Oxygen Therapy

Thanks for posing this question, I'm a new grad RN with a few months under me and some answers would be helpful. I find that MANY nursing schools neglect oxygen therapy. I'm not quite sure why. Hello??? Is it because there's RT? Because when there's no RT guess who comes next? R to the N! =D

I think one of the things that may be tripping you up is the blurring of units of measure. For example, your post references %, L/min, and pressure. Let me break that down first, because these units of measure all mean different things.

% of oxygen is the concentration of oxygen in the air/gas being delivered. You are correct that room air is 21% oxygen (interchangeable with the term FiO2, or fraction of inspired oxygen, which would be expressed as a decimal rather than a percent; .21). You are also correct that 1L of oxygen via NP is roughly equivalent to 24% oxygen, which is 3% above atmospheric oxygen concentration, not pressure.

Which brings us to our next unit of measure... pressure. Pressure is measured in cmH2O or mmHg (just like a blood pressure would be measured). It is the pressure that oxygen is exerting in the environment and is rarely used as a unit of measure when discussing oxygen, except when talking about blood gasses. The 'normal' ABG PaO2 value that you memorized when learning labs of 80-100 is 80-100mmHg and represents the partial pressure of oxygen dissolved in the blood (not bound to hemoglobin).

Finally L/min. This is simply a measure of the flow of a gas being delivered. For example, that 1L of oxygen via NP is simply 1 liter of flow of oxygen per minute being delivered to the patient.

Now to attempt to answer part 1 of your question - How much oxygen is the patient actually getting... Where this gets confusing is the delivery source of the oxygen and the device being used to deliver the oxygen (NP, ventimask, ventilator). If the delivery source is a flow meter hooked up directly to the 'wall' oxygen, or an oxygen tank, then the gas source is pure oxygen, or 100% oxygen. The 100% oxygen mixes with the room air the patient is breathing and thus lowers the % of oxygen the patient actually breathes in. This is how we can estimate that a pt on (to use your examples) 1L/min NP or 6L/min NP is breathing 24% or 44% oxygen... because 100% oxygen being delivered at 1L/min or 6L/min mixes with the room air the patient is also breathing in, lowering the concentration of oxygen ultimately delivered to the patient to 24% and 44% respectively. This is an example of how liter flow can change the concentration of oxygen delivered to the patient - increased flow increases % of oxygen (and conversely decreased flow will decrease the % of oxygen). Now an example of a device where this is not the case - the ventimask. Once you've selected the concentration (%) of oxygen you want to deliver to the patient, the flow you select does not affect the % of oxygen being delivered to the patient. The % of oxygen delivered to the patient is set. Say, for example, you have a patient on a 35% ventimask set at 8L/min and the patient desats on you while turning, the first impulse may be to increase the flow as one might with a nasal cannula, but increasing the liter flow will not increase the % of oxygen being delivered to the patient as it would with a nasal cannula because the ventimask will simply draw in more room air to mix with the increased oxygen flow from the flowmeter, ultimately keeping the % of oxygen delivered to the patient the same, regardless of whether the flow is set to 8L/min or 15L/min, the % of oxygen remains fixed at 35%.

The second part of your first question has to do with whether we can predict if a certain amount of oxygen will increase oxygen saturation by a set amount. The simple answer is no. There are too many variables affecting how each individual will respond to a given amount of oxygen.

Question 2 - high and low flow oxygen. This is a matter of if you are using a device that is capable of completely meeting a patient's inspiratory flow needs. So, short answer is yes, it is just in reference to the device or method used to deliver flow to the patient. However, one thing to point out is high flow devices are NOT devices that allow rebreathing. A ventimask IS a high flow device and it DOES NOT allow rebreathing. This is another area where I think you were blurring the lines of the units of measure. High and low flow devices are only determined by flow, not the gas source. Whether using them to deliver 21% oxygen or 100% oxygen does not matter, it is whether or not they are capable of delivering enough flow to the patient to meet their inspiratory flow demands. I couldn't remember what the average inspiratory flow for an adult was, so I googled it - wikipedia (lol) informed me that the inspiratory flow rate for adults exceeds 12L/min, and can be in excess of 30L/min when in mild resp distress. I also came across this link when I googled: Oxygen Delivery Systems and that info may or may not help.

I hope this looooooonnnggg-winded response helped, rather than confusing things even further.

Let me chime in with some explanations of physiology, ABGs, and SpO2, too, to help you see the whole system more globally.

One thing to remember is, as vanilla bean has so nicely explained , is that % of oxygen in inspired air (FIO2, fraction of inspired (air) oxygen) doesn't necessarily translate to PaO2 or SpO2. There's an easy formula for figuring out what arterial oxygen partial pressure ought to be at a given atmospheric pressure, but the short answer is that once you figure it out, arterial oxygen (PaO2, pressure of arterial oxygen in mmHg or torr, same thing) works out to be roughly 4-5 x FIO2. So, if you're at sea level and breathing room air (FIO2 = 21%) into normally healthy lungs, your partial pressure of arterial oxygen, PaO2, should be around 80-100 torr. If you are breathing 50% O2, your PaO2 ought to be around 200-250 torr (yep). If you are breathing 100% oxygen, 400-500 torr.

Now, of course we never see PaO2s like that in the hospital when somebody is sick enough to be getting ABGs drawn. The reason is that they have sick lungs that aren't taking in O2 as well as they ought to. So their PaO2 is lower than expected for healthy lungs. The difference is called a gradient, meaning the difference between the partial pressure of oxygen in the inspired gases entering the alveoli (usually noted as "A") and the partial pressure of oxygen actually making it into the arterial (noted as "a," as in, "PaO2") blood. You will see this called, "the A-a gradient," ("alveolar-arterial gradient") and it's an indication of how lousy the lungs are.

The other thing to remember is that the lungs' primary job is not getting oxygen in, it's getting CO2 out. This is why many people have lousy PaO2s but sorta OK CO2s with hyperventilation until their lung disease is fairly well-advanced. It's also why somebody with a big PE shower can have lousy PaO2s and very low CO2s. They are hyperventilating not because their CO2 is up (as you and I do when we exercise and produce a lot of CO2) but because their O2 is so damn low, due to poor blood flow to the alveoli making it hard to pick up O2 from the inspired air.

So if you have someone on 50% O2, his alveoli are getting gases with an O2 partial pressure of 200-250 torr. Yet when you check his ABGs, his PaO2 is 88 torr. "Great, huh?" you say. "Normal range!" No, not great at all, as you can see by the A-a gradient, that's telling you that's the best his lungs can do. But acceptable therapeutic levels to keep his body happy (ier).

(PS,the concept of gradient applies anywhere you measure pressure-- for example, if you have a lousy aortic valve, there can be a blood pressure difference (gradient) across it indicating how lousy it is...)

ABGs Made Simple

You want simple ABGs? Piece o' cake. People who have seen this before, well, just scroll on by. Newbies who want a brief ABG's refresher, take out your pencils and a piece of paper, cuz you'll need to do a bit of drawing .

I taught ABG interpretation for yrs in a way that made it pretty foolproof. You will make your own key to interpret ABG's, and will be able to reproduce it from memory any time you need to with very little trouble if you learn a very few **key concepts**, labeled **thus**..

Take a piece of paper. Make a big box on it, then draw vertical and horizontal lines on it so you have four boxes. I will try to make this come out, but...you should have

AB

CD

where the four boxes a,b,c,d are such that a is above c and b is above d. You don't need to label the boxes a,b,c,d, just get them in the right alignment. (This is WAY easier with a blackboard bear with me).

*Inside* each of the 4 boxes write the following, down the left edge:

pH

CO2

Bic

Now, OUTSIDE the big box do the following: above the "A" box write "resp"; above the "B" box write "metabolic"

To the left of the "A" box write "acidosis" and to the left of the "C" box write "alkalosis"

Now you have a "resp" column and a "metabolic" column, an "acidosis" row and an "alkalosis" row. So you have respiratory acidosis and alkalosis boxes, metabolic acidosis and alkalosis boxes.

With me so far?

Now, you're going to label the PRIMARY DERANGEMENTS, so later you can tell what's the derangement and what's the compensation. OK? In the respiratory column, underline CO2's. In the metabolic column, underline the Bicarb's. That's because in **respiratory disorders, the CO2 gets messed up**, and in **metabolic disorders, the Bicarb is messed up**. You knew that, or could figure it out pretty quick if you thought about it, right? Thought so.

Now. You are going to put upward-pointing and downward-pointing arrows next to the pH, CO2, and Bicarb labels inside every box. Ready?

pH first. In the "alkalosis" row, make up arrows next to pH, because **pH is elevated in alkalosis (by definition)**. Put down arrows in the acidosis row's pHs, because **acidosis means a lower that nl pH**.

Remember that **CO2 is ACID** and **Bicarb is ALKALINE** (this is the end of the key concepts. Not too bad, huh?). (oops, I forgot: **nls are generally accepted as pH 7.35-7.45, CO2 35-45 (nice symmetry there), bic 19-26**)

Now go to the box that is in the respiratory column and the acidosis row. Figured out that CO2 must be elevated? Good. Put an up arrow next to that CO2. Go to the respiratory alkalosis box. Figures that CO2 must be low to cause this, right? Put a down arrow next to that CO2.

OK, now go to the next column, the metabolic one. I think you can figure out what happens here: in the metabolic alkalosis box, put an up arrow next to the Bic, because high bicarb makes for metabolic alkalosis. Put a down arrow next to the Bic in the metabolic acidosis box, because in metabolic acidosis the bicarb is consumed by the acids and is low.

You are now going to put arrows next to the blank spots in your boxes that show compensatory movements. Ready? OK, what does your body want to do if it has too much acid? Right, retain base. Yes, of course if your body has too much acid it would like to get rid of it...but if it can't do that, then retaining bicarb is the compensation. So for every elevated CO2 you see, put an up arrow with its bicarb.( Chronic CO2 retainers always have elevated bicarbs, and this is why.) You will find an up arrow next to the CO2 in the resp/acidosis box.

So if your body is short on acids, what does it do? Right, excrete base. So put a down arrow next to the bicarb in the resp/alkalosis box, because chronic low CO2 makes the body want to get back into balance by getting rid of bicarb.

Likewise in the metabolic/alkalosis box, a high bicarb makes your body want to retain acid, increasing CO2 being the fastest cuz all you have to do is hypoventilate, to bring your pH back towards nl. Put an up arrow next to the CO2 in the met/alk box. See the pattern here? Put a down arrow next to the CO2 in the met/acidosis box, because if your body has too much acid in it (think : ASA overdose? DK**A**?) it will want to get rid of CO2 to compensate, and the fastest way to do that is to hyperventilate.

OK, I hear you wailing: but how do I know whether that elevated or decreased CO2 or Bicarb in my ABG report is primary or compensatory?

Well, now you have your key. So take your ABG reports and look at them. Say, try these. (Notice that O2 levels have nothing to do with acid-base balance ABG interpretation) (OK, if you are VERY hypoxic you can get acidotic...but you see that in the metabolic component, not the O2 measurement, because it's lactic ACID your body is making if it's working in an anaerobic way)

1) pH = 7.20, CO2 = 60, Bic = 40.

First thing to look at is the pH. 1) is acidosis, with a low pH. Look at your acidosis choices (you have two). Find the acidosis where both CO2 and Bicarb are elevated, and you find your answer: respiratory acidosis with metabolic compensation. This is what you see in chronic lungers who have had high CO2's for so long their kidneys have adapted to things by retaining bicarb. (It takes about 24 hrs for your kidneys to make this compensatory effort, so you can tell if your resp acidosis is acute (no or little change in bicarb) or chronic)). (Remember, your lungs' first and most important job is not getting oxygen in, it's getting CO2 out, and when chronic lungers have CO2 retention, they're really getting bad. People with acute bad lungs will often have low oxygens and low CO2's , because their ability to gain O2 goes first, and while they're trying to deep breathe their way back to a decent PaO2, they hyperventilate away their CO2. ....but I digress....)

2) pH = 7.54, CO2 = 60, Bic = 40

pH here? This is alkalosis, with a high pH.

The only box where pH is high and CO2 & Bic are both elevated is metabolic alkalosis with respiratory compensation. Sometimes you'll see this in people who have a bigtime antacid habit. Really. (You can get a short-term metabolic alkalosis with rapid severe vomiting, because the body's nl balance betwreen acid and base has been disrupted due to a sudden loss of acid. Things will equilibrate pretty quickly, though, all things considered.)

So even though you have identical CO2's and Bicarbs, you can look in your boxes, find the match, and see what you have. Remember you underlined the primary disorder in each box?

Wanna try another one?

3) pH = 7.19, CO2 = 24, Bic = 12. Bingo, you found it: an acidosis where the CO2 and the Bic are both low. Only fits in the metabolic acidosis box, so you have a metabolic acidosis with a respiratory compensation effort. Incidentally, this is what you see in diabetic ketoACIDOSIS, when they come in huffing and puffing to blow out that CO2 because their ketosis is so high. Also you see this picture in ASA OD's, because this is acetylsalicylic ACID they ate, and the fastest way to get rid of acid is to blow it off via hyperventilation. Increasing your bicarb takes 24-48 hrs. Another quick way to get a metabolic acidosis is to poop out a lot of diarrhea, because you lose a lot of bicarb that way.

I know this is LONG, but trust me, you'll never go wrong with it, and you can recreate it anytime. It doesn't really even matter how you set up your boxes, so long as you have a metabolic and a respiratory axis and an acid/alkaline axis. Rotate your paper and you'll see what I mean.

Why don't I care about PaO2 here? Well, because ABG's mostly tell you about A/B balance and CO2 and Bicarb, that's why. Probs with them can be serious probs without any abnormality in oxygenation at all.

Remember that PaO2 (arterial oxygen, measured in torr or mmHg) is not the same as SpO2,( hemoglobin saturation, a percentage of red cells carrying oxygen). if you think they are, your pt could be in serious trouble before you do anything. There is a nomogram that shows you the relationship between arterial oxygen and saturation, which I will try to reproduce here. But you can sketch out a basic version...

Draw a graph where sats are on the vertical (left) axis and PaO2's are on the horizontal (bottom) axis. Draw little shaded band across the top at the 95%-100% sat areas. That's your normal saturation. Draw a few dots there indicating a line of PaO2's of 80-100, because those are normal PaO2's.

Now draw a dot for SpO2 of 90 and PaO2 of about 75. Now, another dot showing SpO2 of 85 and PaO2 of about 60. Another dot: SpO2 of about 80 and PaO2 of about 55. Connecting all these dots should give you a sort of S curve, indicating that while the top is pretty flat in the PaO2 80-100, SpO2 95-100 range, PaO2 drops off like a shot at decreasing SpO2 levels.

Your pt with a sat of 85 is not doing OK, he's in big trouble. While a PaO2 of 75 torr isn't too bad at all, a SAT of 75% is heading for the undertaker unless dealt with.

Here's my very favorite ABG of all time: pH = 7.11, PaO2 = 136, PaCO2 = 96, bicarb = 36.

What happened to this lady? What will happen next?

University of All-Nurses.

Here's my very favorite ABG of all time: pH = 7.11, PaO2 = 136, PaCO2 = 96, bicarb = 36.

What happened to this lady? What will happen next?

Yikes! I have my guess as to what happened, but I will hold my tongue and let some others take a stab at it.

Oh, go ahead. It's been 2 days and nobody's guessed yet. :)

Oh, go ahead. It's been 2 days and nobody's guessed yet. :)

ok, I will take a shot at this since have been reviewing ABG lately.

The ABG reflect a partially compensated Resp. acidosis of hyperoxia.

It may be caused by resp. failure which maybe secondary to hypoventilation (COPD) or due to inhaling large amount of smoke or a damage to the brain stem that regulates the respiratory system.

The lungs cant blow off co2 due to respiratory failure because exhalation is a passive process which also leads to co2 being retained.

I still dont know why the patient is hyperoxic but I know it has something to do with Copd

I'll take a stab at it too... was a bit too much oxygen given to a bad COPDer on hypoxic drive? If that was the case, then either minimizing or eliminating the supplemental oxygen will help to correct the problem and perk our lady up (PPV will speed the process).

I'll take a stab at it too... was a bit too much oxygen given to a bad COPDer on hypoxic drive? If that was the case, then either minimizing or eliminating the supplemental oxygen will help to correct the problem and perk our lady up (PPV will speed the process).

Ding-ding-ding, we have a winnah! :anpom: Loveofrn comes in close second, on the right track but not quite there.

This was an old bird with awful COPD who had the bad luck to be admitted at midnight by a new nurse who didn't understand the O2 prescription written by an attending new to the hospital. He wrote for, "O2 3/4 LPM," which the new grad misunderstood as, "3 to 4 LPM." So when the old bird didn't look so hot at 3LPM, she turned her up to 4LPM. Old bird pretty much stopped getting oxygen from her lungs because she wasn't really breathing much anymore. As far as I can tell she was doing her gas exchange in her nasal mucosa or hair follicles or something.

At 0700 crusty old bat RN gets report on the events of the night. She realizes what has happened, runs to old bird's bedside, rips off the O2 and grabs Ambu all in one smooth motion, concurrently explaining that since the old bird's carotid bodies hadn't seen that much oxygen since the Eisenhower administration, they decided to tell the hypoxic respiratory drive center to take the rest of the night off. So although the PaO2 was ducky (for normal people at 130+), the CO2 was ::: this close ::: to lethal levels and would have killed the old bird before her O2 dropped low enough for her hypoxic drive to kick in. But because the old bird was used to high CO2s she had lots of bicarb onboard for her long-term metabolic compensation, so the CO2 of 96 wasn't quite high enough to make her pH low enough to kill her yet (although it was getting there and certainly would have killed you or me).

Dontcha just love physiology?

Hypoxic Drive?

You must make the distinction between the hypoxic drive and the hypoxic drive theory.

Good reading:

[h=1]Oxygen-induced hypercapnia in COPD: myths and facts[/h]

Oxygen-induced hypercapnia in COPD: myths and facts

Quote from the article:

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.

Another good website:

Hypoxic Drive Theory

And yet another great page which is an educational inservice for a hospital.

http://www.nygh.on.ca/cernercbt/files%5CCONTENT_Day_1%5CRT%5COxygen%20Therapy%20Inservice-%20Rev%20July%202012.pdf

An elevated HCO3 can be for many different reasons which is why an ABG is just a small part of the assessment. Those numbers MUST be correlated with other lab data. The basic ABG course does clinicians a big disservice when they leave off the "rest of the story".

Not all people with COPD are CO2 retainers. In fact, very few.

Not all people with COPD have an SpO2 of 88% as their norm. In fact, very few. It is sometimes hard as heck to get someone to qualify for home O2 because their SpO2 or PaO2 is too high on ROOM AIR.

Not all people with the label of "COPD" have actually been tested by spirometry or X-ray to meet the qualifications for a diagnosis. Just smoking for x amount of years and being short of breath are not enough. CMS is cracking down on the actual diagnosis of COPD for a 496 code. ERs are notorious for this which is why extensive education has to be done if we are too prevent readmissions. It takes the correct diagnosis and the correct treatment plan.

Some who actually do have COPD are missed because they have never smoked and thus are not properly treated. (Alpha1 Antitrypsin Deficiency)

Never assume it is the oxygen. Do a complete assessment. Don't dismiss a somnolent patient as just having too much O2.

Understand the now KNOWN mechanisms for why the PaCO2 might rise and be proactive by knowing test results, CXRs and the V/Q mismatch. This can guide you in the administration of pain and sedation medications as well as the readiness of a BiPAP machine to support breathing or BVM. Also be aware of the role of perfusion.

If a patient shuts down from "too much" oxygen, chances are they needed BiPAP or a ventilator from the beginning. They definitely need a further work up.