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.
Thoughts?
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?