Please help me understand COPD!

People who do not have COPD have a hypercapnic drive to breathe. In other words, they breathe because their CO2 level is too high, and breathing helps to reduce it. People with COPD, especially in advanced stages, tend to retain CO2, which means they are hypercapnic all the time. Their bodies adapt in a way to this chronic high CO2 level, and they develop a hypoxic respiratory drive. They breathe because their oxygen level gets too low. So, in a nutshell, giving a CO2-retaining COPD patient too much oxygen will knock out their respiratory drive. I specify CO2 retainers because not all COPD patients are retainers. As the disease progresses, they probably will become retainers.

As for whether it is safe to use a non-rebreather on a COPD patient, a good rule of thumb for SpO2 target is 88-92%. If it takes a non-rebreather or venturi mask to keep them in that range, then it's probably safe to use it. Generally you would use a mask short-term to help recover their sats, but not long-term. If the patient is consistently >92%, it's time to wean the oxygen. For very high pCO2 levels, my facility likes to use BiPAP therapy at least in the short term to help them "blow off" some of the excess CO2.

I hope this helps!

Oxygen and CO2 Retention in COPD

Enough with the "knocking out the hypoxic drive" stuff. It is time to stop teaching the myth and start teaching the real mechanisms so correct therapy and oxygen administration can be given.

The above link is a very condensed summary. The references and comments are good reading.

Also, very few COPD patients are CO2 retainers.

Some patients labeled as COPD have actually never been diagnosed by actual testing nor been appropriately treated by severity due to lack of testing.

Patients with COPD usually have other medical conditions which also cause shortness of breath such as an exacerbation of their cardiac status. These patients are prone to PNAs and sepsis which must be addressed. Look for the V/Q mismatch source.

Do not treat a myth after hearing "COPD".

There was a good article eons ago in Nursing______(year?) Google the following: "Blue Bloater" and "Pink puffer" I think these articles will give you some physiology info that may help you. I agree with Granny, each COPD pt is different,(and she would know!!) You do not want to over oxygenate these folks nor do you want to under oxygenate them, their cells need O2 to function!!! Use the guidelines of your facility and if this area is lacking then bring it to the attention of your nurse educator. COPD is an umbrella term for various respiratory conditions, do a little more research and you will find your answers. This is a very complex condition and usually does require a good understanding of the specific condition and the other conditions that may contribute to someone going into respiratory distress. FYI, the winter is usually prime time for these patients to come into the hospital because of the agravation of underlying respiratory issues. You will see a lot of these type of patients this time of year. It can be a scarey situation, just remember, they need oxygen also and if you can maintain their SPO2 88-90% you are doing OK and so are they.

Slay that dragon, Granny! I was scrolling down to post about the V/Q mismatch and Haldane effect myself...GrannyRRT linked a brief summary for me. The 1949 (Edited to correct the date) research that has lead generations of educators to continue the "hypoxic drive" myth was based upon a poor understanding of the physiology and a misinterpretation of the data. If the pt needs 21% or 100% FiO2 to maintain sats, then that's what we deliver. Granted, high % inspired O2 isn't ideal, so we titrate down ASAP, but hypoxia takes early priority over O2 toxicity.

Edited again to include a direct link to the first reference in GrannyRRT's summary:

Oxygen-induced hypercapnia in COPD: myths and facts

Thank you for all your responses!! :)

"To maintain sats" is the critical point, and it has to be at the patient's baseline, not a "normal" sat. Too many people get O's slapped on them without checking sats, and those COPDrs WILL stop breathing.

The short answer is in the physiology of acid-base, because it's less an oxygen question than a ventilation question. Briefly, you and I breathe more deeply when we exercise not because we need more oxygen (there's no way to increase your blood oxygen by breathing MORE room air), but because we need to get rid of CO2 , the extra we are making when we carry something up the stairs or run. That you CAN blow off the more you hyperventilate.

The way our respiratory center decides whether to do that or not is based on the blood pH it sees circulating by. CO2 works like an acid, lowering the blood pH; lower pH (from whatever reason..we'll get back to that) says, "Hey! More deep breathing needed here! Get rid of this CO2 and get the pH back to normal!"

This is important: The normal respiratory driver is NOT hypoxia (low oxygen), but hypercarbia (high CO2). Your (normal) lungs' first job is to manage CO2 levels, not to manage oxygen. That comes second. Really. Remember that.

Now, when lungs fail, their ability to manage CO2 decreases. CO2 rises in the blood, and eventually that little sensor wears out and stops working. Fortunately, there's a back-up system, which IS an oxygen sensor. In chronic CO2 retainers, their respiratory drive is NOT elevated CO2 levels, it's falling oxygen levels. So, if their ventilation is inadequate, the body doesn't kick in with an elevated respiratory rate and minute volume (that's the total volume of air moved in and out in one minute) until the blood oxygen drops below threshold.

What this means is that someone who is a chronic CO2 retainer is ALWAYS a bit on the acidotic side (see below). It also means that if you give him oxygen to raise his SpO2, his body will say, "Ahh, no need to breathe now, all is well" until he stops long enough to drop his O2 back to make-me-breathe levels. The problem is that some people will stop breathing long enough to raise their CO2 to lethal levels before the oxygen level gets low enough to make them breathe again, and they die. Thus "never give a chronic lunger (well, at least a chronic CO2 retainer, the blue bloater) a lot of oxygen, it's bad for them." Now you know why.

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 whiteboard 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 (for purposes of this discussion and general clinical use) 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 (like, oh, ASA) 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. However, remember that it takes a day or two for the kidney to do this job, and if you have nonfunctioning kidneys they won't do it at all.

Likewise in the metabolic/alkalosis box, a high bicarb makes your body want to retain acid, increasing CO2 being the fastest way to do that because 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? DKA?) it will want to get rid of CO2 to compensate, and the fastest way to do that is to hyperventilate. This is why patients in metabolic acidosis are doing that deep, rapid breathing thing (Kussmaul's respirations).

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 between 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 abnormal 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 abnormally 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. Another classic place for this is in mesenteric artery thrombosis, in which you have a lot of ischemic bowel sitting in there screaming for oxygen and making lactic acid when it can't have any.

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 regret I cannot 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?

There is alot to understand. Sometimes reading about mistakes works for me. Carbon dioxide narcosis due to inappropriate oxygen delivery: a case report