Thoughts on High Flow O2

Mike97

Mike97

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Most of the older books recommend high flow O2 at 15 lpm. Now, we're taught to use O2 more conservatively and treat it like any other drug. However, from what I've read, its very difficult to over-oxygenate a patient at normal pressures. Unless, your in a hyperbaric chamber, it seems like it takes many hours to potentially days of breathing 100% O2 to have adverse effects.

So, considering we care for patients for relatively short period of time, should we be using high flow O2 more? (I know this is probably a question for a medical director, but I'm curious to hear your opinions)
 
Mike97 said:
should we be using high flow O2 more? (I know this is probably a question for a medical director, but I'm curious to hear your opinions)
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No.

There are many studies that show a detrimental effect of oxygen toxicity in ACS and stroke patients. Even in the amount of time we have them.

I think the "extended time required" you're maybe referencing is relating to the switching to hypoxic drive in COPD patients.
 
NPO said:
No.

There are many studies that show a detrimental effect of oxygen toxicity in ACS and stroke patients. Even in the amount of time we have them.

I think the "extended time required" you're maybe referencing is relating to the switching to hypoxic drive in COPD patients.
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Agreed, the "days to adverse effects" sounds more relative to hypoxic drive.
 
This was a tough one for me. I was raised in the school of thought that oxygen had two settings, on and off. If they needed oxygen, blast em. Nasal cannulas were worthless in the acute setting. For years I held these beliefs as fact. Then, as if a switch flipped, I was awakened to the idea that maybe, just maybe, what I had been taught was wrong. That those silverbacks who had taught me the business might have stopped reading and learning a few years back. Mind. Freaking. Blown.

Once the first domino fell, I was open to the idea of reviewing and reconsidering everything. Backboards, gone. Lasix, get it out of here. Once you open up and consider that everything you know might actually be crap and you start to actually read the research and study the data, you’ll see all sorts of nonsense you once thought of as gospel.

We know, not think but know that hyperoxygenation in the prohospital setting(and in the prehospital timeframe) is a real live thing and that we have been harming patients by flooding them with oxygen for years and years. CVA, ACS, chronic respiratory patients, probably other conditions as well.

No, we shouldn’t be using more high flow O2.
 
High flow O2 does have its uses and indications but, by and large, it's not the greatest thing since sliced bread and it shouldn't be the 1st thing you go to when you're thinking about giving oxygen for possible hypoxia. With CVA, ACS, and so on, I don't reach for supplemental oxygen unless I have to and even then, I'll use the minimum necessary to keep the patient in the mid 90's. Short excursions to 90% I don't worry too much about... it's when it's consistently low-ish that I start considering it.

Of course I also start looking more closely at work of breathing and if the patient's starting to look tired, then we generally go to Bi-PAP and skip the whole "high flow" thing.
 
Do an ABG on a patient who has essentially normal respiratory function and placed on a NRB, just watch how quick you can get that tension above 300 mmHg (spoiler: just a few minutes).

High flow oxygen does have its place in treatment, but like all treatments it comes with risks and benefits and therefore is not always indicated. High oxygen flow is known to cause higher rates of free radicals in the blood with causes cellular damage, and high tensions are known to create some intracranial and coronary arterial constriction. It can also close the fetal circulatory shunts which can be devastating to neos/infants/kids with ductal dependent heart disease.

Understand that ventilation and respiration in much more complex than just how much oxygen you can flow. There are many vent dependent patients who are on room air, most in the hospital are going to be somewhere between 40-60% FIO2. Most patients who use CPAP or BiPAP at home are on room air. There are many bronchiolitics who benefit from a lower FIO2 given at a higher flow rate through HHF than if they were given just the oxygen without the increased flow which is more about decreasing the anatomical dead space than giving the oxygen.

I suggest you look into the countless other topics here, but understand that there is not going to be a black and white answer to giving supplemental oxygen.
 
If a patient has no shunt (i.e. no issues absorbing oxygen into the bloodstream) a very rough "rule of thumb" is that the PaO2 should be 4+ times the FiO2. That means a normal person should achieve a blood gas PaO2 of 80+mmHg when breathing 21% oxygen. Likewise, if receiving true 100% (NRM only deliver about 60% oxygen at best), a normal person can easily reach 300+ mmHg (as stated above). Many patients are at risk for a shunt of some sort, but nothing that requires a blast of high flow oxygen. Too high of a PaO2 and it can be bad. That's why we base oxygen therapy on the outcome (based on SpO2 levels), not on what we administer.

A huge, huge issue is that too many practitioners hold back on O2 delivery despite incredibly low SpO2 levels with the thought that "I know the SpO2 levels are in the low 80's but we're told that too much oxygen can kill him". You may very well need high flow oxygen via a NRM just to get the SpO2 up to a reasonable level.

In the end, nasal cannula should suit most of your needs, however keep the NRM handy must in case.
 
I was raised on the belief that everyone gets a NRB at 15LPM, regardless of complaint. chest pain? NRB at 15. toe pain? NRB at 15. get hit by a truck? on the high way? NRB at 15. sprain your ankle? NRB at 15. It was actually almost a critical failure on my NYS trauma examination back in 2001. When I questioned the stupidity of the over application, I was told there is no downside, and it might help. and the book said to do it. So it must be my ignorance. And every time we brought a patient into the ER on a NRB, the first thing the nurse would do is take the NRB off the person.

Fast forward a few years, and we are getting away from EMS dogma, and moving towards evidence based medicine. don't do something just because that's always the way we have done it, but understand why. We know the over application of O2 does have negative side effects (free radicals, etc).

If the patient has difficulty breathing, and is not oxygenating enough, high flow oxygen is needed. If they are showing signs of poor perfusion, than yes, high flow oxygen can help.

But the rest of the time it is either not helping or potentially hurting the patient. So why do it?
 
Correct me if I’m wrong but isn’t there a relationship between nitrogen and surfactant? Somehow I seem to remember that a decrease in N2 leads to a decrease in surfactant production which can in turn lead to, obviously, atelectasis. Not that you’ll see it in the 30 minute window you have the patient under your control, but again, if it’s bad long term why are we doing it? If we were only concerned with what has an immediate effect we wouldn’t admin Solu-Medrol.
 
lightsandsirens5 said:
Correct me if I’m wrong but isn’t there a relationship between nitrogen and surfactant? Somehow I seem to remember that a decrease in N2 leads to a decrease in surfactant production which can in turn lead to, obviously, atelectasis.
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It sounds like you are thinking of absorption atelectasis.

Room air is mostly (~78%) nitrogen, which does not cross the alveolar-capillary membrane and is the primary contributor to the ~2mmHg natural PEEP that keeps your alveoli open. When you use a high fi02, you replace the nitrogen in the alveoli with oxygen, which is of course highly soluble and crosses the alveolar-capillary membrane readily. It has been demonstrated that significant atelectasis can occur in a healthy patient in the time that it takes to pre-oxygenate prior to an intubation attempt.
 
High Flow 02 makes me think of 50 lpm HHFNC not a NRB.
 
I've never been taught to give everybody oxygen; in-fact, I was specifically taught first-off NOT to do so. Perhaps I am too young.

Something like 98% of arterial oxygen saturation is carried on Hb; and about 1% or so dissolved in blood plasma. Under normal circumstances the Hb are fully saturated on whatever normal FiO2 is; 22% or suchlike; so suddenly increasing the FiO2 to 100% is pointless.

I vividly remember being taught in physiology that capillary sphincter control is regulated by oxygen saturation; think about it; if somebody is hyperoxygenated above euoxyaemia then they're going to close off. No wonder patients with STEMI and stroke do worse when given lots of oxygen.

Remember as well if you are giving somebody lots of O2 and making up for a poor SpO2; you could potentially mask respiratory acidosis.

And besides, beyond the unnecessary and potentially harmful effect; you don't want to be replacing your portable oxygen cylinder every five minutes.
 
It’s always a contention issue.i have been taught both HOWEVER in the uk we currently saturate to effect and NEVER give high flow to stroke etc unless patient is clearly hypoxic.this is due to the lining of the brain and the damage it can cause.hope this helps
 
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