Thoughts on hyperoxia

[coffeebythelake]

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Thoughts on hyperoxia for prevention of surgical site infections.
Seems like there is some evidence for this, at least for colorectal surgeries
However doesn't seem like any of my colleagues do this. I don't.

(I'm talking FiO2 80%, regardless of whether patient's SpO2 is 100% at lower FiO2.)

 

[GassYous]

Im pretty sure this has been studied before and found to not work.

 

[abolt18]

Im pretty sure this has been studied before and found to not work.

Though there seems to be more evidence, more obviously noted in people with pre-existing lung disease and in infants, that hyperoxia caused harm and we should titrate the FiO2 as low as possible for an O2 SpO2 in the mid 90s.

 

[MoMoGesiologist]

Not a fan. Have colleagues that leave pt on FiO2 100% the whole case. Can’t be good to be on that much O2 for long cases... it ain’t natural!

 

[GassYous]

I think with the haldane effect and the maldistribution of perfusion due to the adverse effect on hypoxic pulmonary vasoconstriction, hyperoxia is just poor practice, especially in people who cannot tolerate it. Whenever I see a partner running O2 at 6 L I just shake my head. I usually run my flows around 0.5-1 with around 40% oxygen aiming for a sat of around 95-99 because then I have a rough idea of the pao2. When the sat is 100 it could be 100 or 500 and is just unnecessary.



In this issue of Anesthesiology, Stæhr et al. 1report the lack of effect of perioperative hyperoxia on preventing surgical site infection (SSI) in obese patients undergoing laparotomy. The study was a secondary analysis of data from the PROXI Trial, a Danish multicenter study of 1,400 patients undergoing elective or emergency laparotomy who were randomized to receive a 30% or 80% oxygen concentration intraoperatively and for the first 2 h after surgery.2Although no significant reduction in the frequency of SSI was observed in the high-concentration group in that trial, it was hypothesized that the results for the subpopulation of 213 obese patients (body mass index ≥30 kg/m2, 15% of the sample) might be different. However, on reanalysis the researchers again found no significant differences in the rates of SSI or pulmonary complications.

Anesthesiology

pubs.asahq.org

 

[deleted875186]

There have been a couple big studies on this, one that actually measured tissue PaO2 if I remember correctly, results aren’t conclusive that it helps, although I don’t have the studies saved and it’s been a while.

I would consider doing hyperoxia for a short case, where infection would be a big deal (total joints). It makes no sense for abdominal surgeries, the abdomen is already well perfused, probably makes more sense for extremities and such.

 

[coffeebythelake]

There have been a couple big studies on this, one that actually measured tissue PaO2 if I remember correctly, results aren’t conclusive that it helps, although I don’t have the studies saved and it’s been a while.

I would consider doing hyperoxia for a short case, where infection would be a big deal (total joints). It makes no sense for abdominal surgeries, the abdomen is already well perfused, probably makes more sense for extremities and such.

Interestjng unanswered questions are brought up.. The ?flawed premise is that adequate perfusion and tissue oxygenation improves outcomes. Intuitively it makes sense that tissue vasoconstriction varies depending on central vs periphery.. Does the use of pressors increase the risk for SSI? Does the use of vasopressin increase the risk for organ space SSI by preferentially constricting gut vasculature?

 

[Hoya11]

Thoughts on hyperoxia for prevention of surgical site infections.
Seems like there is some evidence for this, at least for colorectal surgeries
However doesn't seem like any of my colleagues do this. I don't.

(I'm talking FiO2 80%, regardless of whether patient's SpO2 is 100% at lower FiO2.)

It does sound like sketchy evidence.

But if a surgeon asked me to do a case with 100 percent oxygen, just to go with the flow I would do it. I really see little downside. Negative effects of high pao2s (outside of fire risk) have been something that have been only theoretical in my career. 2-3 hours intubated at 100% fio2, I really doubt harm is going to come from that....

 

[Urzuz]

I’ll play devil’s advocate.

I regularly run patients on an FiO2 of 1.0 in the OR. Why? For me, the potential benefits outweigh the risks. The risks of a few hours of hyperoxia, barring any comorbidities like ILD etc, are mostly theoretical. Sure, there may be free radicals that cause some degree of tissue damage at a molecular level with prolonged exposure, sure there may be some diffusion atelectasis (once again after several hours of exposure), etc. But ventilating at 100% FiO2 buys you time in the event of an emergency, which in my opinion, is much more likely to cause tangible long-term consequences to a patient. The loss of an airway (eg: ETT becomes dislodged - happened to my partner just the other day), bronchospasm due to anaphylaxis or reactive airway disease, etc - these things IMO are much more likely to cause long term harm in an otherwise healthy patient, so buying precious minutes by having your FRC saturated with oxygen outweighs any negative consequences of having hyperoxia for those hours that they’re intubated for. In patients with comorbidities where hyperoxia may have real, tangible harm (eg: ILD), I do ventilate at a lower FiO2.

 

[coffeebythelake]

I’ll play devil’s advocate.

I regularly run patients on an FiO2 of 1.0 in the OR. Why? For me, the potential benefits outweigh the risks. The risks of a few hours of hyperoxia, barring any comorbidities like ILD etc, are mostly theoretical. Sure, there may be free radicals that cause some degree of tissue damage at a molecular level with prolonged exposure, sure there may be some diffusion atelectasis (once again after several hours of exposure), etc. But ventilating at 100% FiO2 buys you time in the event of an emergency, which in my opinion, is much more likely to cause tangible long-term consequences to a patient. The loss of an airway (eg: ETT becomes dislodged - happened to my partner just the other day), bronchospasm due to anaphylaxis or reactive airway disease, etc - these things IMO are much more likely to cause long term harm in an otherwise healthy patient, so buying precious minutes by having your FRC saturated with oxygen outweighs any negative consequences of having hyperoxia for those hours that they’re intubated for. In patients with comorbidities where hyperoxia may have real, tangible harm (eg: ILD), I do ventilate at a lower FiO2.

1. Does it really make things safer? I question your assumption. For induction and emergence we routinely do 1.0 FiO2 to extend time to desaturation and that makes sense because they are monitored second by second. I would argue doing this during the entire case would actually be less safe because it would delay recognition of a problem. the first temporizing measure is to go up on your FIO2 while trying to work the problem.

2. Unless you have Art line and checking PaO2 you have no idea what it is. You get a lot more information when you have a sat of 100% at 0.3 FIO2 than you gave with a sat of 100% at 1.0 FIO2.

3. Not worried about O2 toxicity for most patients. But I do worry about atelectasis.

 

[Urzuz]

1. Does it really make things safer? For induction and emergence we routinely do 1.0 FiO2 for this reason and that makes sense because they are monitored second by second. I would argue doing this during the entire case would actually be less safe because it would delay recognition of a problem. the first temporizing measure is to go up on your FIO2 while trying to work the problem.

If your ETT becomes dislodged, or you have severe bronchospasm affecting oxygen uptake, or some other problem that is compromising oxygen delivery to that degree, you will have several other signs prior to the patient becoming hypoxic that something is amiss. I would rather buy myself extra time with that FRC and rely on myself paying attention to my monitors.

Plus, in these events where you can’t ventilate the patient, what good is turning up your FiO2 after the fact?

 

[coffeebythelake]

If your ETT becomes dislodged, or you have severe bronchospasm affecting oxygen uptake, or some other problem that is compromising oxygen delivery to that degree, you will have several other signs prior to the patient becoming hypoxic that something is amiss. I would rather buy myself extra time with that FRC and rely on myself paying attention to my monitors.

Plus, in these events where you can’t ventilate the patient, what good is turning up your FiO2 after the fact?

Have u actually had any of these things happen or are u talking hypothetical. I've never had something like what u describe. It seems highly unlikely. So I question why a patient would develop sudden onset bronchospasm for no apparent reason in the middle of a case when it didn't happen with induction and initial placement of the tube...

And if the reason is light anesthesia, then maybe u deepen it to break the bronchospasm and go up on fio2 to temporize problem. Again I dont necessarily see 1.0 FIO2 as a safety measure in the middle of a case.

(I routinely run my patients on 50/50 air oxygen which is about 0.65 FIO2. I think it offers plenty of time before desat while also allowing FIO2 to be bumped up as needed. In patients of concern without art line, every once in a while I adjust the FIO2 to minimal to see when SpO2 drops to estimate the PaO2)

 

[deleted875186]

Have u actually had any of these things happen or are u talking hypothetical. I've never had something like what u describe. It seems highly unlikely. So I question why a patient would develop sudden onset bronchospasm for no apparent reason in the middle of a case when it didn't happen with induction and initial placement of the tube...

And if the reason is light anesthesia, then maybe u deepen it to break the bronchospasm and go up on fio2 to temporize problem. Again I dont necessarily see 1.0 FIO2 as a safety measure in the middle of a case.

(I routinely run my patients on 50/50 air oxygen which is about 0.65 FIO2. I think it offers plenty of time before desat while also allowing FIO2 to be bumped up as needed)

I have heard the “airway events are more common” argument, and I think they are more theoretical. I’d rather have a person with less atalectasis than have a 100% sat in 1.0 FIO2.

what happens if your sat starts to decrease if your on FIO2 1.0. Now you have no temporizing measure, now your unsure if it’s atelectasis or something worse. Maybe it’s a main stem or a mucous plug that was unrecognized for an hour because you had a high FIO2.

 

[Urzuz]

Have u actually had any of these things happen or are u talking hypothetical. I've never had something like what u describe. It seems highly unlikely. So I question why a patient would develop bronchospasm for no apparent reason in the middle of a case when it didn't happen with induction and initial placement of the tube...

Luckily I myself have never had anything like that happen, but I have heard several M&Ms of tubes being displaced or coming out altogether. You haven’t?

Additionally, our job is all about risk mitigation. If you only employ practices to prevent complications that you yourself have seen firsthand, you will be practicing well below the standard of care (to be clear, I’m not implying running an Fio2 < 1.0 is below standard of care).

 

[Urzuz]

I have heard the “airway events are more common” argument, and I think they are more theoretical. I’d rather have a person with less atalectasis than have a 100% sat in 1.0 FIO2.

what happens if your sat starts to decrease if your on FIO2 1.0. Now you have no temporizing measure, now your unsure if it’s atelectasis or something worse. Maybe it’s a main stem or a mucous plug that was unrecognized for an hour because you had a high FIO2.

To each their own. An ETT falling out is definitely not theoretical and is a very real complication that happens with some regularity even with the best of tape jobs. And again, cranking up your FiO2 in that scenario won’t do jack.

Diffusion atelectasis that a little recruitment maneuver or a little IS postop won’t fix? Free radicals causing cell membrane disruption? Those sound more theoretical to me.

 

[coffeebythelake]

Luckily I myself have never had anything like that happen, but I have heard several M&Ms of tubes being displaced or coming out altogether. You haven’t?

Additionally, our job is all about risk mitigation. If you only employ practices to prevent complications that you yourself have seen firsthand, you will be practicing well below the standard of care (to be clear, I’m not implying running an Fio2 < 1.0 is below standard of care).

Seems more a matter of someone not paying enough care and not necessarily increased safety of 1.0 FIO2. Clumsy surgeon perhaps. Or inadequate neuromuscular blockade.. or not good tape job.. Whenever a surgeon is up by the face I double check to tape the tube down very well. Maybe use some mastisol and tegedsrms. If they are doing some bronchoscopy or EGD I hold onto the tube. I also tell the surgeon not to **** with my patients airway. In these select cases I may decide to use a higher FIO2. But recognize that tubes don't just come out for no reason.

 

[Urzuz]

Seems more a matter of someone not paying enough care and not necessarily increased safety of 1.0 FIO2. Clumsy surgeon perhaps. Or inadequate neuromuscular blockade.. or not good tape job.. Whenever a surgeon is up by the face I double check to tape the tube down very well. Maybe use some mastisol and tegedsrms. If they are doing some bronchoscopy or EGD I hold onto the tube. In these select cases I may decide to use a higher FIO2. But recognize that tubes don't just come out for no reason.

To each their own. I’ll continue assuming the risks associated with an Fio2 of 1.0, you continue assuming the risk of an unlikely airway emergency. That’s the beauty of developing your own practice style.

 

[coffeebythelake]

It does sound like sketchy evidence.

But if a surgeon asked me to do a case with 100 percent oxygen, just to go with the flow I would do it. I really see little downside. Negative effects of high pao2s (outside of fire risk) have been something that have been only theoretical in my career. 2-3 hours intubated at 100% fio2, I really doubt harm is going to come from that....

Some of the earlier studies were convincing but it seems like the tide has changed with newer studies. Some describe increased morbidity and mortality without much benefit. So definitely not benign intervention.. The WHO actually made a broad recommendations (i think it was sometime after 2010) for using hyperoxia to prevent SSIs which was heavily criticized by Hedenstierna et al 2017 (A&A) as not evidence based and potentially causing harm.

 

[GassYous]

Intuitive thinking is what caused countless septic patients to drown iatrogenically for a decade during the era of goal directed therapy. We gave unnecessary oxygen to countless MI patients and all we got was increased mortality. I don't know how you are taping your tubes but sounds like you need to pay more attention during taping and draping. I don't even tape many of my lmas and magically none of them have ever gotten dislodged. FiO2 of 100% doesn't prevent tube dislodgement or anaphylaxis and you should be able to fix it in time.

I'd rather have an issue with the airway during the case when I'm there with the patient 1:1 than in the pacu afterwards. Most of my patients do fine on room air after extubation. The few times I run 100% oxygen are during one lung ventilation when the sat is <90.

 

[Urzuz]

I don't know how you are taping your tubes but sounds like you need to pay more attention during taping and draping. I don't even tape many of my lmas and magically none of them have ever gotten dislodged.

Never happened to me, but has happened to many experienced partners and colleagues. But again, it is about risk mitigation. It hasn't happened to you, until it has.

Intuitive thinking is what caused countless septic patients to drown iatrogenically for a decade during the era of goal directed therapy. We gave unnecessary oxygen to countless MI patients and all we got was increased mortality.

You're comparing apples to elephants if you're trying to draw a parallel between EGDT+fluids, O2+MIs, and a patient having a surgical anesthetic for several hours with an FiO2=1.0.

FiO2 of 100% doesn't prevent tube dislodgement or anaphylaxis and you should be able to fix it in time.

It doesn't prevent it, which is exactly my point. If it did happen, would you rather have been ventilating your patient for the past 30 min on an FiO2 or 1.0 or 0.5? And to say "you should be able to fix it in time" is naive. That's like asking, "why preoxygenate a patient before intubation? Just induce them immediately while they're breathing room air - you should be able to intubate them in time."

I'd rather have an issue with the airway during the case when I'm there with the patient 1:1 than in the pacu afterwards. Most of my patients do fine on room air after extubation.

I'd rather not have an airway issue, period. Give them a recruitment maneuver at the end of the case if you are that concerned about diffusion atelectasis and you have the best of both worlds.

Coincidentally, the patients who you really worry about any degree of atelectasis compromising them postoperatively (e.g.: morbidly obese, Pickwickian patients, etc) are the patients who you should probably doing recruitment maneuvers on regardless prior to extubation. Additionally, they are also the ones who, IF your airway gets compromised during the case, you will take every drop of additional oxygenation you can since their sats will tank quickly.

I'm not here to argue with you or convince you that running a patient on 100% oxygen is the only way to do things. I'm here offering a different perspective, and providing a rationale for why it isn't completely crazy to run a patient on a high FiO2. Until there is solid evidence to show an actual morbidity/mortality benefit of running a lower FiO2, I'll keep ventilating most patients at a high FiO2.

 

[GassYous]

I don't preoxygenate every patient either. I'll have monitors on and the patient tubed within 4 minutes of their arrival to the OR. Do you have epi drawn up for every case because they might have bronchospasm or anaphylaxis? Ordering types and screens for appys due to the possibility of bleeding? Mixing up dantrolene daily because you're using triggering agents? It's just unnecessary.

 

[Urzuz]

I don't preoxygenate every patient either. I'll have monitors on and the patient tubed within 4 minutes of their arrival to the OR. Do you have epi drawn up for every case because they might have bronchospasm or anaphylaxis? Ordering types and screens for appys due to the possibility of bleeding? Mixing up dantrolene daily because you're using triggering agents? It's just unnecessary.

Lol ok guy. Yup, having a patient take three breaths of 100% oxygen as I’m pushing propofol is a sign of weakness as an anesthesiologist and shows the lack of confidence I have in my skills.

Now that you mention it, why even put monitors on? Are your inductions so ****ty that you are afraid of hypotension or arrhythmias?

 

[deleted875186]

Lol ok guy. Yup, having a patient take three breaths of 100% oxygen as I’m pushing propofol is a sign of weakness as an anesthesiologist and shows the lack of confidence I have in my skills.

Now that you mention it, why even put monitors on? Are your inductions so ****ty that you are afraid of hypotension or arrhythmias?

100%, not doing good preoxygenation is indefensible if there’s an airway issue. There will be a small amount of people with unanticipated difficult airways. I’ll always take the extra 2 mins if needed to get the etO2 up.

 

[teacher2md]

The risks of a few hours of hyperoxia, barring any comorbidities like ILD etc, are mostly theoretical.

To play devil's advocate: the data regarding hyperoxia are more than theoretical. There is a bunch of observational data for critically ill patients showing worsened outcomes associated with hyperoxia in certain subgroups: stroke, MI, post cardiac arrest. Here's a review paper [https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30479-3/fulltext]

There was the recent ICU-ROX trial that showed no improvement for conservative vs. 'normal' oxygen therapy, so I think it's fair to say that there's not clear difference either way.

But if you are only convinced by RCT's, then you shouldn't feel the need to use low tidal-volume ventilation either, and should feel comfortable cranking away at 10mL/kg [Effect of Intraoperative Low Tidal Volume vs Conventional Tidal Volume on Postoperative Pulmonary Complications in Patients Undergoing Major Surgery: A Randomized Clinical Trial - PubMed]

 

[Urzuz]

To play devil's advocate: the data regarding hyperoxia are more than theoretical. There is a bunch of observational data for critically ill patients showing worsened outcomes associated with hyperoxia in certain subgroups: stroke, MI, post cardiac arrest. Here's a review paper [https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30479-3/fulltext]

There was the recent ICU-ROX trial that showed no improvement for conservative vs. 'normal' oxygen therapy, so I think it's fair to say that there's not clear difference either way.

Cross-applying ICU data in critically ill patients to the intraoperative setting is of little to no relevance. As an example of what you're doing, it's like saying, esmolol infusions were shown to reduce mortality in septic shock patients in the ICU by targeting a HR of 80-94 bpm, therefore you should start an esmolol infusion in every operative patient you have whose HR is >95 bpm. Seems rather silly, no?

But if you are only convinced by RCT's, then you shouldn't feel the need to use low tidal-volume ventilation either, and should feel comfortable cranking away at 10mL/kg [Effect of Intraoperative Low Tidal Volume vs Conventional Tidal Volume on Postoperative Pulmonary Complications in Patients Undergoing Major Surgery: A Randomized Clinical Trial - PubMed]

Not sure what relevance this has to the discussion but ok.

 

[nimbus]

To play devil's advocate: the data regarding hyperoxia are more than theoretical. There is a bunch of observational data for critically ill patients showing worsened outcomes associated with hyperoxia in certain subgroups: stroke, MI, post cardiac arrest. Here's a review paper [https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30479-3/fulltext]

There was the recent ICU-ROX trial that showed no improvement for conservative vs. 'normal' oxygen therapy, so I think it's fair to say that there's not clear difference either way.

But if you are only convinced by RCT's, then you shouldn't feel the need to use low tidal-volume ventilation either, and should feel comfortable cranking away at 10mL/kg [Effect of Intraoperative Low Tidal Volume vs Conventional Tidal Volume on Postoperative Pulmonary Complications in Patients Undergoing Major Surgery: A Randomized Clinical Trial - PubMed]

I imagine if anybody studied hyperoxia vs normoxia in the intraop setting, the result would show no difference like the tidal volume paper. I used large tidal volumes for years because that’s what everybody did when I trained. The patients did fine. I have not seen a change in any outcome using lower tidal volumes. It may be more the current fashion.

 

[teacher2md]

Cross-applying ICU data in critically ill patients to the intraoperative setting is of little to no relevance. As an example of what you're doing, it's like saying, esmolol infusions were shown to reduce mortality in septic shock patients in the ICU by targeting a HR of 80-94 bpm, therefore you should start an esmolol infusion in every operative patient you have whose HR is >95 bpm. Seems rather silly, no?

I actually agree with you— I’m just pointing out that many of our common practices in anesthesiology are extrapolated from ICU literature, and a lot of them probably can’t be applied to otherwise healthy anesthesia patients.

Low tidal volume ventilation, transfusion thresholds, MAP goals, etc; all of these come from ICU literature.

 

[Ronin786]

To each their own. An ETT falling out is definitely not theoretical and is a very real complication that happens with some regularity even with the best of tape jobs. And again, cranking up your FiO2 in that scenario won’t do jack.

Diffusion atelectasis that a little recruitment maneuver or a little IS postop won’t fix? Free radicals causing cell membrane disruption? Those sound more theoretical to me.

What about your patient with bibasilar atelectasis in the laparoscopic trendelenburg position that you don't even think about because of how high your FiO2 is? Or your mainstem intubation that isn't picked up on because your FiO2 is making up for the one lung ventilation? Those are much more common events that you're potentially missing than the rare accidental ETT dislodgment.

Do you also call ENT for every airway in case you can't intubate/ventilate?

 

[coffeebythelake]

I don't preoxygenate every patient either

did u initially train in ER? Jkjk

 

[Urzuz]

Do you also call ENT for every airway in case you can't intubate/ventilate?

why are you being snarky (similar to our other friend who I was talking to before) rather than addressing the points I brought up before? Or is it that some anesthesiologists have their heads so far up their own asses that they can’t understand that people practice differently?

 

[Ronin786]

why are you being snarky (similar to our other friend who I was talking to before) rather than addressing the points I brought up before? Or is it that some anesthesiologists have their heads so far up their own asses that they can’t understand that people practice differently?

I did address the points you asked. Your premise is that 100% FiO2 buys you time in case of an ETT malfunction. You're ignoring much more plausible scenarios in favor of the 99th percentile outcome.

 

[zizzer]

I imagine if anybody studied hyperoxia vs normoxia in the intraop setting, the result would show no difference like the tidal volume paper. I used large tidal volumes for years because that’s what everybody did when I trained. The patients did fine. I have not seen a change in any outcome using lower tidal volumes. It may be more the current fashion.

Not to pick on you specifically, but I see this anecdotal reasoning all the tone and out kind of drives me crazy for a couple of reasons. One is that many types of complications manifest later after surgery, so just because you don't notice a difference in PACU doesn't mean there isn't one. Second, many of these interventions create a statistically significant, but not dramatic difference in outcomes. Are you telling me you expect to anecdotally notice a difference between let's say a 2% and 5% incidence in post op ICU ARDS for example?

On the other hand, people who need a RCT to convince themselves of common sense interventions we can base on or reasoning and medical knowledge can be a bit out of hand as well.

 

[zizzer]

I haven’t seen any studies coming out the the OR comparing low vs high tidal volumes ventilation. Everybody just adopted low tidal volumes based on ICU literature. If there is a difference, I’m willing to bet it is insignificant. And there’s even a chance that high tidal volumes are better for certain outcomes.

Maybe you're right in this specific example, and ARDSnet was even criticized because its "conventional" TVs were 12 mL/kg. I'm just not a fan of the reasoning along the lines of: "I've never noticed a difference, so three probably isn't one."

 

[nimbus]

Maybe you're right in this specific example, and ARDSnet was even criticized because its "conventional" TVs were 12 mL/kg. I'm just not a fan of the reasoning along the lines of: "I've never noticed a difference, so three probably isn't one."

Maybe it’s better to state “I’ve never noticed a difference so the difference is not large.”

And without RCTs, we don’t know the effect of common sense interventions. A noteable example being the POISE trial, which showed that perioperative beta blockers (at the doses given) reduced perioperative myocardial ischemia but increased perioperative strokes and death.

 

[GassYous]

Starting beta blocker naive patients on metoprolol 200 is not a common sense intervention. It's just stupid.

 

[zizzer]

Regarding FiO2, I used to be in the lowest possible concentration camp but have recently decided to use hyperoxemia more often. I tape and protect my ETT well, but as others have mentioned, accidents aren't unheard of and bronchospasm and laryngospasm can happen regardless of how the tube is secured. The criticism that you lose the ability to switch to 100% oxygen as a temporizing measure doesn't make sense. You don't gain anything by switching to 100% over already being on 100% when they start desaturating.

The other criticism is that those of us who use higher FiO2 won't catch things such as mainstem intubation is a bit narrow minded as well. You don't think we realize that hypoxemia won't be an early presenting sign of something like that and remain mindful of ETT depth, position changes, and plateau pressures? Besides, in a supine position, there usually is some hypoxemia with a mainstemmed ETT because it creates a large shunt. Give us a little credit for being able to understand the tradeoffs of our choices and remain vigilant for the likely complications. I don't use 100% FiO2 to avoid some of the atelectasis, but I usually don't use 21% either.

 

[zizzer]

Starting beta blocker naive patients on metoprolol 200 is not a common sense intervention. It's just stupid.

Similar to the ARDSnet criticism.

I'm trying to strike a reasonable middle ground approach. Some people need RCTs to convince themselves of interventions where no good RCTs exist. Others dismiss studies frequently because of their own anecdotal experience. I think the best approach is critically evaluating evidence and not being afraid to use medical knowledge and clinical reasoning to fill in the gaps where there aren't convincing RCTs.

 

[SDF1]

Really depends on the culture of the institution you are at. During our cardiac cases - we routinely run patients on 100% oxygen.

 

[Urzuz]

I did address the points you asked. Your premise is that 100% FiO2 buys you time in case of an ETT malfunction. You're ignoring much more plausible scenarios in favor of the 99th percentile outcome.

Sorry, whatever point you were making was overshadowed by you making a snarky comment like a prick.

But to address your point, it isn’t JUST the ETT coming out. In any sort of emergency, whether it’s unanticipated bleeding, arrhythmia, ST changes, bronchospasm, etc, one of your first interventions will be (or should be) to increase the FiO2. So, rather than having to increase the FiO2 to buy time at the time of emergency, in my opinion, it is better to have that safety net already in place. Keep in mind, as mentioned before, turning the FiO2 up after the event will be utterly useless in some of these scenarios.

I also like how you say that an ETT coming out is a super rare event, and then cite mainstemming an ETT and ventilating a patient in steep trendelenburg as being "common occurrences" to lend support to your argument. Sorry, I can't remember the last time I mainstemmed an ETT. Additionally, you talk about bibasilar atelectasis as if ventilating a patient at a lower FiO2 prevents it in steep T-burg, which is idiotic. Regardless of if you've run the patient on an FiO2 of 0.5 or 1.0 through the entire case, if a patient is in steep T-burg for a prolonged period of time (and especially if they've had an insufflated abdomen), you should be giving a good recruitment maneuver at the end since atelectasis is unavoidable.

Out of curiosity, as a side note, how long have you been out of training for? I feel like the posters on this topic that are unwilling/unable to see the value in doing things a different way, in addition to posting with a douchey, resident-like, know-it-all attitude (when in reality you come across as an ignorant asshat), are the posters with the least amount of experience. Maybe I am wrong though since I don't know how long you've been out for, but something tells me that the more dogmatic and rigid someone is, the less experience they have.

 

[GassYous]

For someone who is constantly complaining about snark and attitudes, you sure don't come across as Mr. Nice Guy. You sound like the weak anesthesiologists who spend 20 minutes talking to a patient about meaningless crap and obsessing about useless things like how to tape a tube. The guys that know what they're doing don't need to puff themselves up and try to put others down constantly.

 

[Urzuz]

For someone who is constantly complaining about snark and attitudes, you sure don't come across as Mr. Nice Guy. You sound like the weak anesthesiologists who spend 20 minutes talking to a patient about meaningless crap and obsessing about useless things like how to tape a tube. The guys that know what they're doing don't need to puff themselves up and try to put others down constantly.

Reread the thread and tell me who was putting others down...if I recall, we were having a fine discussion and keeping it topical until you came along with:

I don't preoxygenate every patient either. I'll have monitors on and the patient tubed within 4 minutes of their arrival to the OR. Do you have epi drawn up for every case because they might have bronchospasm or anaphylaxis? Ordering types and screens for appys due to the possibility of bleeding? Mixing up dantrolene daily because you're using triggering agents? It's just unnecessary.

 

[coffeebythelake]

Sorry, whatever point you were making was overshadowed by you making a snarky comment like a prick.

But to address your point, it isn’t JUST the ETT coming out. In any sort of emergency, whether it’s unanticipated bleeding, arrhythmia, ST changes, bronchospasm, etc, one of your first interventions will be (or should be) to increase the FiO2. So, rather than having to increase the FiO2 to buy time at the time of emergency, in my opinion, it is better to have that safety net already in place. Keep in mind, as mentioned before, turning the FiO2 up after the event will be utterly useless in some of these scenarios.

I also like how you say that an ETT coming out is a super rare event, and then cite mainstemming an ETT and ventilating a patient in steep trendelenburg as being "common occurrences" to lend support to your argument. Sorry, I can't remember the last time I mainstemmed an ETT. Additionally, you talk about bibasilar atelectasis as if ventilating a patient at a lower FiO2 prevents it in steep T-burg, which is idiotic. Regardless of if you've run the patient on an FiO2 of 0.5 or 1.0 through the entire case, if a patient is in steep T-burg for a prolonged period of time (and especially if they've had an insufflated abdomen), you should be giving a good recruitment maneuver at the end since atelectasis is unavoidable.

Out of curiosity, as a side note, how long have you been out of training for? I feel like the posters on this topic that are unwilling/unable to see the value in doing things a different way, in addition to posting with a douchey, resident-like, know-it-all attitude (when in reality you come across as an ignorant asshat), are the posters with the least amount of experience. Maybe I am wrong though since I don't know how long you've been out for, but something tells me that the more dogmatic and rigid someone is, the less experience they have.

Take a step back and relax a bit. You sound like you are about to rupture an aneurysm..

 

[coffeebythelake]

Really depends on the culture of the institution you are at. During our cardiac cases - we routinely run patients on 100% oxygen.

Do you extubate your cardiac patients in the OR? Fast track? Or do they go tubed to the ICU? And what fio2 are they run in thr ICU (I assume much lower than 1.0). Seems to be if a tube is going to get dislodged it is most likely to happen in an ICU setting with all yhr interventions performed (in line suctioining, repositioning and retaping tube, manipulations of the head of bed,, etc) than in maintenance phase of the OR.

 

[Urzuz]

Take a step back and relax a bit. You sound like you are about to rupture an aneurysm..

im fine, thanks for checking. I just have little tolerance for people who try to act like they know everything online, post ad hominems like “Do you also call ENT for every airway in case you can't intubate/ventilate?” and “Do you have epi drawn up for every case because they might have bronchospasm or anaphylaxis?”, and then suddenly he wants to play victim when I call him (them) snarky pricks. I didn’t try to put them down and was having a fine debate with you and others up until that point, but again, for some reason they seemed personally offended and felt the need to talk about me and my abilities since they couldn’t comprehend that there are anesthesiologists that practice differently than them (hence why I feel like they are probably residents or junior attendings in bumble**** nowhere). If you care, I encourage you to reread the thread to see where it derailed.

But you’re right, I called them out and now will refocus the discussion (if anyone cares to).

 

[Urzuz]

Do you extubate your cardiac patients in the OR? Fast track? Or do they go tubed to the ICU? And what fio2 are they run in thr ICU (I assume much lower than 1.0). Seems to be if a tube is going to get dislodged it is most likely to happen in an ICU setting with all yhr interventions performed (in line suctioining, repositioning and retaping tube, manipulations of the head of bed,, etc) than in maintenance phase of the OR.

see my post before. It isn’t just about the tube being dislodged. During any/every emergency (and in the cardiac room you get more than your fair share), turning up the FiO2 to maximize oxygen carrying capacity (though it only increases it a little with a normal sat) will be one of your first interventions.

 

[SDF1]

Do you extubate your cardiac patients in the OR? Fast track? Or do they go tubed to the ICU? And what fio2 are they run in thr ICU (I assume much lower than 1.0). Seems to be if a tube is going to get dislodged it is most likely to happen in an ICU setting with all yhr interventions performed (in line suctioining, repositioning and retaping tube, manipulations of the head of bed,, etc) than in maintenance phase of the OR.

We extubate our robotic cardiac procedures. But generally no we do not extubate in the OR. They run usually 40% in the unit.

Totally agree with you - I was a bit against running patients on 100% FiO2 but I can see why you would do it (especially in the cardiac OR). Usually you are flying solo - doing TEE, bed up/down, titrating drips, etc - it is easy to set my FiO2 to 100% and forget it.

 

[vector2]

We extubate our robotic cardiac procedures. But generally no we do not extubate in the OR. They run usually 40% in the unit.

Totally agree with you - I was a bit against running patients on 100% FiO2 but I can see why you would do it (especially in the cardiac OR). Usually you are flying solo - doing TEE, bed up/down, titrating drips, etc - it is easy to set my FiO2 to 100% and forget it.

Trial just started:

" Conventionally, a relatively high level of fraction of inspired oxygen (FiO2) has been used for secure a margin of safety in patients undergoing cardiac surgery using cardiopulmonary bypass (CPB). Since the potential adverse effects of hyperoxemia (via reactive oxygen species, vasocontriction, perfusion heterogeneity, myocardiac injury, etc.), various studies on this topic has been performed. However, the results are conflicting and inconsistent, and the consensus about whether the use of additional oxygen supply in cardiac surgery using CPB has not been reached among practitioners yet. "

ClinicalTrials.gov

clinicaltrials.gov

 

[Urzuz]

However, the results are conflicting and inconsistent, and the consensus about whether the use of additional oxygen supply in cardiac surgery using CPB has not been reached among practitioners yet. "

And this beautifully encompasses my point (though I was referring to non-cardiac cases as well) - the data is inconsistent and conflicting, and arguments can be made for both high FiO2 and more moderate FiO2. There is no right or wrong on this subject, and as with almost everything in medicine, it’s a shade of gray rather than black or white.

 

[vector2]

And this beautifully encompasses my point (though I was referring to non-cardiac cases as well) - the data is inconsistent and conflicting, and arguments can be made for both high FiO2 and more moderate FiO2. There is no right or wrong on this subject, and as with almost everything in medicine, it’s a shade of gray rather than black or white.

I agree that there's not a strongly evidenced based answer yet but I am not a fan of high FiO2 if the argument is just for a degree of safety, especially for easy intubation supine ASA 1-3 who are getting low to moderate risk surgery. Running 100% FiO2 for a few hours is probably fine- it just rubs me the wrong way mentally cause I know it's detrimental if it's prolonged even if it's fine in the short term.

 

[Urzuz]

I agree that there's not a strongly evidenced based answer yet but I am not a fan of high FiO2 if the argument is just for a degree of safety, especially for easy intubation supine ASA 1-3 who are getting low to moderate risk surgery. Running 100% FiO2 for a few hours is probably fine- it just rubs me the wrong way mentally cause I know it's detrimental if it's prolonged even if it's fine in the short term.

And I respect and understand that viewpoint. As I said earlier in the thread, I’m not trying to convince anyone that running 100% is the only right way to do things - just providing a rationale for why I do it.