COPD and O2 sat

In my view, you are practicing in a controlled acute care environment. It is possible and recommended that ABGs are checked with exacerbated COPD patients. Therefore, there is no guessing as to how the short term oxygen therapy is influencing their hypercapnia and acidosis.

Having said that, I find it sad that a nursing home patient with this constellation of medical dx is not a hospice or palliative beneficiary.

68% sats on 4L and not a DNR? Grab a nonrebreather and give the patient some relief. And call respiratory! She's in a crisis, and you are correct, the benefits far outweigh the risk of increasing oxygen in this scenario.

The resp therapist will turn the O2 down prior to obtaining abgs, and then can adjust the O2 delivery accordingly to get the patient above 90% (hopefully). Ideally, check abgs an hour later to check the balance.

I think the risk of losing the drive to breathe is greater at the 95% ish Sat. For someone at 68%, I don't think there is as much of a risk there. Certainly there should have been interventions done if the patient is at that sat level and isn't dnr.

Soran said:

Recently had a pt transferred from a nursing home to the ER. When she arrived her sats were at 68% on 4L O2 and declining from the transport company (not even an ambulance). Pt reports difficulty "getting air". She has COPD and lung CA with partial lobectomy on left upper lobe. At what point do benefits outway the risks in terms of giving the pt more liters of oxygen? I turned up the amount she was receiving to 6L and her levels gradually rose to 85-89% while others said that would be too much and kill her drive to breathe being COPD. I believe benefits outway the risk of increasing oxygen in this scenario. Someone turned down the 6L I was administering and she began to drop again, respiratory showed up and turned it back up to where I had it, prior to putting on a venti-mask.

I think you did the right thing. Using just enough supplemental O2 to achieve an O2 sat of 89% or greater in the initial stage is correct. Of course, you will also be giving steroids, bronchodilators, and possibly using BiPap.

Please do not wait for an ABG to be done and the results to return before intervening. I would not want to be the one to do an arterial stick on someone with an SpO2 of 68% without intervention nor try to explain this to my licensing board. You should know the clinical signs. In this case, the OP was correct to place the patient on 6 L of oxygen and get the SpO2 to close to 90%.

But, if you do an ABG, the website linked below will give you a synopsis of Acid Base and ABGs. V/Q mismatching and patient position can place a role in oxygenation and ventilation. Affected, unaffected sides and atelectasis all have a role. Having an SpO2 does not mean the patient should be a DNR and if a DNR it does not mean we can not intervene until a "comfort care only" order is taken.

https://acidbase.homestead.com/abg_analysis_rev_2.0.pdf

Now for that "hypoxic drive" stuff.

This generation should not be taught old nursing tales from the 1950s. More than a half of century has passed and we now have science and modern technology to explain oxygen, CO2 and the hypoxic drive. It is time to know the difference between the hypoxic drive and the hypoxic drive theory myth which scares some to the point of being stupid when responding to emergencies.

Oxygen-induced hypercapnia in COPD: myths and facts

Crit Care. 2012; 16(5): 323.

Published online 2012 Oct 29. doi: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682248/

Oxygen-induced hypercapnia in COPD: myths and facts

Quote from the above link:

Quote

Reading these early reports about oxygen-induced hypercapnia in patients with chronic obstructive pulmonary disease (COPD), one might think that not much has changed over the years. Despite subsequent studies and reviews [3] describing the effect of oxygen on the ventilator drive in patients with COPD, disproving the 'hypoxic drive' theorem, many clinicians are still being taught during their medical training that administration of oxygen in patients with COPD can be dangerous given that it induces hypercapnia through the 'hypoxic drive' mechanism; that is, increasing arterial O₂ tension will reduce the respiratory drive, leading to a (dangerous) hypercapnia. This misconception has resulted in the reluctance of clinicians and nurses to administer oxygen to hypoxemic patients with COPD. In most cases, this is an unwise decision, putting at risk the safety of patients with acute exacerbation of COPD. In this concise paper, we will discuss the impact and pathophysiology of oxygen-induced hypercapnia in patients with acute exacerbation of COPD.

Please let us get into the 21st century for understanding "hypoxic drive". Once you understand the relationship of the variables, you will be prepared when you do treat someone who is short of breath and/or hypoxic. Yes, patients can be hypoxic and not "know" it.

Seriously? Anyone clinically evaluating the PATIENT? To hell with a number on a monitor. How about checking respiration rate and quality. Talking with the patient to assess difficulty in breathing or mentation.

Even if the patient was a DNR. Since when is 6L O2 considered resuscitation?

I am totally with you OP. Benefits outweigh myths errrrrr ........ I mean risks.

I would 100% crank the O2 up! Those sats are far too low to be adequately oxygenating that pt- regardless of hx of copd. I wouldn't keep them on it for long- but at least until ABGs were drawn and/or a solution was found to help and a lower level of O2 can be used.

NEVER deprive a patient of oxygen!!!! Yes, in this situation eventually there is going to be a problem with CO2 retention...but that can be addressed later. The immediate problem is oxygenation of vital organs. Sats need to be at least 90%.

I've noticed there's been a swing from one myth to another. At one time, it wasn't unusual to find nurses who believed no COPD'r should get "too much" oxygen", which they incorrectly defined as the amount of oxygen being provided instead of the saturation level. Then, in pointing out that myth another myth was created which was that there is never any harm in keeping a chronic CO2 retainer at sats approaching 100%, which isn't true either.

There's no harm in aggressively treating hypoxia in a COPD'r, particularly in the acute stabilization period, but as even myth-busting articles point out, you still shouldn't aim for more than about 92% in order to avoid oxygen-induced hypercapnia, particularly as an ongoing goal beyond initial stabilization.

In five years of treating acute COPD exacerbations, I have seen oxygen-induced hypercapnia exactly ONCE.