Physiological effects of Oxygen

[medicdan]

Yes, one more oxygen thread... but I hope this one is different. I've been scouring the interwebz and this forum for true academic discussion of the prevalence of free-radicals and not found much. I've turned to a friend who is particularly adept at physiology, and as an EMT, tries to put Oxygen on every patient he can, which I disagree with. What follows is his discussion and understanding of the effects of oxygen. I certainly don't have the knowledge-- but I'm interested in hearing how you reconcile this understanding with your own and published literature.

It is true that oxygen is a vasoconstrictor. Something that these articles didn't note is that O2 is a LOCAL vasoconstrictor that will act primarily in arterioles. In this case it will act in a mechanism called flow auto-regulation. However, in this case the myocardial muscle cells would likely be low in oxygen conditions (expecially if SATing below 94%), creating a gradient of oxygen dissociation and a quick equilibrium directly into the muscle cells. O2 only causes vasoconstriction when in the vasculature, not in the muscle cells.

In addition, there would likely be another process at work called active hyperemia. The myocardial cells would be using up oxygen and producing CO2 (in fact, they wouldn't have enough O2, so the equilibrium would lie in favor of CO2. CO2 is a known LOCAL vasodilator and could cancel out the effects
of any hyperoxia.

Finally, hyperoxia would be unlikely in any case (in my opinion) for multiple reasons:

1) the obvious reason of the MI itself

2) the harder concept of fluid dynamics. There are two main ways that o2 can travel in the blood stream, by hemoglobin and by dissolving in the blood. To give you an idea of the normal physiology, there are about 200ml of o2 in a normal liter of blood. 197 ml are hemoglobin bound and only 3 are dissolved. This is because Henry's Law states that the dissolving of a gas is proportional to its partial pressure. HOWEVER, it is also due to the fact that O2 has a low solubility in H2O. This being said, consider the following:

The hemoglobin of a normal pt. should be saturated or almost saturated, so take that out of the equation. All that's left is dissolved O2. Yes dissolved O2 will rise because the partial pressure of O2 is way more at 15 lpm. However, it will still most likely be negligible in comparison to Hbg O2 content. Therefore, risk of hyperoxia seems low to me.


MY CONCLUSION:

What is above is only speculation based on physiological knowledge.

All of this being said, the research is inconclusive. In terms of O2 administration, no strong benefit is shown, nor is strong harmful effect.

Also, while I know more than your average EMT-B about cardiac physiology, and maybe even more that your average paramedic, I am by no means an expert. I think that in light of recent research, EMTs should make their own decisions about O2 administration.

For me that means O2 should always be administered when O2 SAT is below 94%...I don't see enough reason not to give high flow O2 in this case (unless the pt. looked totally fine, in which case maybe NC). Perhaps when the pt has reached an acceptable level of O2 SAT, I would consider stopping O2 administration depending on pt status.

The most important thing is that we still have eyes and ears. We should all be thinking about and evaluating our treatments mid-call constantly. In the real world, if I give O2, and its making it worse, I'm gonna take it off. It it's making it better, hell yeah im gonna use it lol.

I do strongly agree with you and the other EMTs that all EMTs should be better educated about this dispute, and they should not be taught all O2 all the time.

Thoughts?

 

[JPINFV]

Your friend is mistaking global hypoxia for ischemia (think local hypoxia). Vasodilation isn't going to dilate the atherosclerotic plaque. The big issue with MIs isn't so much the vasoconstriction so much as the reperfusion injury following uncorking the artery.

 

[Fish]

Your friend is mistaking global hypoxia for ischemia (think local hypoxia). Vasodilation isn't going to dilate the atherosclerotic plaque. The big issue with MIs isn't so much the vasoconstriction so much as the reperfusion injury following uncorking the artery.

Hence Hypothermia Protocols for Cardiac Arrest

Lots of studies coming out that pertain to "Toxic" o2 levels, ie. placing an NRB on every patient you run into.

 

[medicdan]

JP, I think you were misunderstanding the original point...

What I am arguing against is LOCAL vasoconstriction of the coronary vasculature. I'm not even arguing that net vasoconstriction will help the pathophysiology. That would be silly, as it would contradict my own initiative to give oxygen (active hyperemia would be more potent without O2).

What I am trying to say is that O2 causing vasoconstriction problems in the coronary vasculature is not a valid concern to me when I measure it against the possible benefits of raising global O2 Sats...

Sent from my DROID2 using Tapatalk

 

[firetender]

Source?

It would be helpful if you could identify the person you're quoting or cite a reference source that he/she is using. It would make it easier for us. As it stands, all you're saying is my friend thinks this, and that's not enough.

Personally, I'd like to hear how Rogue Medic would respond.

 

[Brandon O]

Hi Dan, Russ.

There are two approaches here, I think.

The most valid one is empirical. The body is very complicated, and try as we might, we're often wrong when we predict the way things will happen. To quote a friend, there are all kinds of things that make perfect sense but just aren't so. So we're best off considering studies that actually put people on oxygen and examine whether they do better or worse.

The other method is physiological, and if nothing else it's good fun and a nice mental workout. But we have to decide what we're talking about. Is it the effect of blood oxygen levels on myocardial tissue survival after an ischemic (obstructive) cardiac event? Okay.

If there is damage, what causes it? A large part is presumably caused by hypoxia -- oxygen is not reaching cells, so they're dying. Some, however, is presumably caused by reperfusion -- circulation is restored, oxygen floods the ischemic tissues, and the return to normal perfusion causes damage. The big shift in the past 10 years has been the recognition that this latter is actually very significant and may actually be responsible for much of the damage.

So perhaps there are two opposing threads:

1. Will giving supplemental oxygen to this patient reduce hypoxic coronary damage?

2. Will giving supplemental oxygen to this patient increase reperfusion injury?

Again, we're just spitballing here. But much of the current thinking reflects the answers: probably no, and probably yes.

Mind you this assumes no global hypoxemia. If they're satting 80% they probably need to improve that. But if they're satting 96%, will 100% benefit them? How much more oxygen is actually being carried here? In terms of hemoglobin-bound O2, not a huge amount. Moreover, how much is reaching the injured tissue? Since the whole problem is obstruction, probably not much. Can there be minimal or collateral circulation which we can "superoxygenate"? Yes, but does this small improvement counterbalance the reperfusion issue? Perhaps we're just creating a more dangerous solution to flood the area once we do obtain reperfusion (via thrombolysis or PCI).

Furthermore, and although I haven't heard this stated explicitly, one of the implicit ideas many people seem to hold is that tissue oxygenation is improved by high hemoglobin saturation (since this is, by far, where we can transport significant amounts of O2), but reperfusion injury is increased by high levels of dissolved oxygen -- PO2. Put another way, if you're satting 100%, and then I radically increase your PO2 by flooding your lungs with high partial pressures of oxygen, your saturation will not increase (can't beat 100%), but your PO2 will go up. Is this good?

Just throwing around ideas here, and I'm no physiology wiz myself. But given the AHA's current recommendations to titrate oxygen only to maintain >94% sats, they seem to agree with the general gist. Again though, this is all just kitchen table stuff; serious protocol and care decisions should be based on outcome-based research.

 

[Aprz]

Beautiful post Brandon Oto. +1

 

[Tigger]

It would be helpful if you could identify the person you're quoting or cite a reference source that he/she is using. It would make it easier for us. As it stands, all you're saying is my friend thinks this, and that's not enough.

Personally, I'd like to hear how Rogue Medic would respond.

I think that's kind of the point of his question? This is friend's theory and he is seeking commentary on it, seems to be enough to me.

Who is Rouge Medic and why does his opinion carry so much weight?

 

[JPINFV]

Who is Rouge Medic and why does his opinion carry so much weight?

www.roguemedic.com

Somethings you just have to read for yourself.

 

[Tigger]

www.roguemedic.com

Somethings you just have to read for yourself.

I appreciate his message, and agree with what he says, though admittedly much of it is entirely over my head at this point. However, I have a hard time taking an anonymous blogger's work as any sort of evidence into an argument. Maybe that's just the political-science major in me.

 

[firetender]

Rogue is a proponent of "evidence-based medicine" and as he discusses the nuts and bolts, he backs what he says up with references. At the least, he's a good role-model when it comes to supporting claims or questioning the status quo.

By the way; rouge is what you put on the cheeks of a corpse to make it look lively.

 

[Tigger]

Rogue is a proponent of "evidence-based medicine" and as he discusses the nuts and bolts, he backs what he says up with references. At the least, he's a good role-model when it comes to supporting claims or questioning the status quo.

Don't get me wrong, I appreciate what he is doing. Not enough people are vocal enough like he is to bring about change. There is a limit the amount of evidenced based medicine that I can personally practice, given that my scope is quite limited. Still, I try to do what is proven to be useful, and then some partners look at me like I have four heads. Someone smarter than me is going to have bring about systematic change I am afraid.

By the way; rouge is what you put on the cheeks of a corpse to make it look lively.

:embarrassed:

 

[Brandon O]

In fairness he'd probably disagree with anyone appealing to his authority anyway. That's not how he rolls.

 

[mycrofft]

So how does this impact the empiric statements about O2 and decompression syndrome?

One of the very first threads I weighed in on (and got shown I was wrong) was whether or not atmospheric pressure oxygen was of help in cases of "the bends", and it was shown that there are references that say it is (oxygenation through collateral circulation). If O2 causes peripheral vasoconstriction, then it would seem that at atmospheric pressures but elevated concentrations, it could make things worse?

 

[medicdan]

One of the very first threads I weighed in on (and got shown I was wrong) was whether or not atmospheric pressure oxygen was of help in cases of "the bends", and it was shown that there are references that say it is (oxygenation through collateral circulation). If O2 causes peripheral vasoconstriction, then it would seem that at atmospheric pressures but elevated concentrations, it could make things worse?

Divers Alert Network, out of NOrth Carolina has studied this, and if I recall, shown that supplemental o2 at atmospheric concentrations is beneficial. I am not at my computer now, but can look it up tonight.

Sent from my Droid.

 

[uminchu]

Respiratory Drive Suppression

I think the one problem w/just tossing O2 on everyone is that some Pt's O2 sat is constantly 95% or lower, simply because of the age of the Pt or their hx of smoking, exposure to damaging chemicals, poor circulation in general etc. High flow 100% Oxygen in this case will of course assist them w/raising their 02 saturation but will limit their need to breathe, as their bodies have grown accustomed to a diminished level of 02 circulating generally. This would subsequently lead to an increase in the levels of CO2 and other waste products to build up within the body potentially making the person's own blood toxic to them in effect doing more harm then good.
I personally think O2 is an excellent treatment strategy for a majority of EMS patients, but I believe that any time you administer any medication you must be judicious in your follow up care, monitoring those vitals, looking for trends in the Pt's condition and if they begin to deteriorate despite a rise in their 02 saturation you have to decrease the flow, or remove the O2 altogether.
All that being said, excellent discussion IMO.

 

[Cawolf86]

High flow 100% Oxygen in this case will of course assist them w/raising their 02 saturation but will limit their need to breathe

I personally think O2 is an excellent treatment strategy for a majority

Hypoxic drive is a minor/false consideration in my mind and has been largely dismissed.

Oxygen is an excellent treatment when needed - definitely not any majority of my patients.

 

[JPINFV]

High flow 100% Oxygen in this case will of course assist them w/raising their 02 saturation but will limit their need to breathe, as their bodies have grown accustomed to a diminished level of 02 circulating generally. This would subsequently lead to an increase in the levels of CO2 and other waste products to build up within the body potentially making the person's own blood toxic to them in effect doing more harm then good.

You do realize that the primary physiological parameter used to determine ventilation rate is CO2 levels and not O2 levels?

 

[Veneficus]

Hypoxic drive is a minor/false consideration in my mind and has been largely dismissed.

"I find your lack of faith...

...disturbing."


It is not that hypoxic drive is false, it exists in a specific subset of patients, end stage copd of the blue bloater variety.

Pulmonology actually sees it a lot.

Because these people are often institutionalized, and may be a DNR, it is unlikely EMS has much interaction with them, and consequently over exaggerate the incidence.

Just like spinal injuries and a host of other conditions.

 

[Cawolf86]

"I find your lack of faith...

...disturbing."

QUOTE]

Apologies - my intent was to say that it is so rarely encountered that it should not be applied to every patient or COPD patient we encounter.