Oxygen administration

>
Just because someone has obstructive lung disease, DOES NOT mean they are "more that likely" to be chronically hypercapnic, although some COPD'rs are "CO2 retainers". Furthermore, a chronically hypercapnic Pt DOES NOT rely on the mythical "hypoxic drive" to breathe. On rare occasions a Pt's pCO2 may increase when recieving high concentration supplemental oxygen by other mechanisms than hypoventilation. The "hypoxic drive" theory is hogwash, please read the link I posted earlier.

Sorry have not been back in awhile. While research may say it is a myth, the reality is seeing a patient who has lived on an anerobe drive for several years at 3 lpm NC, increased to 6 LPM-by a well meaning nurse. Get somnolent and respiratory rate drop to 8 from 20 and SaO2 drop from 91% to 73% until we returned his O2 to 2-3 lpm. So, it doesn't matter to me what the research says, it is more important what happens to a patient who is not in distress and does not NEED the oxygen. There is a difference.

Hmmm I replied to the other post, but will again. It is not hogwash. Have personally seen it happen. You are correct though, not all COPD patient's rely on a hypoxic drive. You need to asses blood gases and patient's response to O2 to determine their level of need for O2. Again correct, you don't deny a patient O2 if they NEED it. Not all COPD patient's need higher flows of O2. It may have more to do with their disease process and ability to diffuse O2/CO2. Raising their O2 does not necessarily resolve the issue of their shortness of breath and low SaO2, but can increase the problem. PATIENT ASSESSMENT OF NEED,

You're mssing the point, and obviously did not read the study. There is no singular "hypoxic drive", in other words just because a chronicly hypercapnic person's central and peripheral chemoreceptors have aclimated to raised CO2 levels, CO2 still remains the principle factor in ventilation. On rare occasion (such as your single anecdote) said person may experience further increased CO2 by other mecahnisms than hypoventilation and suffer CO2 narcotization.

I did read the article. If a patient needs O2 they are always titrated to maintain the best sats and respiratory response. If they need ventilation they get it, if they need BiPap or CPAP they get it. In no way do I advocate the withholding of O2, whether they are COPD patients or not and they need it. You have to look at the whole patient and see what they need. However, in a patient who is stable, like any medication, O2 needs to be titrated to need. Just because someone is a COPD patient does not mean they need 6 lpm O2 either. * absorption atelectasis, oxygen toxicity, and depression of ciliary and leukocyte function at FIO2 values above 0.5 has been noted. Now to address the hypoxic drive I can understand the premise of the article and I know what they are saying. All I can say is how I have seen people react to oxygen delivery and the improvement of someone's respiratory status by titrating down the O2. It may not be due to the "Hypoxic drive" per se and that's fine, but nonetheless that particular patient (and by the way I have seen it in more than one patient and we discussed it in our office and more than one therapist has seen several cases where that has happened) did not tolerate high levels of oxygen. It is something you have to watch out for no matter what the studies say. The patient woke up and their respiratory status and SaO2's improved with decreased O2. You can't just quote a report and say it never happens whether it is the "Hypoxic drive or not".