driving O2 into the blood. In x amount of time, if half of that oxygen is absorbed (as it will be if there's no ventilation of those alveoli), the volume of those alveoli is now 0.5 mL but the partial pressure of the O2 is still 730 mmHg.

Meanwhile, perhaps some CO2 diffuses into those alveoli ... approaching the 50-60 mmHg level you referenced in your post. So now maybe you've got roughly 0.55 mL of O2 and CO2 with the O2 partial pressure around 670 and CO2 around 60. Roughly.

There's STILL a pressure gradient here driving O2 into the blood ... and there will be until the great majority of the O2 has been absorbed.

Y minutes later, more O2 has been absorbed. Now the alveoli might be 0.2 mL ... but the partial pressure of oxygen is still 670 and CO2 (which is at equilibrium) is still at 60.


Point being, absorption atelectasis doesn't violate any laws of physics. That doesn't make it clinically significant though ...

At least, that's my understanding of it, and if I'm wrong, I'd like to learn why.

 

[militarymd]

With absorption atelectasis, the partial pressure of oxygen in the alveoli is minimally change, at least initially. The volume of the alveolus decreases as O2 is absorbed.

Consider a cluster of alveoli have a combined volume of 1 mL and you fill them with 100% oxygen at 730 mmHg ... with maybe 30 of water vapor. There is an A-a gradient here driving O2 into the blood. In x amount of time, if half of that oxygen is absorbed (as it will be if there's no ventilation of those alveoli), the volume of those alveoli is now 0.5 mL but the partial pressure of the O2 is still 730 mmHg.

Meanwhile, perhaps some CO2 diffuses into those alveoli ... approaching the 50-60 mmHg level you referenced in your post. So now maybe you've got roughly 0.55 mL of O2 and CO2 with the O2 partial pressure around 670 and CO2 around 60. Roughly.

There's STILL a pressure gradient here driving O2 into the blood ... and there will be until the great majority of the O2 has been absorbed.

Y minutes later, more O2 has been absorbed. Now the alveoli might be 0.2 mL ... but the partial pressure of oxygen is still 670 and CO2 (which is at equilibrium) is still at 60.


Point being, absorption atelectasis doesn't violate any laws of physics. That doesn't make it clinically significant though ...

At least, that's my understanding of it, and if I'm wrong, I'd like to learn why.

200 ml per minute is how much oxygen is absorbed.....spread over 5 liters of lung volume....

with the partial gas laws that can not be violated....

along with just simple experience with critically ill patients on varying amounts of oxygen, peep, and seeing their CT scans...

Myth.

 

[Planktonmd]

Some people are confused about how the alveoli react to changing volume: always think about the example of a soap bubble.
When the pressure inside the bubble decreases initially the bubble shrinks until it reaches a certain breaking point where it just collapses, it does not keep shrinking to zero as some people might be imagining.
So you don't need to have the alveoli completely empty for them to collapse, all you need is for the gas content to go under a critical value.
This is why absorption atelectasis are real and they happen all the time.
The clinical importance or significance of absorption atelectasis is relative to the underlying pulmonary function, so a patient who has marginal lungs to start with might not tolerate any aditional atelectasis.
Also atelectasis in general could become infected and become a very "clinically significant" pneumonia.

 

[hoyden]

Obviously you don't understand the physiology here! (no surprise)
Under anesthesia and in the supine position there are areas of the lungs that simply do not get any ventialtion because of decreased FRC and increased closing volume.
The alveoli in these non ventilated areas could remain open if they contained nitorogen since that nitrogen will not get absorbed, but if you remove the nitrogen and replace it with 100 % oxygen during preoxygenation (while these areas were still getting ventilated), then these alveoli are going to collapse and create atelectasis later when they are no longer ventilated, because 100% of their gas content is going to get absorbed.
Makes sense now genius?

except that if absorption athelectasis happens to the alveoli that are in non ventilated areas HOW does 100% O2 get there in the first place? And if it gets there to wash out the N2 why can't it get there after that as well?

Obviously I know the whole concept of 100% O2 and absorption athelectasis... I just happen to not 100% believe it because the ends do not meet in this concept.

 

[Planktonmd]

You preoxygenate while the patient is still awake and breathing spontaneously so these dependent areas of the lungs can still be ventilated, then when you induce anesthesia and switch to PPV the ventilation-perfusion distribution pattern changes and some areas that have become full of 100% O2 during preoxygenation will now become non ventilated and eventually collapse.

except that if absorption athelectasis happens to the alveoli that are in non ventilated areas HOW does 100% O2 get there in the first place? And if it gets there to wash out the N2 why can't it get there after that as well?

Obviously I know the whole concept of 100% O2 and absorption athelectasis... I just happen to not 100% believe it because the ends do not meet in this concept.

 

[hoyden]

You preoxygenate while the patient is still awake and breathing spontaneously so these dependent areas of the lungs can still be ventilated, then when you induce anesthesia and switch to PPV the ventilation-perfusion distribution pattern changes and some areas that have become full of 100% O2 during preoxygenation will now become non ventilated and eventually collapse.

see, what is confusing is the proportion of this collapsed alveoli and also the rate by which they are collapsing ( both disputed already by other forum members) and therefore clinical significance of the process.
Anyway, thanks for the input and - Merry Christmas!

 

[Planktonmd]

I partially agree on the clinical significance part of the discussion because absorption atelelctasis are only one factor in the formation of perioperative atelectasis and compression atelectasis seem to play a more significant role here (clinically speaking).
But I disagree with saying that absorption atelectasis are a "myth", because they are not.
Merry Christmas to you too.

see, what is confusing is the proportion of this collapsed alveoli and also the rate by which they are collapsing ( both disputed already by other forum members) and therefore clinical significance of the process.
Anyway, thanks for the input and - Merry Christmas!

 

[DScully]

But I disagree with saying that absorption atelectasis are a "myth", because they are not.

Just out of curiosity, is there a way to measure / determine the level of atelectasis? Whether it is absorption or compression?

And I assume that we still pre-oxygenate pts because the benefit of SaO2 100%
is greater than the amount of atelectasis it inevitably creates?

 

[pgg]

Just out of curiosity, is there a way to measure / determine the level of atelectasis? Whether it is absorption or compression?

I guess if you really wanted to, in order to satisfy your curiosity, and you didn't mind sending off a couple of ABGs, you could calculate a shunt fraction before & after preoxygenation (but before induction). Increasing the area that's perfused but not ventilated is what atelectasis and small airway collapse does so that should be reflected in the shunt fraction.

You can do the math, or just consult a nomogram. And I bet you wouldn't measure much of a difference.

And I assume that we still pre-oxygenate pts because the benefit of SaO2 100%
is greater than the amount of atelectasis it inevitably creates?

Yes. Most of us who believe absorption atelectasis exists under certain circumstances also believe that it is clinically irrelevant unless you go out of your way doing dumb things to create it. Ordinary preoxygenation is not going to cause problems.

 

[DScully]

I guess if you really wanted to, in order to satisfy your curiosity, and you didn't mind sending off a couple of ABGs, you could calculate a shunt fraction before & after preoxygenation (but before induction).

Interesting. So theoretically speaking, you can do a study to find the "optimal" percentage of O2 for pre-oxygenation to maximize the benefits and risks (if any) with such measures (eg. repeated ABGs). Though it will probably not clinically significant....