Sometimes the oxymizer is referred to as a “nasal moustache” because the reservoir is positioned under the nose, as in this instructive 1-minute video from RT Clinic.
What’s the conversion between oxymizer and nasal cannula?
Roughly 1:2––For example, 3 L by oxymizer delivers approximately the same amount of FiO2 that 6 L NC does. Some oxymizer devices can provide oxygen at a 1:4 level (so 1 L oxymizer=4 L NC) and deliver up to 20 L NC! Pretty cool.
What are the advantages of using an oxymizer?
For patients at home, oxymizers make portable oxygen tanks last longer (because the flow rate is lower). How much longer? It depends on the individual patient’s O2 needs and activity level. The lower flow rate also decreases nasal dryness and the discomfort of oxygen blasting into the nares all the time. From a pragmatic standpoint, most clinicians would be nervous about keeping patients at 7-8 L NC at all times (especially on a general medical floor), but an oxymizer can be used to keep patients with higher O2 requirements who are otherwise stable on the floor. For most patients with long-term, high-flow oxygen needs, oxymizers just make more sense.
If it’s “better” than nasal cannula, why don’t we use it all the time? Are there any downsides to the oxymizer?
Cost-wise, oxymizers can be expensive. Not all insurance companies cover oxymizers. The retail price of a single device is (as of this post) about $400 and the manufacturers recommend replacing the device every 3-4 weeks to ensure the membrane continues to work properly. In addition, some patients find the heavier tubing uncomfortable to wear. As far as I know, that’s pretty much it.
Disclaimer: I don’t get paid by Big Respiratory to write this. I have noticed more and more patients wearing oxymizers in the past couple of years who have been able to stay out of stepdown units and ICUs just because they “need more than 6 L NC, which is too much for the floor.”
Let’s say you have a 57 year old patient breathing comfortably on room air, and when you walk in the next morning, he’s suddenly on 6 L O2 by nasal cannula. He doesn’t look like he’s in respiratory distress, but you decide to investigate by getting an ABG.
He is satting 93% on 6 L NC. Is that good? Is that bad? How does his O2 sat compare to the PaO2 on his ABG?
Normal PaO2=80-100 mm Hg. PaO2 is affected by age (tends to be lower) and altitude (tends to be lower).
As you can see, under normal conditions, an O2 sat of 90% correlates with a PaO2 of 60 mm Hg (bonus points if this makes you realize an O2 sat of 90% is not totally normal, although for sick, hospitalized patients, it is acceptable). This curve is useful because it shows that giving supplemental O2 is most useful when someone has an O2 sat <90%. The curve also shows that O2 sat falls slower than the PaO2–a change in PaO2 from 96 to 70 may only show up as a change in O2 sat from 97% to 92%.
FiO2 can also affect an ABG reading. The PaO2 on your ABG should equal FiO2 x 500. If it doesn’t, there’s probably an A-a gradient. The PaO2/FiO2 ratio (or P/F ratio) is useful for categorizing hypoxia as potentially severe (when applied to ARDS).
So what about the patient above? His PaO2 of 68 mm Hg correlated perfectly with an O2 sat of 93%. However, he was also on 6 L NC, and the FiO2 was 40%. This implied that there was a significant A-a gradient
Random notes below:
Why are air bubbles bad? The PO2 of room air is 150 mm Hg, which means any air bubbles trapped in the ABG sample will shift the oxygen value towards 150 mm Hg. When does the ABG have to be put on ice? If it can’t be processed in 15 minutes. (Residual blood cells will continue to use oxygen and make the PaO2 seem lower than it really is.) An ABG on ice can still be analyzed for up to an hour after collection. If I get a value like PaO2=213, what does that mean?! At least you know the patient’s not hypoxic? PO2 is measured directly via electrode. The electrode is calibrated for values between 0-140. Therefore values >150 are of unclear accuracy. Remember that FiO2 affects the value as well.
AKA “pulmonary hygiene.” Pulmonary toilet is advocated by many people, and does sound like a good idea in theory. However, the literature on whether pulmonary toilet actually improves outcomes for various patient populations is very mixed. In general, the patients who seem to benefit most are the cystic fibrosis and critically ill/intubated populations.
The purpose is to THIN and LOOSEN secretions. Having an awake, alert patient who can cough on their own is the best kind of pulmonary toilet.
What are the specific components of pulmonary toilet?
Mucolytic (such as NAC or Mucomyst): NAC in particular has become less popular because of lack of demonstrated utility (a good example is this meta-analysis on cystic fibrosis). I still see it used in the ICU, though.
Hypertonic (7%) saline: may cause bronchospasm, coughing
Deep tracheal suctioning gets lower respiratory secretions and can be very satisfying, but should only be done in intubated patients
Bronchoscopy: using a bronchoscope to “wash out” secretions for atelectasis. This is only helpful in patients who are critically ill/intubated who cannot do any other kind of secretion clearance on their own. My personal observation is that when BAL is used for pulmonary toilet, it turns into a problematic cycle of provoking even more secretions and the need for repeated bronchs. A bronch is also not a completely benign procedure and may be associated with barotrauma, temporarily worsened oxygenation, etc.
When is pulmonary toilet useful? This clinical review is pretty negative. It states that chlorhexidine oral rinses are the only intervention that reduces rates of nosocomial pneumonia, and that other common practices like mucolytics and chest PT are not associated with improved outcomes and may in fact cause harm like bronchospasm and mechanical trauma, respectively. (A lot of evidence comes from pre-2000’s papers/guidelines, though). Let’s look at some common situations:
COPD: This meta-analysis reports that daily oral NAC was associated with fewer COPD exacerbations in patients who had a spirometric diagnosis of COPD, but also in patients who did not have a spirometric diagnosis of COPD. However, this joint paper from ACP-ACCP states that multiple trials have not found benefit for mucolytics or chest PT in COPD exacerbations.
Cystic fibrosis:Yes to chest PT. There is also good evidence that dornase alfa (DNase) and hypertonic saline have small effects.
Atelectasis: for acute atelectasis, if patients cannot cough on their own, chest PT is helpful. (The same review talks about how “bronch for airway clearance” is only indicated in selected cases of atelectasis that are multilobar or severe.)
Post-surgical patients :There is very limited objective evidence that pulmonary toilet decreases pulmonary complications (pneumonia, atelectasis, edema, etc.) in the postoperative period. This Cochrane review shows that in patients who underwent upper abdominal surgery, incentive spirometry didn’t make a difference. Maybe this will make us feel better about all those unused incentive spirometers sitting by patients’ bedsides.
It is common to set the O2 saturation goal for hospitalized patients with COPD exacerbations at 88-92%, and patients without COPD to 94-98%. This is in accordance with British Thoracic Society guidelines. The O2 sat goals are lower for patients with COPD because of the risk of hypercapnenic respiratory failure.
I’m not questioning the O2 sat goals. What I do want to discuss is one of the oft-cited mechanisms for this respiratory failure: that a higher O2 sat will depress the respiratory drive in these patients. Is this true?
Not really. The explanation is very well stated in LITFL. Patients with COPD suffer from parenchymal damage that increases V/Q mismatch. To compensate for this, those smart pulmonary arterioles vasoconstrict to deliver O2 preferentially to the parts of the lungs with the least damage. Giving someone supplemental O2 in this scenario causes the pulmonary arterioles to dilate, causing increased blood flow to the damaged parts of the lungs, too, which increases V/Q mismatch again. See this article for helpful diagrams and more detailed explanation. In addition, due to the Haldane effect (=introducing more O2 will cause CO2 to dissociate more readily from hemoglobin), adding supplemental O2 theoretically causes COPDers’ CO2 levels to increase. I’m not sure that anyone has actually demonstrated this experimentally, but it makes sense.
This review from Respiratory Care on the use of supplemental O2 cites a 2010 study of about 400 patients with COPD exacerbations. They were randomized into a 88-92% O2 sat group and a non-titrated group (so presumed >94%); each group could get as much supplemental O2 as needed to reach those goals. The titrated group had a 58% reduction in hypercapnea and respiratory failure compared to the non-titrated group.
In conclusion: patients with COPD exacerbations should have a lower target O2 sat, but the justification for this is not that it will affect their respiratory drive–instead, think about V/Q mismatch and CO2 dissociation.
What if a patient has COPD but does not have an exacerbation while they’re in the hospital? I couldn’t find a clear answer but would assume that since the same physiologic properties above are in play, it makes sense to continue the lower O2 sat goal.
“Breath stacking” is a term that often applies to severe bronchospasm/COPD. This is when patients take a breath in, but are unable to get that air out, so it builds up and up in their lungs. If they are on a ventilator, you can see it as the volume getting progressively higher with each breath, and the patient not completing a full expiration before trying to inspire again.
If breath stacking is really bad, you can paralyze them with atracuronium.