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Posted

So its the chemo receptors that are detecting a correction in ph that causes hypoxic drive? I did not know that

Do forgive my complete brain fart. But what would the contraindications be for o2....Besides A good spo2 saturation

Like chbare said, certain congenital heart defects are a contraindication for high flow oxygen because they can end up having undesired blood pathway shunts which bring oxygenated blood where it isn't supposed to be, like the pulmonary trunk causing the ductus arteriosus to remain patent and messing with the pulmonary and cardiac pressures. That's one case where less is more.

Other precautions for oxygen use include AMI and stroke, due to the risk of free radicals increasing the size of the infarct.

Posted (edited)

Like chbare said, certain congenital heart defects are a contraindication for high flow oxygen because they can end up having undesired blood pathway shunts which bring oxygenated blood where it isn't supposed to be, like the pulmonary trunk causing the ductus arteriosus to remain patent and messing with the pulmonary and cardiac pressures. That's one case where less is more.

That has to be one of the most confusing statements regarding congenital heart defects and oxygen I have ever read!

Generally when people talk about oxygen being harmful in CHD it is with ductal dependent lesions where you actually need the ductus to remain patent as it is life-saving. In these cases in an infant, if you give oxygen it can cause the ductus to close and that may be the only way that the body is getting ANY blood flow or oxygenation. Increased oxygen levels contributes to closure of the PDA not causing it to remain patent. If you want to close when it shouldn't be open, they are treated with Indomethacin or surgery.

You're partially right in that it can also cause undesirable shunting and in in some cases cause the lungs to be flooded which can be detrimental in some lesions. Oxygen can decrease pulmonary vascular resistance which can cause more of a left to right shunt and flood the lungs with too much blood flow in some cases. It's not a matter of bringing oxygenated blood where it's not supposed to be but more a matter of too much blood flow that interferes with oxygenation of the blood in the lungs.

However very few people are going to have enough of an understanding of all the potential cardiac defects and hemodynamics to differentiate which defect oxygen is going to be detrimental to. Since they are the minority rather than the majority of cases it would be more harmful to withhold oxygen than to give it and titrate it to effect.

IF the patient condition does not improve or deteriorates with oxygen then it should be removed. That is in regards to CHD in any case.

Edited by Aussieaid
Posted (edited)

Aussie, you're right, I got that one all sorts of twisted up. Shows how long it's been since I've studied up on that stuff! You're correct that oxygen is what stimulates the closure of the neonatal heart ducts, and that certain duct dependent congenital heart diseases will experience an exacerbation of their condition with high flow oxygen due to the closure of those necessary ducts.

P.S. The funny thing is my presentation for paramedic school was on congenital heart disease!

Edited by Bieber
Posted
For instance, one trial from 1976 found nine out of 80 heart attack patients who got oxygen died, compared to just 3 out of 77 who got compressed air. Although that difference could have been a statistical fluke, it was still bad news for oxygen.

Hardly a convincing statistic, there could certainly be a lot of under factors at play here. However, as said earlier in this thread, there is no reporting on the amounts particular amount of 02 given to subjects in this study. Howver, this is an interesting piece, I look forward to more study on the subject.

Posted

Hardly a convincing statistic, there could certainly be a lot of under factors at play here. However, as said earlier in this thread, there is no reporting on the amounts particular amount of 02 given to subjects in this study. Howver, this is an interesting piece, I look forward to more study on the subject.

What should also be considered here, is that this is in 1976, so it's pre-reperfusion era. No angioplasties, no thrombolytics. In this time period, the treatment for MI is mostly wait-and-see, not unlike modern day stroke care. You either die or get better, and a lot of people end up disabled. It's really hard to generalise this sort of study to modern day care.

Posted

This is a pet hate of mine, really it is, it just fucks me off no end seeing people forcing oxygen down everybodies gob by non re-breathing mask and makes me want to hit them with a blunt object to the noggin ... *eyes oxygen tank, hmmm, well it would be of more benefit at least than it is to the patient!

The whole issue is quite complex involving arteriolar and capillary tone regulation, chemoreceptors, oxygenation vs ventilation, hypoxaemia both chronic and acute, hyperoxaemia, the electron transport chain, hypoxaemia vs ischaemia, some basic physics and a bunch of other crap that I can't be arsed typing up now.

The 20 on it is this: you can give somebody too much oxygen, it can be very harmful and the good ole ambo trick of "more is better" does not apply here; oxygen is a treatment for hypoxia not a 'general treatment'

Posted

Yeah I agree Kiwi,

I rarely ever use an NRB unless totally nessesary, however I think that the research cited for this article is woefully incomplete and some new research could be very illuminating.

Posted (edited)

There was a recent meta-analysis that I am too lazy to find. I think it was in Annals of EM. It showed that there is a tendency towards harm in MI pts who were placed on hi-flow O2, but it was not statistically significant and more study was needed.

Edited by ERDoc
Posted

There was a recent meta-analysis that I am too lazy to find. I think it was in Annals of EM. It showed that there is a tendency towards harm in MI pts who were placed on hi-flow O2, but it was not statistically significant and more study was needed.

Come on there must be something out there, even some sort of yetti or shemales or something that came down from Canada that is better than anal, oh you said annals, never mind bro just my Kiwiness we don't readz so good

I think the two most important things here are that oxygen is a treatment for hypoxia not something to be dished out or crammed down everybodies gob willy nilly, that hyperoxia causes capillary and small arterioles to constrict and that ventilation is not oxygenation and ischaemia is not hypoxia.

Wait, that's more than two thats like five or something you know two plus two is five right? Kiwi maths bro :D

Posted

There was a recent meta-analysis that I am too lazy to find. I think it was in Annals of EM. It showed that there is a tendency towards harm in MI pts who were placed on hi-flow O2, but it was not statistically significant and more study was needed.

There was this in Heart [1], but they excluded everything except 2 RCTs, one of which is the 1976 data people have mentioned [2]. The other was 50 patients, post streptokinase, who received either air via face mask or a nasal cannula at 4 LPM for 24 hours [3]. But the study was designed to investigate the occurence of hypoxemia and the ability of the physicians to recognise it clinically. So they didn't report much useful data.

[1]Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley. Routine use of oxygen in the treatment of myocardial infarction: systematic review. Heart 2009;95:198–202. doi:10.1136/hrt.2008.148742

[2] Rawles JM, Kenmure AC. Controlled trial of oxygen in uncomplicated myocardial infarction. BMJ 1976;1:1121–3.

[3] Wilson AT, Channer KS. Hypoxaemia and supplemental oxygen therapy in the first 24 hours after myocardial infarction: the role of pulse oximetry. J R Coll Physicians Lond 1997;31:657–61

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