Oxygen, anyone?

Here - take a whiff of this

The good gas or not so good - that is the question. And a question it will remain (especially in EMS practice) until a substantive body of evidence indicates changes are needed for better clinical outcomes. Small studies in healthy patients are interesting at best but won't cut the mustard with the medical types, conservative lot that they are.

They just might need a little more convincing.

Mind you there is also a trap here for we ambo types that has been revisited more than once in the past and caused more problems than it has solved.

So and so said.....and he had this amazing study which showed such and such.
We need to put all our research together systematically as part of a process not part of conversation. (These remarks aren't intended for you SMASH by the way).

The easy step is introducing topics of conversation and presuming you have a point. The hard bit is proving it conclusively and seeing change result.

Just my thoughts.

MM
 
Small-ish thread necro. The systems here have ALS providers which are uniformly of the belief that all patients, period, must have oxygen. Sat 99% on RA with complaint of cut on foot sans any other illness, injury, or clinical concern? Gets at least nasal cannula, min. of 4 LPM.

I know this, as the fire medic had a fit and I questioned my boss, who upheld that all our patients must be given oxygen of at least 4 LPM. Of course, they also mandate at least a saline lock on all patients, per the hospital's "request." And transport all codes with L&S. And don't count scene time if it's in the back of an ambulance. And it really gets worse.

Luckily, I'll be (back) out of the business for good soon. Quite tired of silly medical decisions being made by people who have no collegiate medical history whatsoever.
 
Treatment without benefit is a potential tort and an unnecessary expense.

Ths study is an anecdote. Maybe we see the body "decompensating" in a healthy subject because it's receptors have sensed that O2 is up, so a lower degree of cardiopulmonary activity is adequate...in otherwords, it is compensating for a heightened O2 level.
Maybe.

If that occurs to an otherwise compromised pt, then it is bad, but if those receptors are still working properly, the pt should not exhibit the same sort of response as the healthy ones.

Folks, "Thuh Meeedia" doesn't use even junior high school science to decide which "studies" or "experts" to expose to "Thuh Peepul" for their edification. We need to be "critical consumers of 'fact' ", as my statistics prof used to teach us to be.
 
Hal9000 said:
Small-ish thread necro. The systems here have ALS providers which are uniformly of the belief that all patients, period, must have oxygen. Sat 99% on RA with complaint of cut on foot sans any other illness, injury, or clinical concern? Gets at least nasal cannula, min. of 4 LPM.

I know this, as the fire medic had a fit and I questioned my boss, who upheld that all our patients must be given oxygen of at least 4 LPM. Of course, they also mandate at least a saline lock on all patients, per the hospital's "request." And transport all codes with L&S. And don't count scene time if it's in the back of an ambulance. And it really gets worse.

Luckily, I'll be (back) out of the business for good soon. Quite tired of silly medical decisions being made by people who have no collegiate medical history whatsoever.
Click to expand...

Lol mandatory oxygen and IVs for all patients, is archaeic. wasteful and probably even detrimental. What if the pt with the cut foor gets phlebitis?
 
mycrofft said:
Ths study is an anecdote. Maybe we see the body "decompensating" in a healthy subject because it's receptors have sensed that O2 is up, so a lower degree of cardiopulmonary activity is adequate...in otherwords, it is compensating for a heightened O2 level.
Maybe.

If that occurs to an otherwise compromised pt, then it is bad, but if those receptors are still working properly, the pt should not exhibit the same sort of response as the healthy ones.
Click to expand...

So happy to see someone else had this idea. My first thought when reading the the short version (as I haven't looked at the article yet, but I'll get there) was "well duh". It had seemed to me that with greater O2 availability, the heart wouldn't have to work as hard. Would like to know if it was actual coronary tissue perfusion (oxygen exchange) that was reduced or was it just coronary blood flow that was reduced? Same for systemic circulation.
 
The myocardium extracts about 75% of delivered oxygen at rest. So it's essentially supply-dependent - it's already using almost all of the delivered oxygen. [This is a much greater value than in most other organs.]

If we reduce coronary oxygen delivery, we're also going to be limiting the total amount of oxygen extracted by the myocardium. High pO2 results in coronary and cerebral vasoconstriction, and vasodilation in the other peripheral vascular beds.

So if you cause a decrease in coronary blood flow, the oxygen extraction probably isn't going to be able tobe adjusted to compensate.

The trouble with this reasoning, is that while physiological mechanisms are appealing --- "if we give oxygen, we cause coronary vasoconstriction, limit coronary blood flow and reduce oxygen delivery which results in cardiac ischemia, dysfunction and poor outcomes in conditions X, Y and Z" is that so far we've only demonstrated the first half to be true.

I love physiology, but it's possible to postulate plausible physiologic mechanisms for many things, including a beneficial effect for high dose epinephrine in cardiac arrest, or routine hyperventilation in closed head injury. We have to do outcomes-based trials to demonstrate a treatment effect.
 
The myocardium extracts about 75% of delivered oxygen at rest. So it's essentially supply-dependent - it's already using almost all of the delivered oxygen. [This is a much greater value than in most other organs.]
Click to expand...

Wanna try again with that figure or at least give a source for it so I can go smack whomever feed you this crap? You got the last sentence (in brackets) correct, but your figures are massively off. If you were to actually have a functioning organ like that in the absence of exercise or disease, you'd not be able to stress the organ very much at all. Not to mention that it exceeds the theoretical maximum oxygen extraction capability severalfold.

BTW, most organs (other than the brain and heart) run around 2-6% extraction on a % volume basis. Oddly enough, the intestines are one of the organs at the higher end of this.
 
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Sure:

Tune JD, Gorman MW, Feigl EO. Matching coronary blood flow to myocardial oxygen consumption. J Appl Physiol 2004 97:404-415 online .pdf here: http://jap.physiology.org/content/97/1/404.full.pdf+html

If you're looking to slap someone, it appears that you can find Feigl here: http://depts.washington.edu/pbiopage/people_fac_page.php?fac_ID=11

I've never met the man, but he's got the look like he's got a trick or two up his sleeve. I bet a good slap would be met with some wirey old man strength, and some sort of subtle and cunning plan.
 
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The issue here, is that I'm talking the percentage of delivered oxygen, i.e. %DO2, and you're talking the absolute volume of oxygen extracted (i.e. CaO2- CvO2).

So, if you're trying to say that there's no way I can extract 75 ml of oxygen from 100 ml of blood, I'd agree. This would require fully-saturated blood, and a hemoglobin of something ungodly, like 50 g/dl.

However, if you're suggesting that the heart is incapable of extracting around 15 ml of oxygen from every 100ml of oxygenated blood that passes through it at rest, i.e. ~ 75% of delivered oxygen, or 75% DO2, then we're in disagreement.

I've seen your previous posts, and I think you're a pretty intelligent guy, so I'm going to suggest that we're actually in agreement here.
 
*facepalm* I really need to stop reading the forums after having a few beers. You're right. I misunderstood what you said and thought you were talking about % volume and not % delivered.

BTW, one of the authors is going to get a good laugh out of this. I've talked to him before.
 
Totally cool. Beer and the internet is fun, but potentially problematic :)
 
As far back as 2000, the AHA started talking about reducing oxygen delivery to stroke patients. The reason is that higher O2 levels cause hypocapnia which in turn causes vasoconstriction which reduces blood flow to the brain. That in it's turn cause the stroke to expand across the penumbra. Which of course is bad for the patient. There is also an Australian study which shows greater morbidity for patients given Albuterol with O2 as opposes to Albuterol with Normoxic air. The article referenced here in "Chest" is very interesting.

Finally, there are studies of neonatal resuscitation that show babies resuscitated on room air do better than those resuscitated on high flow O2.

Maybe it's time that EMS discarded the "Chicken Soup" school of medicine.
 
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