Too much oxygen?

[nypamedic43]

http://www.reuters.com/article/2012/01/11/us-oxygen-patients-idUSTRE80A26A20120111

I was perusing some pages on Facebook and ran across this article. I can see giving too much oxygen to a COPD'r that is normally on 2-3 liters via cannula. I try to keep them at 2-3 liters while transporting to the ED unless more is warrented or more aggressive intervention is needed. I found it interesting and it is just a theory at this time, there isnt any proof...per se.

[Happiness]

My question would be what is an acceptable level of O2. If using the pulseox do they want it at 80% or should it be 95%.

[DFIB]

The article talks about too much O2 but is not very specific. If I remember correctly the EMT-B orange book mentions that in COPD patients O2 should be given with care but never withheld. I will have to look up the specific text.

[chbare]

The hypoxic drive of death is a scarecrow that for some reason continues to haunt this site among others. However, there has been much research into the problems associated with prolongued exposure to higher than normal FiO2's. I suggest you guys take a look at the 2010 AHA guidelines as a starting point. At this point, the general suggestion is to titrate to a SPO2 of around 94%.

A summary of the 2010 guidelines:

http://guidelines.ecc.org/pdf/90-1043_ECC_2010_Guidelines_Highlights_noRecycle.pdf

However, I also suggest you guys look at other types of literature as well.

[runswithneedles]

From what I understand the hypoxic drive does take some time for it to develop. Am I wrong?

[Bieber]

Routine oxygen use for uncomplicated strokes and MI's has been discontinued in the newest AHA guidelines. Unfortunately, our current protocols still require at least 2 lpm for those, but all other patients oxygen use is basically provider's discretion. I don't put someone on oxygen unless I feel they need it (or unless I'm required by protocol).

Oxygen is a drug just like any other, it has indications, contraindications, and adverse effects. You wouldn't push epi without considering all of those, would you?

[chbare]

From what I understand the hypoxic drive does take some time for it to develop. Am I wrong?

Well, I think we need to look at things with more detail. I am going to oversimplify a bit because I'm not sure how well you may understand chemistry, particularly equilibrium reactions and I think I can convey the concept without all the detail in any event.

First, many people are under the misguided opinion that CO2 is the primary respiratory stimulus. That's is not exactly the case. Ph changes are actually very important to consider. It just so happens that an increase in CO2 will often decrease Ph and trigger central chemoreceptors. However, this is because the CO2 is transported in the form of HCO3- and H+ ions (for the most part). So, CO2 is converted into an acid and the associated Ph change stimulates breathing. (One of the mechanisms).

However, consider a patient in DKA. They are ventilating like a big dog. often, they have a very low CO2, so what is going on? Well, their Ph is low and remember what we just discussed regarding Ph and respiratory stimulation. Where am I going with this?

Consider the following. A COPD patient has chronically elevated CO2. What happens with chronically altered respiratory related Ph changes? We develop renal compensation and the body creates more HCO3-. Do, we have a patient with a chronically elevated CO2, but their Ph is relatively normal due to renal compensation. So, in this situation, we would not expect respiratory stimulation because our Ph is relatively normal.

Where exactly is this hypoxic drive in what I discussed above? Well, the hypoxic drive theory many not even apply in many patients or it may not play a significant role in the deterioration of COPD patients. It may exist, but the traditional way we look at it is not really all that valid.

Edited January 15, 2012 by chbare

[runswithneedles]

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

Oxygen is a drug just like any other, it has indications, contraindications, and adverse effects. You wouldn't push epi without considering all of those, would you?

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

Edited January 16, 2012 by Mike Ellis

[chbare]

That was not exactly the point I was trying to make.

Regarding problems and possible Oxygen contraindications:

Consider cyanotic heart defects and paraquat toxicity.

[systemet]

Respiratory control is complicated, as chbare is explaining.

Very few COPDers will stop breathing when given high concentration oxygen.

When they do, it's often secondary to increased carbon dioxide retention, which may have little or nothing to do with any supression of a hypoxic drive component to their respiratory control. There may be a small percentage of patients that are dependent on a hypoxic drive, who may go apneic with supplemental O2, but even this is very controversial and hotly debated. The idea that you must avoid supersaturating COPDers because they might stop breathing has been greatly over-emphasised in EMS training. [* We should avoid supersaturating them because it's pointless.]

There is some small amount of evidence that hyperoxygenating MI / CVA patients to high pO2s is associated with poor outcomes. I don't think these studies have met causality, although there's some plausible mechanisms by which high levels of oxygen could increase free radical formation and oxidative damage. This data has been sufficient for the AHA to recommend against routine oxygenation in patients without detectable hypoxia.