Oxygen does harm ?

[ReD]

what about throwing COPD pt's into this mix? ive heard alot of people argue about giving COPD pts O2. "they will stop breathing if you give them O2!"......well, with no oxygen....you will die.

im only a basic, and fairly new (been doin this for a year), but im a firm believer that if someone does need O2, GIVE IT TO THEM!

[Guest]

ReD, You're right by saying that if someone needs O2, DON't DENY IT to them. Just because they have COPD, doesn't mean they don't get O2, just means you have to be more careful and observe them more intently.

Why though, does it do harm? Because ... COPDers have develloped the 'hypoxic drive' . Instead of their chemoreceptors being triggered by higher PCO2 levels as is the norm in most individuals, they respond to low PO2, so if you give them supplemental O2, the brain interprets that as "oh, well theres lots of oxygen being supplied now ... i can slow the breathing rate right down!' (quite crude, but that's the best I can explain it).

~Zach~

[BEorP]

what about throwing COPD pt's into this mix? ive heard alot of people argue about giving COPD pts O2. "they will stop breathing if you give them O2!"......well, with no oxygen....you will die.

AFAIK (not speaking from experience) it usually takes more time than there is in a perhospital setting for them to stop breathing from being on O2 and even if they did their body will cause them to start breathing again once the oxygen is off.

[Ace844]

USAF,

Thganks for the O2 info., and double thanks for not posting Winter's formula...I think I would have had to leave my comp and go bang my head against the wall several times if you had.....

"rid," I definately think we should allow this scientist to try out his theory on HIMSELF in realtime...perhaps we could even change the CO2 to be the actual percentage of atmospheric Nitrogen...I bet that'd make him happier, then we could even tape the whole thing and see how much "practicality" his research holds....

:twisted: :!: :idea: LOL

Out here,

Ace

[rocket]

So this is in essence a hyperventilation issue?

If so then I suppose the issue might require one to reconsider what "hyperventilation" actually means in the prehospital setting.

Would tracking resp rate and/or depth be sufficient? I'm thinking no. I'm also thinking that if the effect were as pronounced as (perhaps) suggested in the original article then we'd often see a marked increase in respiratory rates in patients following the administration of oxygen therapy (non those with controlled resps of course).

Now I'm just a newbie and have only a "handful" of runs under my belt so far but I don't believe I have seen this occur in the field. Why not? Either counting resps is not terribly accurate in the field (I could see the potential for that occurring) and we "miss" the O2-driven effect or perhaps the leaky adjuncts that T_D_D describes is the culprit.

I tend to think it'd be the leaky adjuncts. That makes the most sense to me.

Back to measurement: I don't think yer standard ranges (e.g., 12-20) or depths (how can that be measured other than subjectively anyway with say a NRB on the patient?) wouldn't be enough to determine how close a patient was to hyperventilation. Seems to me that you'd need something more tangible to measure the state of the patient's exhaled gases...which is what we are most interested in anyway...to be sure.

So maybe capnography...like Buddha suggests...would be the best way to definitively prove/disprove the presence of the condition?

Cool discussion BTW. Thanks for posting it. 8)

-Trevor

[RamVacEms]

NOPE!!!! O2 has no contraindications!!! Pts with COPD are really not supposed to be on High Con 02 for extended periods of time. But in the EMS field we has no contraindications!

[Ace844]

"RamVacEms",

There is at least one absolute contraindication to O2 therepy and many more"relative" ones. The "absolute" is a paraquat, cumquat ingestion or suspicion there of. As far as the relative, well there are many... I posted a scenario either here or on the old board and I can't seem to find a link, so if anyone has it, I'd appreciate it if you'd help out and post it.

Hope this helps,

Ace844

[THE_DITCH_DOCTOR]

OK....a few points

1. NOT all COPD'ers have a functional hypoxic drive. It takes prolonged (and I'm talking weeks) of markedly elevated PaCO2 levels before the CO2 receptors that normally help adjust ventilation rates become insensitive and this normally only occurs in end stage patients. The rule to keep in mind is that you should use the lowest possible FiO2 necessary to maintain adequate tissue oxygenation- but this applies to ALL patients, not just COPD'ers.

2. CO2 levels are not primarily dependent upon oxygen levels. CO2 is most rapidly changed through ventilation. You can put a person upon 100% O2 and if they maintain a normal minute ventilation (around 5 liters of air per minute), most people's CO2 levels will not decrease that much (because they are still producing the same amount of O2 every minute, but it's not being exhaled at a greater rate).

3. Oxygen levels (on SpO2 for instance) are not adequate measures of appropriate ventilation. The one thing I see a great deal of confusion among EMT's and paramedics is the differences between oxygenation and ventilation. These two mechanisms are intertwined but separate and the adequacy of each is determined through different measures.

Oxygenation is the absorption, delivery and use of oxygen by the tissues. It is effectively assessed either through SpO2 or by the PaO2 reading on a blood gas. It can be affected by derangements in ventilation (hypoventilation has a greater effect than hyperventilation), by changes in oxygen binding levels (example: the greater affinity of hemoglobin for carbon monoxide decreases blood oxygen levels by decreasing the amount of hemoglobin free to bind with O2), or by impairment of tissue utilization of O2 (example: the mechanism of cyanide toxicity is impairment of an enzyme necessary for the use of O2 in cellular metabolism), and a few others. Oxygenation is basically the result of adequate ventilation combined with adequate perfusion if the pulmonary capillary beds....it gets pretty complicated but suffice to say that indicators of sufficient oxygenation do not also imply sufficient ventilation.

Ventilation is the physical movement of air in and out of the lungs, and is best reflected by CO2 levels (ETCO2 is a rough approximation of the PaCO2 level we obtain in hospital when we do blood gases). Impairment of ventilation can be due to:

Physical hindrance of lung expansion (tension pneumothorax, skeletal misalignment (scoliosis for example), skeletal trauma (rib fractures, etc))

Changes in pulmonary compliance (a measure of how easily the lungs expand- increased compliance (as occurs in COPD) means the lungs expand more easily (but also tend to not recoil as much upon exhalation leading to more air trapping), where as decreased compliance means that lungs tend to be "stiffer" and take more force to expand ("hard to bag") and the best example of this is acute respiratory distress syndrome (ARDS) or severe sarcoidosis.

Airway obstruction

Decrease in drive to breathe (head injury, narcotics OD, etc),

Etc.

Any questions, please let me know......

[bravofoxtrot]

Good thing that in the US we don't actually have true NRB only semi-NRBs. Something about patients used to suffocate. I don't really buy into this research though. I'd also be interested to know how much the patient's superficial arteries would dilate during shock compared to the expansion of arteries in vital areas.

[THE_DITCH_DOCTOR]

You mean how much would the peripheral veins constrict in relation to the dilation of "vital" areas? Right?