Fatties and anesthesia

[epidural man]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

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[dhb]

Can't think of a more ******ed concept than weight loss surgery:
We'll cut out half your gut so you don't absorb all the crap you eat

 

[Robotic Wis-Hipple]

In these patients I always want to see a pulse ox in preop. I'd bet they aren't sitting at 95-100% supine/semi-recumbent at rest.

But of course you have to rule out badness, find the mode on whatever vent you have that provides the best volume/pressures for them, and roll with it.

 

[G-Man82]

I would have had the peep much higher. Quite often I start these patients at 15 of peep. The peak pressures don't matter as much; it's the transpulmonary pressures that really matter (Plateau - pleural). For these kinds of patients, their chest wall compliance will be quite different and a lot of the pressure being delivered dissipates as it moves the chest wall, before adding to ventilation.

A rule of thumb I've learned is that an acceptable plateau pressure, if you don't have a good way to measure pleural pressures (e.g. esophageal probe), is equal to BMI. In these patients you're probably safe going over the usual 40.

Look at ARDS high peep ladder - can go as high as 24 in those patients. As long as volumes remain protective and your driving pressure is acceptable, the risk of volu- or barotrauma is low. So far I've had no problems.


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[Iso4ane]

I would have had the peep much higher. Quite often I start these patients at 15 of peep. The peak pressures don't matter as much; it's the transpulmonary pressures that really matter (Plateau - pleural). For these kinds of patients, their chest wall compliance will be quite different and a lot of the pressure being delivered dissipates as it moves the chest wall, before adding to ventilation.

Only a CA-1, but one of my attending often stresses the first two/three points. Another way to think about is you lungs are like balloons. If you compare a balloon in room air with one underwater, the one surrounded by water requires a lot more pressure to reach the limit of distensibility before it pops. (And for lap cases, you know insufflation is going to be at 15cmH20, so I have seen some advocate starting PEEP at 15)

The extreme case where this comes into play is robotic gyn cases. Not only is that patient population on the larger end, but then are sitting on on their head in severe Trednelenburg, for HOURS. You bet I turn up that PEEP and high pressure alarm.

 

[deleted697127]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

Not to be a dick and you probably meant this but: *you didn't see a pneumothorax on ultrasound. You did not rule it out.

 

[Ezekiel2517]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

something seems off about this case. I've managed patients for cases like this with BMI's well over 50's and have never had this problem. These pts are usually otherwise healthy with good cardiac and pulmonary function. With the patient in reverse trend and paralyzed and on high FiO2, you should be able to get much better volumes and sats than 400 and 90% with those kind of peak pressures. Even with laparoscopic cases I've done with pts with BMI of 60's in steep trendelenberg, I've not had issues with sats. Hard to say what the problem was, but something unusual more than just atelectasis is going on here.

 

[Planktonmd]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

Peek pressure of 40 is too conservative in this population if you are using volume control ventilation, another option is to use pressure control and try to titrate the pressure to obtain a tidal volume around 600 ml. This would also give a better plateau pressure without a high peek pressure that is usually useless.

 

[pjl]

Peek pressure of 40 is too conservative in this population if you are using volume control ventilation, another option is to use pressure control and try to titrate the pressure to obtain a tidal volume around 600 ml. This would also give a better plateau pressure without a high peek pressure that is usually useless.

Definitely use PC, or the vol af/PRVC modes on the machine.


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[G-Man82]

I would argue that there really is no difference between PC and VC. Just set the pressure limits higher in this situation. Again, the PIPs are of little clinical value here. It's all about the pressure "seen" by the alveoli.

Also .... you could just accept some hypercapnia if it lets you avoid the high tidal volumes.


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[jthedestroyr]

1)Pressure control vol guaranteed mode FTW

2)adjust peep as necessary, we start higher as suggested above.

We have a lot of large ppl in my institution. BMI 40-50 is pretty much the norm and we dont seem to have issues.

 

[Ronin786]

I:E ratio. Always amazes me how little people mess with this. In obese patients without underlying lung issues, a 1:1 ratio can do wonders to your peak pressures and tidal volumes.

I know tidal volumes aren't supposed to affect oxygenation, but if all you're ventilating is anatomical dead space then you're not going to exchange oxygen either.

 

[Hoya11]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

Agree with what others have said.

In the end the only way to really increase oxygenation is PEEP and FiO2. SO keep them on 100% and play with the PEEP to optimize sat.

I would worry that with a 1:1 ventilation ratio and steep tberg and a fat patient that they would not have enough E time and start retaining CO2..

I had a case on fatty the other day and the pulse ox was consistently in the 80s. Good wave form, 3 asterix on the screen, no "low signal quality" warning. However we had an aline and the PaO2 was always 150-200. Anyone have that experience? It has made me consider checking an ABG when sats are low and I cant figure out why..

 

[partydoc]

I had a case on fatty the other day and the pulse ox was consistently in the 80s. Good wave form, 3 asterix on the screen, no "low signal quality" warning. However we had an aline and the PaO2 was always 150-200. Anyone have that experience? It has made me consider checking an ABG when sats are low and I cant figure out why..

I've had this happen before where the pulse ox gets pulled on the finger and is sitting a little sideways. Good waveform, good pao2. The ambient light that finds its way in drags the reading closer to 85

 

[cleansocks]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

How did you confirm being above carina?

 

[nimbus]

How did you confirm being above carina?

There's only one way....bronch.

 

[Noyac]

When Sats are crappy put a probe on the ear. It is always at least a few points higher.

 

[pgg]

There's only one way....bronch.

Auscultation?

 

[Noyac]

I would worry that with a 1:1 ventilation ratio and steep tberg and a fat patient that they would not have enough E time and start retaining CO2..

Sorry but I'm not following this logic. I would think that the Tberg would assist expiration.
But the decreased expiratory time would hinder it.
I worry about auto-peep in this case, not so much about CO2 retention. But if the expiratory wave form is flat I'm pretty sure there isn't auto-peep.

 

[Noyac]

I just finished a case from last night that fit in this thread. I was all ready for war but it never happened. BMI >50 for laparoscopic LSO 2nd to torsion. She ended up also having a large colon mass and gen surg was called in.
HTN and subaortic stenosis.

Sats were 100% for the majority of the case. Lowest was 98% until I was waking her up and then they dropped to 94% for a minute or less. I thought is was gonna be worse. Didn't even have to use the ear probe.

Another thing that drives me nuts is when people try to use the extra large BP cuff on these pts with cone shaped arms. They never stay in place. I just put a regular cuff on the forearm. Problem solved.

 

[deleted162650]

Expiration and short E times are just not a problem in these pts. There's so much mass in the chest wall that air is rapidly/forcibly exhaled. It's pretty much the exact opposite problem you see in emphysema where the lungs are very compliant on inhalation but there's no elasticity left to push air out on the exhale. Those are the pts that can breath stack/auto peep but even then it's pretty rare.

 

[jthedestroyr]

Another thing that drives me nuts is when people try to use the extra large BP cuff on these pts with cone shaped arms. They never stay in place. I just put a regular cuff on the forearm. Problem solved.

Yes x1000 !! They never fit well. I just use the "regular arm cuff size" on fore arm as well. When i get a skinny patient that i van actually out a normal BP cuff on without issues, its like hitting the jack pot!!

 

[Hoya11]

Sorry but I'm not following this logic. I would think that the Tberg would assist expiration.
But the decreased expiratory time would hinder it.
I worry about auto-peep in this case, not so much about CO2 retention. But if the expiratory wave form is flat I'm pretty sure there isn't auto-peep.

With 1:1 ventiltation I would worry about CO2 retention, autopeep, and expiratory wave form not returning to baseline. Regardless of position. I would worry more about these things than any miniscule oxygenation benefit. I would stick to adjusting PEEP and maximizing Fio2 while assuring my vent setting had the exp wave returning to baseline and no upsloping Co2 curve.

With a fat patient in Tberg, Im going to have high peak pressures (40-50), which means im going to have relatively low TVs (400-600), which means Im going to have a high resp rate (~16-20) to maintain MV... which means my I:E time really matters and even more chance to have that wave form not return to baseline and start the process of inadequate exhalation, auto-peep, co2 retention. This in probably in addition to a set peep of 5-10. I would worry that autopeep plus set peep would push me beyond optimal peep and actually hinder oxygenation

 

[nimbus]

With 1:1 ventiltation I would worry about CO2 retention, autopeep, and expiratory wave form not returning to baseline. Regardless of position. I would worry more about these things than any miniscule oxygenation benefit. I would stick to adjusting PEEP and maximizing Fio2 while assuring my vent setting had the exp wave returning to baseline and no upsloping Co2 curve.

With a fat patient in Tberg, Im going to have high peak pressures (40-50), which means im going to have relatively low TVs (400-600), which means Im going to have a high resp rate (~16-20) to maintain MV... which means my I:E time really matters and even more chance to have that wave form not return to baseline and start the process of inadequate exhalation, auto-peep, co2 retention. This in probably in addition to a set peep of 5-10. I would worry that autopeep plus set peep would push me beyond optimal peep and actually hinder oxygenation

All our machines have spirometry. You can see it immediately if there is breath stacking and I've never seen it even with high RR high peep and I:E 1:1.

 

[Ronin786]

With 1:1 ventiltation I would worry about CO2 retention, autopeep, and expiratory wave form not returning to baseline. Regardless of position. I would worry more about these things than any miniscule oxygenation benefit. I would stick to adjusting PEEP and maximizing Fio2 while assuring my vent setting had the exp wave returning to baseline and no upsloping Co2 curve.

With a fat patient in Tberg, Im going to have high peak pressures (40-50), which means im going to have relatively low TVs (400-600), which means Im going to have a high resp rate (~16-20) to maintain MV... which means my I:E time really matters and even more chance to have that wave form not return to baseline and start the process of inadequate exhalation, auto-peep, co2 retention. This in probably in addition to a set peep of 5-10. I would worry that autopeep plus set peep would push me beyond optimal peep and actually hinder oxygenation

Lower I:E ration means you can deliver larger tidal volumes at the same peak pressures. You don't need as fast a rate as a result.

 

[pgg]

All our machines have spirometry. You can see it immediately if there is breath stacking and I've never seen it even with high RR high peep and I:E 1:1.

Agree, I've had the same experience. I often change the I:E from the default 1:2 to 1:1.5 or 1:1.

Breath stacking shouldn't be a problem in patients who are only obese, i.e. have a restrictive pattern to their pulmonary function. And I can't say I've ever witnessed it in these patients, unless they also had obstructive disease. And in truth you can usually get away with 1:1 even in COPD'ers, just have to watch out for breath stacking.

 

[Hamhock]

There's only one way....bronch.

ultrasound bilateral diaphragmatic excursion

HH

 

[Noyac]

.

 

[fakin' the funk]

OP -

You were doing weight loss surgery. At some point well into the case you say you went into steep rev tberg. What position were you in before??!!

 

[fakin' the funk]

I had a case on fatty the other day and the pulse ox was consistently in the 80s. Good wave form, 3 asterix on the screen, no "low signal quality" warning. However we had an aline and the PaO2 was always 150-200. Anyone have that experience? It has made me consider checking an ABG when sats are low and I cant figure out why..

Yep

 

[fakin' the funk]

So I don't do anesthesia much on really really big people....I know that is standard for many of you.

But I have a question for those that do.

I did a laprscopic case (weight loss surgery) yesterday. BMI 53. The patient was persistently hypoxia (84 to 89%) which I am 99% sure the shunting was from decreased FRC and atelecasis. I know this because I was stressed at the beginning - confirmed tube placement above carina, ruled out pneumo with ultrasound, and the kicker was when we put patient in steep reverse T-berg, everything improved.

Anyway, I had PEEP at 8, peek pressures at 40, and ventilating lung volumes at around 400-450. With multiple attempts with lung recruitment maneuvers, I could not get pulse ox much above 90% ever.

Are there any pearls of wisdom for cases like this?

Let me be clear. Once I learned for sure the shunt was definitely from atelectasis, I didn't care about the hypoxia (since O2 delivery is essentially the same for an SPO2 ofhf 90-100). Hypoxia isn't the problem. Knowing WHY they are hypoxia is the problem.

Anyway....

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

Your plateau pressures are key. What were they?

Good chance you were mainstemmed.

 

[Hoya11]

Lower I:E ration means you can deliver larger tidal volumes at the same peak pressures. You don't need as fast a rate as a result.

The modest increase in TV you can attain from switching to 1:1 would probably only let you decrease your rate by 1-2 breaths/min while dramatically shortening your E time for every breath of the cycle. Obesity and COPD are definitely not mutually exclusive.

I cant tell you how many times Ive come into the room and there is clear breaths tacking going on with exp wave not returning to baseline, upsloping CO2 curve. Its usually improved by lengthening E time from 1:1 that they had it set at (or dont even realize what I:E means). Then I disconnect the circuit and WOOSH autopeep gone.

 

[Ronin786]

The modest increase in TV you can attain from switching to 1:1 would probably only let you decrease your rate by 1-2 breaths/min while dramatically shortening your E time for every breath of the cycle. Obesity and COPD are definitely not mutually exclusive.

I cant tell you how many times Ive come into the room and there is clear breaths tacking going on with exp wave not returning to baseline, upsloping CO2 curve. Its usually improved by lengthening E time from 1:1 that they had it set at (or dont even realize what I:E means). Then I disconnect the circuit and WOOSH autopeep gone.

In my experience it's usually the opposite. Folks turning up the I:E because the Co2 is too high, even though obesity is a restrictive lung disease and they have no difficulty getting that air out. Then you end up with very high peaks and crappy Vt. I'm with you on COPD needing a bit higher expiratory time, but straight obesity definitely benefits from a 1:1 ratio.

 

[deleted162650]

With 1:1 ventiltation I would worry about CO2 retention, autopeep, and expiratory wave form not returning to baseline.

You keep confusing two different physiologic principles. CO2 retention and autopeep/breath stacking are not the same thing. CO2 retention is the result of inadequate MV. Autopeep is not allowing the full volume of inspired gas to be exhaled - gradually leading to distended lungs and increased pressures. Your CO2 wave form tells you nothing about the presence of autopeep. For that you look at your pressure wave form. Again, 1:1 is not a problem in the obese whose massive chest walls forcibly push out air faster than even a normal habitus patient, and it's a good way to keep your pressures at reasonable levels. I'll agree that COPD and morbid obesity are not mutually exclusive, but I have never come across a morbidly obese patient that also had severe emphysema. There are only so many hours in a day, and if your lips are occupied by a cigarette for the majority of your waking hours, there just isn't enough time left to severely over-eat.

It should also be noted that overly high PEEPs and pulmonary pressures can worsen V/Q matching and lead to worsening sats.

 

[deleted162650]

Also, scientific question for residents and then the rest. Can neosynephrine cause increased VQ mismatch?

You need to get your mental hand out of your mental pants.

 

[epidural man]

something seems off about this case. I've managed patients for cases like this with BMI's well over 50's and have never had this problem. These pts are usually otherwise healthy with good cardiac and pulmonary function. With the patient in reverse trend and paralyzed and on high FiO2, you should be able to get much better volumes and sats than 400 and 90% with those kind of peak pressures. Even with laparoscopic cases I've done with pts with BMI of 60's in steep trendelenberg, I've not had issues with sats. Hard to say what the problem was, but something unusual more than just atelectasis is going on here.

Yeah...exactly. I thought so too...but that is why I asked the question here - because I don't do a lot of these cases.

I of course did pressure control ventilation because - duh...why wouldn't you always ventilate that way - I'm not an idiot (jk to all you VC folks...sheesh...relax).

I did 1:1 I:E ratio - and thought about even trying 1.5:1 or 2:1 - wondered what you all thought of that as well (kind of like they do on ARDS in the unit - hold those lungs open as long as possible). I wasn't at all worried about autopeep for the reasons others have described.

I don't think I was main-stemmed because it didn't look like I was main-stemmed - but that is why I checked because I thought I might be.

And snapperrocks - good point. I would have never documented it as "ruled out". I ruled out nothing.

Fakin' - We started supine. Doesn't everyone start supine for laproscopic? Oh wait...this may have been a joke about me standing up (that just occurred to me...sorry..slow on the uptake).

 

[epidural man]

So good info - I needn't be fearful of higher PEEP and higher pressures in these patients. Thanks.

 

[Hoya11]

You keep confusing two different physiologic principles. CO2 retention and autopeep/breath stacking are not the same thing. CO2 retention is the result of inadequate MV. Autopeep is not allowing the full volume of inspired gas to be exhaled - gradually leading to distended lungs and increased pressures. Your CO2 wave form tells you nothing about the presence of autopeep. For that you look at your pressure wave form. Again, 1:1 is not a problem in the obese whose massive chest walls forcibly push out air faster than even a normal habitus patient, and it's a good way to keep your pressures at reasonable levels. I'll agree that COPD and morbid obesity are not mutually exclusive, but I have never come across a morbidly obese patient that also had severe emphysema. There are only so many hours in a day, and if your lips are occupied by a cigarette for the majority of your waking hours, there just isn't enough time left to severely over-eat.

It should also be noted that overly high PEEPs and pulmonary pressures can worsen V/Q matching and lead to worsening sats.

I appreciate the discussion... Maybe im using the wrong terms.. but inadequate minute ventilation is not the same to me as CO2 retention. Inadequate MV is hypoventilation...

When you have an upsloping CO2 curve, this indicates that inadequate exhalation/obstruction is occuring, as the CO2 is rushing out into the spirometer but is abruptly cut off by the inspiratory cycle starting. Like any COPDer, you have an upsloping CO2 curve and higher baseline levels of PaCO2. Hence COPDers losing their hypercapnic drive to breath.. its because they have airway obstruction AND retain CO2.

If you see an upsloping CO2 curve you are seeing inadequate exhalation. That means the CO2 that could be leaving is still staying in the system (retained?) contributing to increased auto-peep as the volume that should be exhaled remains in the airway/lung. This means the ETCO2 that you see is not an accurate reflection of the PACo2 as not all is being exhaled.

If you leave someone with an expiratory wave that doesnt return to baseline for the whole case what will happen? You will have autopeep and a larger gradient of PaCO2 to ETCO2. This is what i means by Co2 retention...

Again I appreciate the discussion and honestly never heard of moving to 1:1 to get a little more volume to (somehow) improve oxygenation.. but interesting...

 

[epidural man]

Again I appreciate the discussion and honestly never heard of moving to 1:1 to get a little more volume to (somehow) improve oxygenation.. but interesting...

I'm surprised that this isn't taught more - my residents never understand this either.

I always use 1:1 or 1:1.5 to get more volume for less pressure in patients without lung disease.

I've never seen an upsloping CO2 curve in a normal-lung patient I don't think.

 

[deleted162650]

If you see an upsloping CO2 curve you are seeing inadequate exhalation.

You're understanding of what causes the upslope is a little flawed. You need to re-read a good textbook chapter about capnography because I'm not sure I can explain it clearly over the internet.

That means the CO2 that could be leaving is still staying in the system (retained?) contributing to increased auto-peep as the volume that should be exhaled remains in the airway/lung.

This is the part that isn't really true. You can certainly have both in the same patient, but an upsloping capnograph doesn't mean that autopeep is developing.

This means the ETCO2 that you see is not an accurate reflection of the PACo2

This is true

If you leave someone with an expiratory wave that doesnt return to baseline for the whole case what will happen? You will have autopeep

This is true of the pressure wave on the vent, not true of the EtCO2.



Take an awake COPD'er and have them breath spontaneously through the mask. They will have an upsloping capnogram due to their obstructive lung disease. Does that mean they are autopeeping with each breath? Of course not - that would mean that their lungs would be gradually overdistending with every breath they take, and their chests would have exploded long before they ever made it to your OR.

 

[vector2]

Autopeep is not allowing the full volume of inspired gas to be exhaled - gradually leading to distended lungs and increased pressures. Your CO2 wave form tells you nothing about the presence of autopeep.

This isn't entirely accurate. If you're significantly autopeeping the ETCO2 waveform isn't going to return to baseline. But yeah, the upsloping plateau phase has nothing to do with autopeep.

 

[Hoya11]

You're understanding of what causes the upslope is a little flawed. You need to re-read a good textbook chapter about capnography because I'm not sure I can explain it clearly over the internet.



This is the part that isn't really true. You can certainly have both in the same patient, but an upsloping capnograph doesn't mean that autopeep is developing.



This is true



This is true of the pressure wave on the vent, not true of the EtCO2.



Take an awake COPD'er and have them breath spontaneously through the mask. They will have an upsloping capnogram due to their obstructive lung disease. Does that mean they are autopeeping with each breath? Of course not - that would mean that their lungs would be gradually overdistending with every breath they take, and their chests would have exploded long before they ever made it to your OR.

Again appreciate the discussion, not to be argumentative just trying to understand the logic...

So an awake COPDer is going to have an upsloping CO2 curve.. So is an asleep non-copder who doesnt have a long enough E-time.. They have the same disease, they dont exhale CO2 adequately.. yes for different reasons, but both have distended lungs (from too much peep be it auto or whatever you want to call it), upsloping CO2 curves, and an increased PaCo2 to ETCO2 gradient.

You are creating a COPD physiology with an E time that is too short... and you get all the stuff that goes along with COPD physiology like CO2 retention (or an increased PaCo2 to ETCO2 gradient is what i really mean)

In the end, we are talking about increasing ventilation (through the increased TV that we can get with the decreased pressure at 1:1) to improve oxygenation. A hard sell that increasing the TV increases oxygenation... if you are struggling to ventilate the patient sure.. but again with hypoxia this wouldnt be my first move

 

[Hoya11]

I'm surprised that this isn't taught more - my residents never understand this either.

I always use 1:1 or 1:1.5 to get more volume for less pressure in patients without lung disease.

I've never seen an upsloping CO2 curve in a normal-lung patient I don't think.

Make the E time 3:1 at a high rate and you will

 

[deleted162650]

Again appreciate the discussion, not to be argumentative

Same here - hope I'm not sounding like a dick.

Thanks to @vector2 for the pics (I had tunnel vision and was only thinking about the upslope when I said the capnograph won't show autopeep). They clearly illustrate that an "obstructive" EtCO2 trace does not imply autopeep. The failure to return to baseline does.

In VC you can make almost anyone breath stack if you make the settings extreme enough. In PC not so much (I won't say impossible, but you reeeeeaaaaly have to try) and PC is really what you should be using in the fat-fat-fatties. Think about APRV and "inverse ratio" vent strategies in the ICU. Hypoventilation can become a problem, but not autopeep since the driving pressures are fixed.

Make the E time 3:1 at a high rate and you will

No you won't. See vector's post. You may see breath stacking, but you won't magically give them obstructive lung Dz.

 

[cleansocks]

Again I appreciate the discussion and honestly never heard of moving to 1:1 to get a little more volume to (somehow) improve oxygenation.. but interesting...

Increasing mean airway pressure, not volume, is what gives more oxygenation. PEEP is the most commonly known form of this concept, but any maneuver that increases average airway pressure per unit time will increase oxygenation. The extreme of this concept are those uncomfortable ICU vent settings (IRV, APRV, etc) where the machine holds high airway pressures for an extended period of time and then releases it for a brief period of exhalation.

 

[Hoya11]

Same here - hope I'm not sounding like a dick.

Thanks to @vector2 for the pics (I had tunnel vision and was only thinking about the upslope when I said the capnograph won't show autopeep). They clearly illustrate that an "obstructive" EtCO2 trace does not imply autopeep. The failure to return to baseline does.

In VC you can make almost anyone breath stack if you make the settings extreme enough. In PC not so much (I won't say impossible, but you reeeeeaaaaly have to try) and PC is really what you should be using in the fat-fat-fatties. Think about APRV and "inverse ratio" vent strategies in the ICU. Hypoventilation can become a problem, but not autopeep since the driving pressures are fixed.



No you won't. See vector's post. You may see breath stacking, but you won't magically give them obstructive lung Dz.

A great discussion thank you. I think we are seeing eye to eye but missing on semantics...I was incorrectly interchanging upsloping CO2 curve with what i meant for breath stacking and autopeeping. Yes you cannot get intrinsic lung disease from short E time... I see what you were getting at. But the only point im trying to make is watch out for breath stacking with short E times. your right in the person in the example you would not see an upsloping curve even if you did see breathstacking..thanks for clarifying

 

[Hoya11]

Increasing mean airway pressure, not volume, is what gives more oxygenation. PEEP is the most commonly known form of this concept, but any maneuver that increases average airway pressure per unit time will increase oxygenation. The extreme of this concept are those uncomfortable ICU vent settings (IRV, APRV, etc) where the machine holds high airway pressures for an extended period of time and then releases it for a brief period of exhalation.

a great point thx

 

[dhb]

Increasing mean airway pressure, not volume, is what gives more oxygenation. PEEP is the most commonly known form of this concept, but any maneuver that increases average airway pressure per unit time will increase oxygenation. The extreme of this concept are those uncomfortable ICU vent settings (IRV, APRV, etc) where the machine holds high airway pressures for an extended period of time and then releases it for a brief period of exhalation.

Up to a certain point: if your airway pressures are higher than perfusion pressure you're going to ger more shunt.

 

[nimbus]

Up to a certain point: if your airway pressures are higher than perfusion pressure you're going to ger more shunt.

More dead space, not more shunt.

 

[Ronin786]

I'm surprised that this isn't taught more - my residents never understand this either.

I always use 1:1 or 1:1.5 to get more volume for less pressure in patients without lung disease.

I've never seen an upsloping CO2 curve in a normal-lung patient I don't think.

My bet is it has to do with medical schools' basic teaching of ventilation. It's oversimplified to PEEP/FiO2 for oxygenation and Vt/RR for ventilation. Anatomic shunting, dead space and V/Q mismatch are "theoretical" concepts that most medical schools do a terrible job of explaining. Heck, most physicians don't truly understand them.