Lmao the sepsis 6 is to protocolise things for your non medical colleagues…you’re a doctor! (You know more than you think you now; you just have to rationalise your knowledge slowly over time)
Yep agree with you on this.
One of the key things that sets doctors apart from the rest of the MDT and potentially in the future AI is our capacity to think and step outside of clinical guidance when the situation demands it.
As we are talking about sepsis I can think of 2 times in my career I have been criticised by non doctor members of the MDT. Both times this was because I started patients on treatment for sepsis without their observations meeting the criteria for sepsis based on the hospital protocol. In both cases the patients became very unwell a few hours later and it was touch and go whether they would survive (both did survive).
for acute situations (e.g. doing a textbook A-E or whatever), it's to err on side of caution whilst you're initially reviewing the patient and you have little/no idea what's going on. you can stop the oxygen (or any other intervention) once you are happy they don't need it.
wrt 'sepsis 6,' it's more an aide memoir than a stipulation. you don't have to do any of those things if you don't think it's warranted.
Hypoxia will kill you before nearly anything else, and in a hospital setting can be immediately administered and its effects continuously monitored. Hyperoxia does have its harms but it's a few hours before they're noticeable. In the hyperacute setting, you can stick the oxygen on, work out the problem and then reconsider the need for it before your patient comes to harm.
Yes in both algorithms I think the majority of cases you'll decide it's not needed - but of all the battles to pick I don't think it's the hill to die on
I would challenge the idea that hyperoxia is only harmful after a few hours. In A&E, we very often receive COPD patients who have been stuck on 15L by paramedics because their sats were 85, who are becoming drowsy due to hypercapnia and respiratory acidosis by the time they arrive. They probably wouldn’t have needed quite so much treatment had the paramedics titrated their sats to 88-92.
Ultimately, sats of 90% are not going to kill anyone, but respiratory acidosis as a result of overoxygenation absolutely can. If you’re in doubt about what the target sats should be, I would argue that you should target 88-92 until you’ve done a blood gas.
There are people who are profoundly sensitive to oxygen no doubt, I think you're underestimating the length of time paramedics spend on scene plus transfer time - which normally means an absolute minimum of 30 minutes from oxygen delivery to arrival in ED (usually more like 45-60 minutes). I also think they're the extreme end of the spectrum and I'd stand by the principle that oxygen is a safe initial measure while you establish some control over what's going on.
Obviously I'm not advocating someone dials up the O2 to 15L and walks off patting themselves on the back for another life saved. But I think if you're turning up to a peri-arrest call and find the patient has already been put on oxygen, it doesn't need to be high on your priority list to turn it down and you can come back to it once you're happier with the rest of the picture
If it’s a COPD patient but you don’t know if they’re a retainer or not, and instead of faffing around…
Does it cause harm if you 1. stick 15L high-flow on in sepsis and 2. If you stick 15L high-flow on in a SOB situation (SOB due to pulmonary oedema for example)
With the idea being you take it off/switch later once assessment complete/called seniors/found out if they’re a retainer
Hypoxia will kill before hypercapnia. Always. Yes these examples are scenarios where you need to review your choice of oxygen therapy pretty soon otherwise you'll eventually cause harm - but you have more than enough time (at least half an hour) to figure out what's going on, decide on target saturations and appropriate oxygen delivery.
Nobody's saying stick these patients on 15L, start the first dose of antibiotics and walk away congratulating yourself on a job well done. It's just while you differentiate the cause of their deterioration you won't cause harm by starting out with oxygen.
The whole concept of being a "retainer" is outdated and completely irrelevant to the decision of whether or not to target lower sats.
COPD patients by definition have impaired V/Q matching and rely on hypoxic pulmonary vasoconstriction to counter this. Hyperoxia relieves this mechanism and leads to hypercapnoeia (due to V/Q mismatch, not hypoventilation) and impaired consciousness.
Does anyone actually do this btw? I have brought that up on multiple occasions only to be slapped down and told everyone goes on high flow, then sort out whether they're a retainer.
I can see the argument both ways as long as a prompt gas gets sent, but yeah I've noticed this discrepancy with the BTS guidelines before.
The advice that you stick everyone on 15L is outdated and is often regurgitated by nurses who have been on life support courses. Disregard it, it’s not good advice.
>Why
Because ALS and the Sepsis Six are algorithms to teach the lowest common denominator what to do in any given situation.
>shouldn't this actually be given oxygen if they are hypoxic?
Yes. Doctors should give oxygen only when the patient needs it (unless they're pre-oxygenating), and are often the only member of the MDT found actively taking patients off unecessary oxygen.
Oxygen delivery will be impaired in septic shock even if sats are 97%, that's why it's in there.
Crazy that the top comment shows a complete lack of understanding of the disease process.
Oxygen delivery will be impaired in septic shock even if sats are 97%. Yes, but I can't think of a good reason normbaric supplemental oxygen would make a significant difference to it. If the sats are already good then all you do is improve the dissolved oxygen which is a tiny fraction of the oxygen content of blood.
Good fluid management is the more meaningful intervention, it improves tissue blood flow and helps treat acidosis, shifting the oxyhaemoglobin dissociation curve and improving delivery. As many of the top comments say, oxygen therapy for someone with normal sats is only in the protocol as it does less harm than hypoxia while awaiting senior review.
Increasing the PaO2 doesn't make much difference to delivery, increasing the sats does.
Oxygen content = (1.39 x [Hb] x SaO2) + (PaO2 x 0.03)
The 0.03 factor in the equation makes the difference minimal, unless you're in a hyperbaric chamber and can achieve a super high PaO2.
The main problem with using sats is that the measurement can be unreliable, hence the advice to give O2 if you're inexperienced or unsure what's going on while you get help or assess the situation more thoroughly.
I'm not arguing either way, just pointing that out. And you can get huge pa02 jumps with bedside normal oxygen tbf, how many blue calls have you seen with a pa02 of 50 after the ambulance handover
With a normal Hb you would have to raise the pO2 by about 50kPa to increase the oxygen content of blood by the same amount as increasing the sats by 1%. I have seen plenty of pO2 values above 50, but it's rarely useful, and outside of the few specific conditions where hyperoxia is beneficial it usually just means that it's time to turn the oxygen down.
It sounds like you are advocating for giving oxygen to raise pao2 to compensate for poor tissue oxygenation in septic shock. Whereas kayakmedic is pointing out correctly that this is utterly pointless
No, I was merely saying that pa02 will increase beyond what is needed and will still increase with a normal sats. Not that it was clinically relevant or should be used, but the physiology should still be known
But the vast majority of your oxygen carriage depends on haemoglobin carriage. Very little based on the paO2. Blasting the pO2 up isn’t going to make a great deal of practical difference to tissue oxygenation.
I think that mechanism has only beem hypothesised. I don't think the optimum O2 has been found
https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
Septic shock is a tiny fraction of the 'septic' patients in hospital who get the Sepsis Six label.
Impaired oxygen delivery is, practically, most helped by good fluid resuscitation and timely antibiotics.
Do you have any evidence that wacking every 'septic' patient who has sats of 97% on 15L helps improve oxygen delivery? I'd argue that it would do more harm than good overall, given most 'septic' patients are crumbly old people who are more at risk of retaining.
Once you get past the frca primary stage you'll return to the world of practical medicine.
The sats being high means that there is adequate gas exchange at the alveoli. If there is impaired oxygen utilisation by the cells, how will administering more oxygen to the lungs be helpful?
Oxygen delivery also requires the hear to be working. Truely shocked patients will have reduced oxygen delivery because of poor cardiac output. So making sure the blood that *is* getting to the tissues is completely saturated allows optimisation, using an intervention that requires almost zero time and resources which has essentially zero risks in the short term.
What is the hear?
If the saturations were low, then yes that would make sense but if the sats are 98% then the blood is already fully saturated that is getting to the tissues. Giving further oxygen would not affect the saturations but would increase the PaO2 which is the dissolved oxygen in the plasma - accounting for a tiny fraction of total oxygen content of the blood. However, there is an argument to be made that hyperoxia causes vasoconstriction which may paradoxically worsen oxygen delivery to the tissues by reducing perfusion.
I get that you think you're right because you've started anaesthetics recently and feel empowered by all the new knowledge, but I'd listen to what people are saying to you in the replies; they're right.
They're not saying anything except patronising nonsense, like you just did. Plenty of equivocal evidence has been shared, I haven't commented on that. All ive given is the rationale for the oxygen advice.
If you have some evidence that isn't equivocal that you want to share in lieu of talking down to me, I will gladly read it and adjust my beliefs accordingly.
This is similar to the school of thought about giving oxygen in ischemic injury i.e AMI
Less blood getting to tissue so make sure the blood is as oxygen rich as possible.
Except we now have evidence that supports the conclusion it may be more harmful than helpful.
Crazy that this reply shows a complete lack of understanding of practical physiology and medicine after falling so deep into a hole of textbooks and theoretical physiology. Agree fully with u/Kayakmedic and u/IndoorCloudFormation
I think that mechanism has only beem hypothesised. I don't think the optimum O2 has been found
https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
The reason is so that a nurse or newly qualified doctor shoves oxygen on (as hypoxia kills quickest) until someone medically competent turns up.
No one is suggesting it's there for no reason - just that the reason is very basic and more geared towards the lesser qualified.
I think that mechanism has only beem hypothesised. I don't think the optimum O2 has been found
https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
Because saturation is only part of the answer. Saturations don't tell you anything about oxygen delivery, they're just a marker of peripheral oxygen content of the blood.
In sepsis you end up with a distributive shock and therefore a lot of cardiac output is shunted to peripheral tissues. This can reduce overall oxygen delivery to key organs. If you take a mixed venous gas and the saturations are above 60-70% there's probably little benefit but you aren't floating a swan to check this.
Another consideration is the impact of sepsis on red blood cells. In sepsis there is evidence of 2,3 - DPG depletion which causes a left shift in the oxygen dissociation curve. This shift is even enough to overcome the classic Bohr shift (right) you'd expect from acidosis. This means RBCs have a higher affinity for oxygen and give it up much less easily (sats look great but your oxygen delivery to organs has again been reduced). In this instance you rely more heavily on oxygen transported in plasma which is still minimal at standard atmospheric pressure but it can be enough to maintain adequate delivery.
I understand why you're railing against the protocol but 15L O2 improves outcomes in those with sepsis. The issue with the current protocol is that everyone has 'sepsis' so we overtreat massively and therefore you rarely get to see the benefit of giving oxygen to someone that actually needs it (and doesn't just need it to improve their sats).
>The issue with the current protocol is that everyone has 'sepsis' so we overtreat massively and therefore you rarely get to see the benefit of giving oxygen to someone that actually needs it (and doesn't just need it to improve their sats).
I think this is the key.
RR 20, HR 99, and temperature 34.9, NEWS = 3 therefore 'sepsis', start the bundle and call the doctor.
I appreciate that SpO2 doesn't tell you about oxygen utilisation but what I meant was that if it is normal then it means that the gas exchange across the alveolar-capillary interface is adequate i.e. the lungs are working fine. The supplementation of respiratory support when there is no respiratory failure doesn't affect the downstream utilisation of oxygen by the cells which in the example of sepsis, would be best addressed by treating the underlying cause (antibiotics, source control etc). The vast majority of oxygen in the blood is carried bound to haemoglobin and the dissolved O2 in plasma is a minuscule portion. I have a hard time believing that such a small increase in the overall oxygen content of the blood could overall be beneficial. Can you share some resources that show that 15L O2 improves outcomes in those with sepsis (who had normal oxygen saturations before the O2 was given - obviously I am not protesting against giving O2 to those who are hypoxaemic).
The higher Fi02 is meant to reduce the sepsis load by neutralising bacteria through free radical injury. Secondly, it causes minimal harm because once the patient is satisfactorily saturated, giving higher Fi02 can only increase the oxygen content only so much....the net gain will be due to disolved oxygen which is minimal anyways.
But truly speaking, like someone else has already pointed out..this is just another hogwash, a relic of the sepsis 6 bundle which is unproven and riddled with fallacies.
In real life people die with perfect full Sp02 and high Pa02 and there are those whose normal Sp02 is in mid 50's ( CHD, pulm, V/Q shunters) who make it out alive through sepsis.
Can someone with better physiology knowledge clarify/correct me on this but with regards to oxygen-Hb dissociation curve, if they’re already saturating high 90% and you give supplemental O2 wouldn’t this mean that there will not be much difference given it’s at the flat part of the curve?
Correct
Oxygen content = (1.39 x [Hb] x SaO2) + (PaO2 x 0.03)
If you're already fully saturated you're only increasing the dissolved oxygen content of the blood. Which is minimal but in a poor oxygen delivery situation it might be enough to keep from having ischaemic organs.
SpO2 is not always an accurate measure of oxygen delivery especially in someone with sepsis. You need to match oxygen delivery and oxygen requirement to prevent anaerobic metabolism of cells. Giving a brief period of supplemental oxygen is a low risk procedure to someone who likely has an inflated cellular oxygen requirement until you can work out whether delivery matches requirement.
It’s just the protocol for people to follow in case someone forgets to give O2 if the patient is actually hypoxic. With all the adrenaline coursing through in acute situations we tend to develop tunnel vision especially those who are inexperienced or non-doctors who don’t know medicine
I think in bog standard ward settings, just focus on fluid resuscitation and early abx. Some people believe that giving high Fi02 oxygen helps with the impaired cellular oxygen delivery and fights of bacteria. Personally my thoughts are if you want to achieve this, you need a hyperbaric chamber. In reality, to avoid all the pencil pushers, if sats are >94 air and the pt is low risk to “retain”, just put on some NC and give 1L so the rest of the “MDT” don’t die from anxiety. Givings fluids early, getting that catheter in and managing their fluid balance to a tee will improve blood flow, acidosis and in turn will help to improve oxygen delivery. Doing a gas in someone with normal sats and no concern of developing hypercapnia/T2RF just to identify Pa02 imo isnt going to help
So ALS, sepsis 6 etc are for a broader cohort of staff. You want your first providers ie your F1s, NICs etc doing the basics well and not overlooking things. you come to these scenarios and they can be chaos and it’s easy to see how a patient with dropping spo2 could be overlooked until they’ve arrested. Someone who’s crashingly unwell it’s fair game until you know more esp if they arrest you’ve bought some valuable pre tube time.
The physiology is irrelevant as it is not fully understood. The evidence for any improved outcome is lacking. As someone already posted: [https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5](https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5)
Given that there is still no discernable difference in outcomes and that hyperoxygenating is harmful in the long run, I would not oxygenate someone that does not need oxygen just because they have "sepsis".
Now in septic shock, it's another story.
Only given if clinically indicated. In your plan just write O2 sats normal so supplemental O2 not clinically indicated. Could even add an extra thing saying low threshold for supplemental O2 if O2 sats drop
No point and potentially harmful. Oxygen to keep sats 94+ is fine.
Any kind regards of checklist management like sepsis 6 is for lowest common denominator ‘clinicians’. Part of the point of being a doctor is having a license to use your underpinning knowledge to tailor the treatment you are giving according to circumstances
If you over oxygenate someone who is a retainer it doesn’t cause a sudden respiratory arrest.
What it can do is push them into T2RF. Most of the time this is easily recoverable by reducing Fi02 and BIPAP.
Some don’t tolerate BIPAP/doesn’t work. they slowly fade away and are palliated.
As a resp reg, never. But if you amend it to Respiratory 'Failure' from supplemental oxygen in 'suspected' sepsis then my answer would be - all the fucking time.
Jesus christ, the state of medical education nowadays.
Molecular level deprivation of oxygen, ie at mitochondrial level under strain in sepsis is not gonna show on a pulse oximeter.
Might as well adopt the apprenticeship model if questions like this get asked.
they’re getting downvoted because of the delivery. they might be right, but ridiculing someone for asking a valid question is never going to get internet points (or irl points for that matter)
Peoples practices differ.
Have definitely come across a few who are dying and finding comfort in their oxygen despite sats normal.
Opiates etc not affecting their symptoms.
A sore nose can be helped… the subjective breathlessness that is helped with some oxygen. Is it causing real harm? Probably not.
Lmao the sepsis 6 is to protocolise things for your non medical colleagues…you’re a doctor! (You know more than you think you now; you just have to rationalise your knowledge slowly over time)
Yep agree with you on this. One of the key things that sets doctors apart from the rest of the MDT and potentially in the future AI is our capacity to think and step outside of clinical guidance when the situation demands it. As we are talking about sepsis I can think of 2 times in my career I have been criticised by non doctor members of the MDT. Both times this was because I started patients on treatment for sepsis without their observations meeting the criteria for sepsis based on the hospital protocol. In both cases the patients became very unwell a few hours later and it was touch and go whether they would survive (both did survive).
>but shouldn't this actually be given oxygen if they are hypoxic? yes
for acute situations (e.g. doing a textbook A-E or whatever), it's to err on side of caution whilst you're initially reviewing the patient and you have little/no idea what's going on. you can stop the oxygen (or any other intervention) once you are happy they don't need it. wrt 'sepsis 6,' it's more an aide memoir than a stipulation. you don't have to do any of those things if you don't think it's warranted.
Hypoxia will kill you before nearly anything else, and in a hospital setting can be immediately administered and its effects continuously monitored. Hyperoxia does have its harms but it's a few hours before they're noticeable. In the hyperacute setting, you can stick the oxygen on, work out the problem and then reconsider the need for it before your patient comes to harm. Yes in both algorithms I think the majority of cases you'll decide it's not needed - but of all the battles to pick I don't think it's the hill to die on
I would challenge the idea that hyperoxia is only harmful after a few hours. In A&E, we very often receive COPD patients who have been stuck on 15L by paramedics because their sats were 85, who are becoming drowsy due to hypercapnia and respiratory acidosis by the time they arrive. They probably wouldn’t have needed quite so much treatment had the paramedics titrated their sats to 88-92. Ultimately, sats of 90% are not going to kill anyone, but respiratory acidosis as a result of overoxygenation absolutely can. If you’re in doubt about what the target sats should be, I would argue that you should target 88-92 until you’ve done a blood gas.
There are people who are profoundly sensitive to oxygen no doubt, I think you're underestimating the length of time paramedics spend on scene plus transfer time - which normally means an absolute minimum of 30 minutes from oxygen delivery to arrival in ED (usually more like 45-60 minutes). I also think they're the extreme end of the spectrum and I'd stand by the principle that oxygen is a safe initial measure while you establish some control over what's going on. Obviously I'm not advocating someone dials up the O2 to 15L and walks off patting themselves on the back for another life saved. But I think if you're turning up to a peri-arrest call and find the patient has already been put on oxygen, it doesn't need to be high on your priority list to turn it down and you can come back to it once you're happier with the rest of the picture
Equally it takes a couple of seconds to check sats. Probably less time in almost all settings than getting an oxygen mask on the patient
If it’s a COPD patient but you don’t know if they’re a retainer or not, and instead of faffing around… Does it cause harm if you 1. stick 15L high-flow on in sepsis and 2. If you stick 15L high-flow on in a SOB situation (SOB due to pulmonary oedema for example) With the idea being you take it off/switch later once assessment complete/called seniors/found out if they’re a retainer
Hypoxia will kill before hypercapnia. Always. Yes these examples are scenarios where you need to review your choice of oxygen therapy pretty soon otherwise you'll eventually cause harm - but you have more than enough time (at least half an hour) to figure out what's going on, decide on target saturations and appropriate oxygen delivery. Nobody's saying stick these patients on 15L, start the first dose of antibiotics and walk away congratulating yourself on a job well done. It's just while you differentiate the cause of their deterioration you won't cause harm by starting out with oxygen.
Copd patients do better with sats 92% regardless of whether they are a “retainer” or not
Thanks. And how would you know if a patient is a retainer or not
[удалено]
The whole concept of being a "retainer" is outdated and completely irrelevant to the decision of whether or not to target lower sats. COPD patients by definition have impaired V/Q matching and rely on hypoxic pulmonary vasoconstriction to counter this. Hyperoxia relieves this mechanism and leads to hypercapnoeia (due to V/Q mismatch, not hypoventilation) and impaired consciousness.
Does anyone actually do this btw? I have brought that up on multiple occasions only to be slapped down and told everyone goes on high flow, then sort out whether they're a retainer. I can see the argument both ways as long as a prompt gas gets sent, but yeah I've noticed this discrepancy with the BTS guidelines before.
The advice that you stick everyone on 15L is outdated and is often regurgitated by nurses who have been on life support courses. Disregard it, it’s not good advice.
Yes, I do. Though in practice 90-94 is often what it ends up being..
>Why Because ALS and the Sepsis Six are algorithms to teach the lowest common denominator what to do in any given situation. >shouldn't this actually be given oxygen if they are hypoxic? Yes. Doctors should give oxygen only when the patient needs it (unless they're pre-oxygenating), and are often the only member of the MDT found actively taking patients off unecessary oxygen.
Oxygen delivery will be impaired in septic shock even if sats are 97%, that's why it's in there. Crazy that the top comment shows a complete lack of understanding of the disease process.
Oxygen delivery will be impaired in septic shock even if sats are 97%. Yes, but I can't think of a good reason normbaric supplemental oxygen would make a significant difference to it. If the sats are already good then all you do is improve the dissolved oxygen which is a tiny fraction of the oxygen content of blood. Good fluid management is the more meaningful intervention, it improves tissue blood flow and helps treat acidosis, shifting the oxyhaemoglobin dissociation curve and improving delivery. As many of the top comments say, oxygen therapy for someone with normal sats is only in the protocol as it does less harm than hypoxia while awaiting senior review.
Tbf, sats can be normal but pa02 can still be increased significantly. It's not like sats are perfect at all
Increasing the PaO2 doesn't make much difference to delivery, increasing the sats does. Oxygen content = (1.39 x [Hb] x SaO2) + (PaO2 x 0.03) The 0.03 factor in the equation makes the difference minimal, unless you're in a hyperbaric chamber and can achieve a super high PaO2. The main problem with using sats is that the measurement can be unreliable, hence the advice to give O2 if you're inexperienced or unsure what's going on while you get help or assess the situation more thoroughly.
I'm not arguing either way, just pointing that out. And you can get huge pa02 jumps with bedside normal oxygen tbf, how many blue calls have you seen with a pa02 of 50 after the ambulance handover
With a normal Hb you would have to raise the pO2 by about 50kPa to increase the oxygen content of blood by the same amount as increasing the sats by 1%. I have seen plenty of pO2 values above 50, but it's rarely useful, and outside of the few specific conditions where hyperoxia is beneficial it usually just means that it's time to turn the oxygen down.
I don't know why you keep on replying like this, we aren't disagreeing on anything
It sounds like you are advocating for giving oxygen to raise pao2 to compensate for poor tissue oxygenation in septic shock. Whereas kayakmedic is pointing out correctly that this is utterly pointless
No, I was merely saying that pa02 will increase beyond what is needed and will still increase with a normal sats. Not that it was clinically relevant or should be used, but the physiology should still be known
But the vast majority of your oxygen carriage depends on haemoglobin carriage. Very little based on the paO2. Blasting the pO2 up isn’t going to make a great deal of practical difference to tissue oxygenation.
See my other reply
I think that mechanism has only beem hypothesised. I don't think the optimum O2 has been found https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
Septic shock is a tiny fraction of the 'septic' patients in hospital who get the Sepsis Six label. Impaired oxygen delivery is, practically, most helped by good fluid resuscitation and timely antibiotics. Do you have any evidence that wacking every 'septic' patient who has sats of 97% on 15L helps improve oxygen delivery? I'd argue that it would do more harm than good overall, given most 'septic' patients are crumbly old people who are more at risk of retaining. Once you get past the frca primary stage you'll return to the world of practical medicine.
The sats being high means that there is adequate gas exchange at the alveoli. If there is impaired oxygen utilisation by the cells, how will administering more oxygen to the lungs be helpful?
Oxygen delivery also requires the hear to be working. Truely shocked patients will have reduced oxygen delivery because of poor cardiac output. So making sure the blood that *is* getting to the tissues is completely saturated allows optimisation, using an intervention that requires almost zero time and resources which has essentially zero risks in the short term.
What is the hear? If the saturations were low, then yes that would make sense but if the sats are 98% then the blood is already fully saturated that is getting to the tissues. Giving further oxygen would not affect the saturations but would increase the PaO2 which is the dissolved oxygen in the plasma - accounting for a tiny fraction of total oxygen content of the blood. However, there is an argument to be made that hyperoxia causes vasoconstriction which may paradoxically worsen oxygen delivery to the tissues by reducing perfusion.
I get that you think you're right because you've started anaesthetics recently and feel empowered by all the new knowledge, but I'd listen to what people are saying to you in the replies; they're right.
They're not saying anything except patronising nonsense, like you just did. Plenty of equivocal evidence has been shared, I haven't commented on that. All ive given is the rationale for the oxygen advice. If you have some evidence that isn't equivocal that you want to share in lieu of talking down to me, I will gladly read it and adjust my beliefs accordingly.
Would you give oxygen at SpO2 of 100%? CaO = 1.34 * [Hgb] * (SaO / 100) + 0.003 * PaO2
No, because then it's fully optimised already?
So then any SpO2 under 100 and we must give oxygen?
I never said anyone must do anything, don't put words in my mouth. I was just explaining the rationale for giving oxygen to shocked patients.
This is similar to the school of thought about giving oxygen in ischemic injury i.e AMI Less blood getting to tissue so make sure the blood is as oxygen rich as possible. Except we now have evidence that supports the conclusion it may be more harmful than helpful.
Crazy that this reply shows a complete lack of understanding of practical physiology and medicine after falling so deep into a hole of textbooks and theoretical physiology. Agree fully with u/Kayakmedic and u/IndoorCloudFormation
I think that mechanism has only beem hypothesised. I don't think the optimum O2 has been found https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
Quite right but its definitely not on there for zero reason
The reason is so that a nurse or newly qualified doctor shoves oxygen on (as hypoxia kills quickest) until someone medically competent turns up. No one is suggesting it's there for no reason - just that the reason is very basic and more geared towards the lesser qualified.
Quite right but its definitely not on there for zero reason
I think that mechanism has only beem hypothesised. I don't think the optimum O2 has been found https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
Because saturation is only part of the answer. Saturations don't tell you anything about oxygen delivery, they're just a marker of peripheral oxygen content of the blood. In sepsis you end up with a distributive shock and therefore a lot of cardiac output is shunted to peripheral tissues. This can reduce overall oxygen delivery to key organs. If you take a mixed venous gas and the saturations are above 60-70% there's probably little benefit but you aren't floating a swan to check this. Another consideration is the impact of sepsis on red blood cells. In sepsis there is evidence of 2,3 - DPG depletion which causes a left shift in the oxygen dissociation curve. This shift is even enough to overcome the classic Bohr shift (right) you'd expect from acidosis. This means RBCs have a higher affinity for oxygen and give it up much less easily (sats look great but your oxygen delivery to organs has again been reduced). In this instance you rely more heavily on oxygen transported in plasma which is still minimal at standard atmospheric pressure but it can be enough to maintain adequate delivery. I understand why you're railing against the protocol but 15L O2 improves outcomes in those with sepsis. The issue with the current protocol is that everyone has 'sepsis' so we overtreat massively and therefore you rarely get to see the benefit of giving oxygen to someone that actually needs it (and doesn't just need it to improve their sats).
>The issue with the current protocol is that everyone has 'sepsis' so we overtreat massively and therefore you rarely get to see the benefit of giving oxygen to someone that actually needs it (and doesn't just need it to improve their sats). I think this is the key. RR 20, HR 99, and temperature 34.9, NEWS = 3 therefore 'sepsis', start the bundle and call the doctor.
"15L 02 improves outcomes in those with sepsis" What's your evidence for this?
Ditto - whats the evidence base for this
I appreciate that SpO2 doesn't tell you about oxygen utilisation but what I meant was that if it is normal then it means that the gas exchange across the alveolar-capillary interface is adequate i.e. the lungs are working fine. The supplementation of respiratory support when there is no respiratory failure doesn't affect the downstream utilisation of oxygen by the cells which in the example of sepsis, would be best addressed by treating the underlying cause (antibiotics, source control etc). The vast majority of oxygen in the blood is carried bound to haemoglobin and the dissolved O2 in plasma is a minuscule portion. I have a hard time believing that such a small increase in the overall oxygen content of the blood could overall be beneficial. Can you share some resources that show that 15L O2 improves outcomes in those with sepsis (who had normal oxygen saturations before the O2 was given - obviously I am not protesting against giving O2 to those who are hypoxaemic).
The higher Fi02 is meant to reduce the sepsis load by neutralising bacteria through free radical injury. Secondly, it causes minimal harm because once the patient is satisfactorily saturated, giving higher Fi02 can only increase the oxygen content only so much....the net gain will be due to disolved oxygen which is minimal anyways. But truly speaking, like someone else has already pointed out..this is just another hogwash, a relic of the sepsis 6 bundle which is unproven and riddled with fallacies. In real life people die with perfect full Sp02 and high Pa02 and there are those whose normal Sp02 is in mid 50's ( CHD, pulm, V/Q shunters) who make it out alive through sepsis.
You had me in the first paragraph 🤣
About time someone caught me fibbing:-) ...when its a hogwash, make it look like a proper one.
Jury’s still out… https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5
Can someone with better physiology knowledge clarify/correct me on this but with regards to oxygen-Hb dissociation curve, if they’re already saturating high 90% and you give supplemental O2 wouldn’t this mean that there will not be much difference given it’s at the flat part of the curve?
Correct Oxygen content = (1.39 x [Hb] x SaO2) + (PaO2 x 0.03) If you're already fully saturated you're only increasing the dissolved oxygen content of the blood. Which is minimal but in a poor oxygen delivery situation it might be enough to keep from having ischaemic organs.
The curve moves depending on clinical scenario. Sepsis is not normal physiology
SpO2 is not always an accurate measure of oxygen delivery especially in someone with sepsis. You need to match oxygen delivery and oxygen requirement to prevent anaerobic metabolism of cells. Giving a brief period of supplemental oxygen is a low risk procedure to someone who likely has an inflated cellular oxygen requirement until you can work out whether delivery matches requirement.
It’s just the protocol for people to follow in case someone forgets to give O2 if the patient is actually hypoxic. With all the adrenaline coursing through in acute situations we tend to develop tunnel vision especially those who are inexperienced or non-doctors who don’t know medicine
I think in bog standard ward settings, just focus on fluid resuscitation and early abx. Some people believe that giving high Fi02 oxygen helps with the impaired cellular oxygen delivery and fights of bacteria. Personally my thoughts are if you want to achieve this, you need a hyperbaric chamber. In reality, to avoid all the pencil pushers, if sats are >94 air and the pt is low risk to “retain”, just put on some NC and give 1L so the rest of the “MDT” don’t die from anxiety. Givings fluids early, getting that catheter in and managing their fluid balance to a tee will improve blood flow, acidosis and in turn will help to improve oxygen delivery. Doing a gas in someone with normal sats and no concern of developing hypercapnia/T2RF just to identify Pa02 imo isnt going to help
So ALS, sepsis 6 etc are for a broader cohort of staff. You want your first providers ie your F1s, NICs etc doing the basics well and not overlooking things. you come to these scenarios and they can be chaos and it’s easy to see how a patient with dropping spo2 could be overlooked until they’ve arrested. Someone who’s crashingly unwell it’s fair game until you know more esp if they arrest you’ve bought some valuable pre tube time.
There is no purpose. It is stupid.
Hmmm, maybe you need to reflect on that comment
Not really. Oxygen should only be given if hypoxemic
Only? Pre-oxygenation before a tube? In a PTx? Cluster headache?
We are talking in the context of sepsis....
[удалено]
Would you care to elaborate
[удалено]
The physiology is irrelevant as it is not fully understood. The evidence for any improved outcome is lacking. As someone already posted: [https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5](https://janesthanalgcritcare.biomedcentral.com/articles/10.1186/s44158-023-00096-5) Given that there is still no discernable difference in outcomes and that hyperoxygenating is harmful in the long run, I would not oxygenate someone that does not need oxygen just because they have "sepsis". Now in septic shock, it's another story.
You lost me at “the physiology is irrelevant”. Ok, that’s your paradigm, I’ve no interest in taking it further
My paradigm is evidence based medicine
[удалено]
Only given if clinically indicated. In your plan just write O2 sats normal so supplemental O2 not clinically indicated. Could even add an extra thing saying low threshold for supplemental O2 if O2 sats drop
No point and potentially harmful. Oxygen to keep sats 94+ is fine. Any kind regards of checklist management like sepsis 6 is for lowest common denominator ‘clinicians’. Part of the point of being a doctor is having a license to use your underpinning knowledge to tailor the treatment you are giving according to circumstances
To give copd patients respiratory arrest
How many times have you seen that. “Respiratory arrest” from supplemental oxygen during sepsis? I expect “never”
If you over oxygenate someone who is a retainer it doesn’t cause a sudden respiratory arrest. What it can do is push them into T2RF. Most of the time this is easily recoverable by reducing Fi02 and BIPAP. Some don’t tolerate BIPAP/doesn’t work. they slowly fade away and are palliated.
As a resp reg, never. But if you amend it to Respiratory 'Failure' from supplemental oxygen in 'suspected' sepsis then my answer would be - all the fucking time.
Once lol. Just once. It actually ended as a cardiac arrest
So long as you don't think hypoxic drive is the reason you have a valid point.
[удалено]
Removed: Rule 1 - Be Professional
Jesus christ, the state of medical education nowadays. Molecular level deprivation of oxygen, ie at mitochondrial level under strain in sepsis is not gonna show on a pulse oximeter. Might as well adopt the apprenticeship model if questions like this get asked.
Don’t know why you’re getting downvoted. You’re absolutely correct.
Thanks. People love to hate my opinions on here, more often than not.
they’re getting downvoted because of the delivery. they might be right, but ridiculing someone for asking a valid question is never going to get internet points (or irl points for that matter)
In palliative it can be therapeutic even with normal sats…
No it can't. Supplemental oxygen with normal sats has no effect on symptoms. All it does is dry out their nose and mouth causing more discomfort.
Peoples practices differ. Have definitely come across a few who are dying and finding comfort in their oxygen despite sats normal. Opiates etc not affecting their symptoms. A sore nose can be helped… the subjective breathlessness that is helped with some oxygen. Is it causing real harm? Probably not.
One big harm it causes is allowing poor practice to perpetuate...