Too Much Oxygen? hmmmm

[usafmedic45]

It is also a common mistake to believe a 15 L NRB mask is "high flow O2".

You must understand a few terms like hyperoxyia which is determined by an ABG (Arterial Blood Gas) not SpO2 and A-a Gradient which is the the difference between oxygen going into the alveoli and that which is in the artery. You can have an SpO2 of 100% and even with being on 100% oxygen, your PaO2 might just fall into the range on the Oxyhemoglobin Dissociation curve.

The oxyhemoglobin dissociation curve relates oxygen saturation (SO2) and partial pressure of oxygen in the blood (PO2), and is determined by what is called hemoglobin's affinity for oxygen,that is, how readily hemoglobin acquires and releases oxygen molecules from its surrounding tissue.

Hyperoxia is defined by many studies as being over 300 mmHg. If patients have multiple disease processes going on, 300 mmHg might be difficult to achieve even on 100% oxygen or just a 15 L NRB mask.

For some neuro and sepsis patients we will run the PaO2 closer to 90 - 100 mmHg rather than the lower 70 - 90 mmHg or 60 - 80 mgHg for some lung diseases. Some neuro patients will have cerebral vasospasms which require a close attention to FiO2 and fluids. For other medical patients we will monitor SvO2 or StO2 which involves tissue oxygenation.

Does this mean all patients need a 15 L NRB mask? No. But as an EMT do you really know all the disease processes or have enough diagnostic data to make a blanket statement?

Remember, you're talking to a practicing RT and former pulmonary physiology instructor.

This is why we have flight, specialty and CCT teams very prevalent in the U.S. in some regions

It goes WAY beyond that.

O2 induced hypercarbia and acidosis

The study you cited has some issues judging by the abstract. As you correct a COPD exacerbation, you often get a decrease (transient) in pH due to a correction of the V/q mismatch inherent in COPD which becomes more pronounced when you start seeing loss of dynamic coupling, the hyperinflation in a lot of cases, etc. The things you're pointing to are the exact origins of the old myth of the "hypoxic drive".

 

[Journey]

Remember, you're talking to a practicing RT and former pulmonary physiology instructor.

You might also be an RT who hasn't worked in an acute hospital or in an ICU since your clinical days. Do you have a Master's degree in Physiology or RT? Or did you just teach basic pulmonary physiology in a tech school? Signatures don't really mean much here and the first posts I read of yours did not present with alot of RT knowledge. Maybe you were dumbing it down and if you were, I apologize. Some here say they are almost a doctor but still post like EMT-Bs without any additional education.

 

[usafmedic45]

No worries. I did post at a rather basic level, but only because I didn't want to absolutely beat the OP over the head with it since I don't know how much they have in terms of an understanding. Better to give the basics and make sure they are clear and let them show the limits of their knowledge and expand from there. No offense taken.


I have taught the basic and advanced pulmonary physiology courses for RTs and I also present at conferences and do continuing education on the subject (especially pertaining to high altitude physiology). Working on my bachelors at the moment, but my goal is actually a doctoral degree in epidemiology with a focus on injury patterns and injury prevention.

 

[MEDIC802]

yes the pulse ox has a place in your assessment but what about treating the pt and not the equipment? It's very rare that pt's that I have come in contact with over the years need o2 via nrb mask @ 15 lpm, a NC @ 2 lpm will be fine with most pt contacts made, unless they are on home oxygen with 1000yards of tubing tangled around furniture ect then there is a problem.

 

[jrm818]

\

The study you cited has some issues judging by the abstract.

Never judge a book by its cover Really, the study deserves a full read. Regardless of putative physiologic mechanisms, a large mortality difference was found in favor of titrated oxygen.

As you correct a COPD exacerbation, you often get a decrease (transient) in pH due to a correction of the V/q mismatch inherent in COPD which becomes more pronounced when you start seeing loss of dynamic coupling, the hyperinflation in a lot of cases, etc. The things you're pointing to are the exact origins of the old myth of the "hypoxic drive".

I'm a bit unclear as to how your description of the physiology is a "problem" for the study. Is the idea that the acidosis is normal and benign?

And maybe a learning point for me: I never heard the "hypoxic drive" described anything like this. I'd always heard/read it described as an adaptation of the cerebral chemoreceptors to chronic hypercarbia and acidosis, thus blunting the normal breathing stimulus due to accumulating CO2, and leaving only the "hypoxic" component of the respiratory drive. The explination was that O2 administration supposedly abolished this last remaining impetus to breathe. Perhaps there was another version?

 

[usafmedic45]

I'm a bit unclear as to how your description of the physiology is a "problem" for the study. Is the idea that the acidosis is normal and benign?

No, it's that you often see a slight change in pH when you're actually improving the patients condition. To say that O2 is the cause for the spike in mortality or the increase in CO2 is something that I can't see being a valid point without more evidence.

I never heard the "hypoxic drive" described anything like this. I'd always heard/read it described as an adaptation of the cerebral chemoreceptors to chronic hypercarbia and acidosis, thus blunting the normal breathing stimulus due to accumulating CO2, and leaving only the "hypoxic" component of the respiratory drive. The explination was that O2 administration supposedly abolished this last remaining impetus to breathe. Perhaps there was another version?

Some of the original "evidence" for the hypoxic drive (which does exist, but it's clinically insignificant in all but a very small minority of patients) in COPD was that giving O2 to these patients caused a rise in CO2 levels which was attributed incorrectly that the O2 was "suppressing" the minute ventilation. The rise is actually due mostly to the Haldane effect and the reversal of hypoxic pulmonary vasoconstriction. Even in severe end-stage COPD, it's quite unusual to see a decline in minute ventilation of more than 10%.

 

[jrm818]

No, it's that you often see a slight change in pH when you're actually improving the patients condition. To say that O2 is the cause for the spike in mortality or the increase in CO2 is something that I can't see being a valid point without more evidence.

If you haven't read the full text yet, it really is worth a read. I'd argue that this trial provides some rather convincing evidence that the mortality (and probably the hypercarbia) were actually caused by oxygen administration variations. This was a well randomized controlled trial with pretty well matched groups. I've obviously had a bit of a debate over the merits of the study beore (that thread I linked to) but I'd be interested in any more specific thoughts.

Some of the original "evidence" for the hypoxic drive (which does exist, but it's clinically insignificant in all but a very small minority of patients) in COPD was that giving O2 to these patients caused a rise in CO2 levels which was attributed incorrectly that the O2 was "suppressing" the minute ventilation. The rise is actually due mostly to the Haldane effect and the reversal of hypoxic pulmonary vasoconstriction. Even in severe end-stage COPD, it's quite unusual to see a decline in minute ventilation of more than 10%.

I'm with you now: I was aware of the no change in minute volume evidence, so in my mind I sort of discarded the notion that development of hypercarbia is related to the theory.

 

[usafmedic45]

Most likely the spike in PCO2 associated with the O2 administration is due to the reduction in hypoxic induced pulmonary vasoconstriction, rather than a worsening of the patient condition. You start perfusing areas that previously were not perfused but were still ventilated, you're going to see your PaCO2 go up.

I just don't see a causative relationship between the O2 and the rise in mortality. There's correlation, yes, but I don't see it as causative. At very least, there needs to be a larger study done to pin it down and reproduce the results.

 

[jrm818]

Most likely the spike in PCO2 associated with the O2 administration is due to the reduction in hypoxic induced pulmonary vasoconstriction, rather than a worsening of the patient condition. You start perfusing areas that previously were not perfused but were still ventilated, you're going to see your PaCO2 go up.

I just don't see a causative relationship between the O2 and the rise in mortality. There's correlation, yes, but I don't see it as causative. At very least, there needs to be a larger study done to pin it down and reproduce the results.

I think your explanation is probably accurate, especially if you add in the influence of the haldane effect, as you note. However, and perhaps I'm wrong, but I was under the impression that the hypoxic vasoconstriction is rather adaptive in this setting, and its artificial removal may worsen V/Q mismatching and cause pathological CO2 accumulatino because more blood is now perfusing lung areas which are still crummy at removing CO2 even though they are now seeing lots of oxygen.


What is the hang up on the causation thing? RCT's are the type of study that is designed to establish causality: because only one intervention is changed, and the groups are randomized and well matched, the only outcome differences in the groups should be because of the changed intervention. Why is that not an acceptable answer here?

Is it just the numbers (obviously more would be better, but this is really not a small study, and a pre-study power analysis was performed indicating that these are adequate numbers, and statistical significance was easily reached for the mortality claim). Is it that there is no other confirmatory evidence (I think there is some). Do you just doubt the biologic plausibility of the whole idea of O2 induced mortality?

I certianly agree that I'd like to see these results replicated in other populations. Still, I think this study does a lot of work towards demonstrating causation.

 

[Chap]

oxygen use

In my EMT class we were taught..."everyone gets oxygen....15ml/min rebreather" (assuming no facial trauma, etc...)


apparently that isn't the way anymore. I wish I had known that...

 

[usalsfyre]

In my EMT class we were taught..."everyone gets oxygen....15ml/min rebreather" (assuming no facial trauma, etc...)


apparently that isn't the way anymore. I wish I had known that...

The kicker is, it NEVER was this way. EMT-Basic is just too dumbed-down to go into how to select appropriate oxygen therapy, so they went with "treat the worst case and most easily correctable condition".

 

[jjesusfreak01]

The kicker is, it NEVER was this way. EMT-Basic is just too dumbed-down to go into how to select appropriate oxygen therapy, so they went with "treat the worst case and most easily correctable condition".

I had a pt today satting between 94% and 96%, didn't put them on supplemental O2, and it didn't bother me one bit. This was an IFT trip and I was the primary provider. I am an EMT-B. If I have access to a pulseox, and the patient doesn't appear to be in any respiratory distress, I am perfectly capable of titrating supplemental O2 to the patient.

 

[Shishkabob]

I had a pt today satting between 94% and 96%, didn't put them on supplemental O2, and it didn't bother me one bit. This was an IFT trip and I was the primary provider. I am an EMT-B. If I have access to a pulseox, and the patient doesn't appear to be in any respiratory distress, I am perfectly capable of titrating supplemental O2 to the patient.

My old EMT challenged my decision on that one time: No signs of respiratory distress, good pulse ox, good CO2, etc etc etc, every assessment was negative for SOB aside from the family stating she looked short of breath. I kept her on the 2lpm NC... my partner said "Are you sure? I think we should do a non-rebreather at 15"



No, I'm not sure, I make arbitrary decisions of patient care all the time, my years of education be damned.

 

[Neo]

How long do you plan on keep the patient inside an ambulance? Do you there can be some cerebral situations where O2 by mask at 100% is indicated? Do you withhold oxygen to a patient that needs it now to prevent immediate damage to organs for something that might start to happen 24 - 72 hours later?

Are you working adult codes on 21% or have a way to accurately titrate O2 to a specific concentration in an ambulance that is not a Specialty unit?

What Oxygen Curve are you referring to? The Oxyhemoglobin Dissociation curve should how you can have a pulse ox of 94% but very different PaO2 values for each patient depending of the factors that shift the curve.

I think your not talking about the same thing here, of course som patient need it he has to get the right amount of O2. puls ox is unstable to use becouse it reacts on skinn temp. o.s.v we do research on free radicals now, and i think we will see a big change in how we administerd O2 to ROSCH and ESTEMI patient and more. If you wonder how fast the reaction is you can see for your self in this formula. The formation of hydrogen peroxide (H2O2) in the body continuously. The body get rid of most of this through enzymes called peroxidase, which converts H2O2 to two water molecules (the remaining hydro genes come from a molecule that hetet NADPH).

Something H2O2 "escapes" the enzyme and if it comes in contact with divalent iron (which is part of the body) will be formed OH radicals (OH • printed):

H2O2 + Fe2 + -> • OH + OH-+ Fe3 +

• OH is very reactive and will react with other substances, such as unsaturated fatty acids, which are very much in the membrane that surrounds all cells in the body. Let RH be an unsaturated fatty acid, and we get a three-step reaction:

Initiation: RH + OH • -> R • + H2O

Propagenering: R • + O2 -> R-O-O •

and R-O-O • + RH -> R-O-O-H + R •

Termination: Interaction between the radicals and the production of non-initiating and non-propagenerende species.

Propageneringstrinnet can happen a number of times before it stops. The reason for this is that it is both consumed and produced a radical, and radicals are unstable since they contain an unpaired electron.

In propageneringsprosessen is the first step rapidly, and the second step rate determining.

 

[JJR512]

Love is like oxygen. You get too much, you get too high.
Not enough and you're going to die.

 

[18G]

Pennsylvania protocols just released also state to titrate oxygen to SpO2 >94%. Oxygen use has always been a major pet peeve of mine especially when used to treat MI / ACS.

This is an evidence based recommendation. High flow oxygen has been shown to cause coronary vasoconstriction thus decreasing coronary blood flow, decreased CO, and worsening of the ischemia.

 

[lightsandsirens5]

Pennsylvania protocols just released also state to titrate oxygen to SpO2 >94%. Oxygen use has always been a major pet peeve of mine especially when used to treat MI / ACS.

This is an evidence based recommendation. High flow oxygen has been shown to cause coronary vasoconstriction thus decreasing coronary blood flow, decreased CO, and worsening of the ischemia.

It's about freaking time someone changed that one! Maybe more states will follow. I hope to God they do!

 

[jjesusfreak01]

I think your not talking about the same thing here, of course som patient need it he has to get the right amount of O2. puls ox is unstable to use becouse it reacts on skinn temp. o.s.v we do research on free radicals now, and i think we will see a big change in how we administerd O2 to ROSCH and ESTEMI patient and more. If you wonder how fast the reaction is you can see for your self in this formula. The formation of hydrogen peroxide (H2O2) in the body continuously. The body get rid of most of this through enzymes called peroxidase, which converts H2O2 to two water molecules (the remaining hydro genes come from a molecule that hetet NADPH).

Titrating O2 to 95% saturation does not result in any larger amount of O2 in the body than the patient would get when breathing normally in a non-emergent situation. Also, why are you posting the radical formation reaction? I had hoped to never see that again after the MCAT.

 

[JPINFV]

o.s.v we do research on free radicals now, and i think we will see a big change in how we administerd O2 to ROSCH and ESTEMI patient and more.

Just curious, what are the literal translation for ROSCH and ESTEMI? I'm going to go out on a limb and think that they are synonymous with "return of spontaneous circulation" (ROSC) and "ST-elevated MI" (STEMI). I am, however, having problem placing the additional letter.

If you wonder how fast the reaction is you can see for your self in this formula. The formation of hydrogen peroxide (H2O2) in the body continuously. The body get rid of most of this through enzymes called peroxidase, which converts H2O2 to two water molecules (the remaining hydro genes come from a molecule that hetet NADPH).

...don't forget about catalase. The reason hydrogen perioxide bubbles when put onto exposed cuts is not because it's killing bacteria, but because oxidase positive cells (both some types of bacteria and human cells) are breaking it down.

 

[DitchDoctorGabe]

True but dare I say common sense judgment is needed. I don't see a huge issue for a short term transport and the pt. receives high flow oxygen. Granted we are aiming at keeping sats 94% or above and the long term issues is that you have to deal with free oxygen radicals. Plus in the neonates you do run the risk of causing retinopathy of prematurity.