New Tack on Cardiac Arrest: Turn Down the Oxygen, very interesting article on EMS responder.com http://www.emsresponder.com/article/article.jsp?id=13503&siteSection=1
oxygen is bad.....????
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JPINFV
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First semester of medical school included an entire lecture just on reactive oxygen species. In other lectures we covered apoptosis vs necrosis (essentially the foundation of why theraputic hypotermia works). Anyone who says that oxygen is harmless is either ignorant or a lier. What is true, though, is that for the timeframe that EMS operates in, withholding oxygen is generally more bad juju than administering it. What's important is knowing where that bad juju is and where it is not.
There was a guy on the TED website talking about an injectable drug that can essentially put a dying person in stasis, by locking the ability of cells to get oxygen out and dropping metabolism to a near standstill. Strange concept, but it works - and he's wanting to see it used in EMS.
Since we're on the topic of reducing oxygen consumption.
Since we're on the topic of reducing oxygen consumption.
better as part of this dscussion
Originally Posted by got_shoes
Life I will also say that for the most part oxygen should never be with held from a pt that does actually need it. but at the same time a lot of EMS providers think oxygen should always be applied no matter what..
Not directed at anyone, but food for thought.
"When it is needed" is exactly the point.
Lets look at blood loss from trauma. There is a great push to find something that will transport and gie up oxygen in the body.
If you add 15L of NRB but losing the blood that carries the oxygen, all you are doing is adding free radicals. Can we agree that adding oxygen when there is no ability to transport it to tissues doesn't really do anything productive?
consider any shock for that matter.
Look at the plethora of airway diseases where o2 intake is not the issue. If there is already enough O2, how does adding more help?
Forget hypoxic drive, and all the myth surrounding that, if you have one functioning alveoli out of 10 or more, does adding oxygen increase the surface area for gas exchange? How?
Want to see? get a straw and some bubbles. Put one bubble on one end of the straw and a second bubble opposite. They don't equal in pressure, one gets smaller and one gets bigger.
What about oxygen as a vasoconstrictor? Does constricting coronary arteries in an ACS seem like it would be of benefit?
EMS relly boarders on snake oil sales. Mythological magical traditions and catch phrases that withstand evidence to the contrary. Is that the mark of medical professionalism?
"If some is good more is better???"
I am not suggesting oxygen, even at 10L NRB never helps, only that there are relatively few times it does.
It is nice to turn phrases like "don't withold when needed." But with such little need, perhaps withholding is a better standard than flooding in all cases?
Originally Posted by got_shoes
Life I will also say that for the most part oxygen should never be with held from a pt that does actually need it. but at the same time a lot of EMS providers think oxygen should always be applied no matter what..
Not directed at anyone, but food for thought.
"When it is needed" is exactly the point.
Lets look at blood loss from trauma. There is a great push to find something that will transport and gie up oxygen in the body.
If you add 15L of NRB but losing the blood that carries the oxygen, all you are doing is adding free radicals. Can we agree that adding oxygen when there is no ability to transport it to tissues doesn't really do anything productive?
consider any shock for that matter.
Look at the plethora of airway diseases where o2 intake is not the issue. If there is already enough O2, how does adding more help?
Forget hypoxic drive, and all the myth surrounding that, if you have one functioning alveoli out of 10 or more, does adding oxygen increase the surface area for gas exchange? How?
Want to see? get a straw and some bubbles. Put one bubble on one end of the straw and a second bubble opposite. They don't equal in pressure, one gets smaller and one gets bigger.
What about oxygen as a vasoconstrictor? Does constricting coronary arteries in an ACS seem like it would be of benefit?
EMS relly boarders on snake oil sales. Mythological magical traditions and catch phrases that withstand evidence to the contrary. Is that the mark of medical professionalism?
"If some is good more is better???"
I am not suggesting oxygen, even at 10L NRB never helps, only that there are relatively few times it does.
It is nice to turn phrases like "don't withold when needed." But with such little need, perhaps withholding is a better standard than flooding in all cases?
mycrofft
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Show me some dog or pig studies
I just read a "scientific" paper which made it into a journal that used some empiric hocus pocus and pocket calculator mumbojumbo to say that somewhere between, let's see, three and fifty-four percent of the population is at risk for anaphylaxis. Nice tautology but their reality-reasoning was third grade.
We will continue to see articles claiming breakthroughs and new tools or discrediting old tools (for new tools) so long as these people get attention and funding and maybe advertising fees for them.
Show us some lab testing, and the statistical samples and processing to turn em piricist fairytales (and apparent outright lies) into science.
I just read a "scientific" paper which made it into a journal that used some empiric hocus pocus and pocket calculator mumbojumbo to say that somewhere between, let's see, three and fifty-four percent of the population is at risk for anaphylaxis. Nice tautology but their reality-reasoning was third grade.
We will continue to see articles claiming breakthroughs and new tools or discrediting old tools (for new tools) so long as these people get attention and funding and maybe advertising fees for them.
Show us some lab testing, and the statistical samples and processing to turn em piricist fairytales (and apparent outright lies) into science.
Aidey
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I think a huge part of it is that we (the medical and research community) still don't know when it really is needed, with EMS being the most uneducated.
I get the impression that a lot of the people I work with think that oxygen will solve everything, when really, you can't out oxygenate 99.8% of all disease processes.
Hypothetically on my last cardiac arrest the BMV didn't get hooked up to the O2 in the ambulance. The pts CO2 was maintained within 45-55 mm/hg, and his labs weren't all that bad at the hospital, especially considering it was an asthma induced arrest. CO2 started out in the high 80s, and dropped steadily post intubation. The SpO2 was not attached for whatever reason, but the pt started out with localized cyanosis to the fingertips, and ended pink and warm (a nurse actually complimented us for the pt having warm feet...a nice but unusual compliment). Again hypothetically, this patient regained a pulse and 'lived' on life support for a few days.
Thinking about it, how many vent dependent patients do you run into that are on high concentration O2? It seems like when we pick them up they are usually on 1-3lpm, or no supplemental O2 at all. In an arrest patient, once the hypoxia is corrected (or at least improves significantly) wouldn't treating them similar to a vent patient make sense, at least as far as their respiratory system is concerned?
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Sandog
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This sounds like nonsense. Cellular respiration is pretty much hallmark in sustaining a living organisms functions such as, breathing, walking, thinking, heartbeat, etc...
JPINFV
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2 words. Anarobic respiration.
Sandog
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Anaerobic respiration cannot be performed by all human cells, and the ones that are able to can only sustain this condition for a short period of time as lactic acid is formed.
JPINFV
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Lactic acid dehydrongenase is found in the vast majority of cells and, except for some types of muscle cells, represents a last ditch effort to produce ATP. Which, is exactly my point. If you lock out the cells ability to obtain and use oxygen then the cell will switch to anaerobic respiration and, unless quickly reversed, die.
Sandog
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Okay so I am confused, are you supporting or refuting my original post? From this post it sounds like we are in agreement. :unsure:
JPINFV
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My post was directed at abeth86, which would put us in agreement.
Sandog
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Very well then, I will Shad up... :blush:
mycrofft
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We're not refuting peple, we refute claims.
People we just tease, ridicule and flirt with.
Not to argue, but to ask: what is the time frame for formation of all these harmful radicals, and their dire effects?
It's like we need three classes of physiochemistry: "Right Now" (effects in up to say 30 minutes), "Soon" (effects within a couple hours or so) and "Who Cares?", (effects expected long after the pt's life and limb are saved).
People we just tease, ridicule and flirt with.
Not to argue, but to ask: what is the time frame for formation of all these harmful radicals, and their dire effects?
It's like we need three classes of physiochemistry: "Right Now" (effects in up to say 30 minutes), "Soon" (effects within a couple hours or so) and "Who Cares?", (effects expected long after the pt's life and limb are saved).
As fast as the rate of reaction will proceed.
In simple biochemistry, as soon as something that has electrons to donate or weak enough valence electrons to be removed by oxygen the damage will be done. We are not talking about 1 molecule of oxygen, we are talking about 10-15L per minute. I am too lazy to calculate out the molar concentration, but it is a lot.
Based on the entry of oxygen, You are talking about damage to the lower respiratory tissue, heart, kidney, brain, and anywhere else the blood is going. You could kill cells by the millions if not billions in a short transport. (say about 10 minutes)
The injury to cells is not only from direct free radicals which cause necrosis from lysing the cell membrane. Oxygen also starts the mitochondrial apoptotic cascades which are irreversible positive feedback. Which means you kill the cell early, but don't see its complete breakdown for hours to days.
In short, the oxygen applied early will be killing the cells by various mechanisms which will manifest clinically in hours or days.
Let me use one example, MI.
the initial ischemic tissue dies. It then starts to break down in the pattern of coagulative necrosis. (usually it takes about 4-7 days for the cells to be completely broken down) In this period the inflammatory process starts to degrade these dead cells and replace them with scar tissue so there is not a hole in the organ. the immune cells also break down some of the healthy cells on the perimeter. If necrosis proceeds in an area large enough, the fibroblasts cannot create scar fast enough and the heart wall ruptures. As well if the damage is deep enough the heart loses its ability to effectively contract, so even without the hole, if the patient is lucky they are going to get an LVAD. If not lucky, well... their problems are over.
Because excess oxygen causes reperfusion injury via apoptosis (described above) you lose even more cells which cannot be reversed/treated. (over 4-7 days) making the likely hood of rupture greater. Even if you don't have rupture you could go from losing (lets make it massive to keep numbers simple, but it could apply to any amount) 10% of superficial ventrical to a complete transmural loss of 30-40% increasing not only the risk of death to the patient, but also leaving the patient with considerably more disability then what they might have endured.
In summary, the damage is done early (seconds to minutes), but the effects are seen days later.
Aidey
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So can I start telling people to stop putting 15lpm on stubbed toes because they are killing their patients?
Kidding....mostly....
Kidding....mostly....
Not sure what the "TED" is, but it sounds like he may be talking about this:
http://www.ncbi.nlm.nih.gov/pubmed/19628092
This obviously is not quite the same as "turning off" cellular respiration. we need clarification on if this is the same idea, but the VPA is supposed to be injectable, prevent cell death despite cellular hypoxia, and certianly holds possibilities for the EMS world, so it may be the same thing.
I heard the 1st author speak about this a few days ago (first I had heard of it....brilliant physician, very very cool work imho), and he was especially interested in moving this into the pre-hospital and military environments. They're envisioning an autoinjector setup, apparently.
In all fairness, many of the cells killed have already been weakend by another injurious stimuli.
But some cells will be killed no matter what. One of the original scintists that defined/studied pharmacology, (his name escapes me, but I remember he was an alcoholic) said: "all drugs are poisons."
It wasn't a don't use drugs campaign, it was to point out your treatment should not be worse than your disease. If you consider how pharmacological agents work at the molecular level, there is absolutely no difference in actions for medications then there are for poisons. He didn't have the benefit of molecular biology in his day, so I guess he was kinda smart.
MonkeySquasher
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Okay, so, in an attempt to walk myself through this and understand...
We're talking about reperfusion injuries in that... When perfusion stops and cells switch to anaerobic respiration, lactic acid is produced, etc, and the resulting movement of blood circulation again basically spreads the icky bad stuff everywhere. Got all that down.
But the stasis-inducing drugs are meant to completely stop the respiration, aerobic or otherwise? Therefore, no lactic acid is produced, as the cell doesn't do anything. And you can correct the problem and reperfuse properly without having to worry about circulating the icky bad stuff... Correct?
Similar to cryogenically freezing, stops everything cold?
We're talking about reperfusion injuries in that... When perfusion stops and cells switch to anaerobic respiration, lactic acid is produced, etc, and the resulting movement of blood circulation again basically spreads the icky bad stuff everywhere. Got all that down.
But the stasis-inducing drugs are meant to completely stop the respiration, aerobic or otherwise? Therefore, no lactic acid is produced, as the cell doesn't do anything. And you can correct the problem and reperfuse properly without having to worry about circulating the icky bad stuff... Correct?
Similar to cryogenically freezing, stops everything cold?