CO2 vs PCOS?

203bravo, MSN, APRN · Mar 28, 2015

you measure the CO2 from the expired breaths and PCO2 from an arterial blood sample as part of the ABGs... the CO2 can indicate that the lungs are adequately exchanging CO2 and O2.. and PCO2 can be an indicator of respiratory portion of acid-base balance regulation.

GrannyRRT · Mar 28, 2015

CO2 from a metabolic panel lab work is more indicative of HCO3. If you did an ABG, the HCO3 will be close to the CO2 on the metabolic panel. This is the acid base part. I rarely need an ABG to know a patient's chronic respiratory status if I have a other lab work

If your instructor goes into the anion gap (CO2 is part of equation) in the ABG lecture, you have a great instructor and will have a more though understanding of acid base and respiration.

PaCO2 from the artery is a direct measurement for respiration valve.

PvO2 from a venous sample can also be used with the understanding it slightly higher than PaCO2.

Exhaled CO2 is ETCO2 or End Tidal CO2. It also has diagnostic value for V/Q mismatch when compared to PaCO2. If the waveform is available on the monitor, it also offers alot of useful information.

nurseprnRN, BSN, RN · Mar 28, 2015

Look at the units.

One says "mmHg" or "torr"-- and if you remember from when you took chemistry, those are measures of pressure. Gases are measured by pressure.

The other says something like "mmol" or "mEq." You will remember from when you took chemistry that those are measures of substances in solution.

Does that help you figure it out yourself?

nurseprnRN, BSN, RN · Mar 28, 2015

you measure the CO2 from the expired breaths and PCO2 from an arterial blood sample as part of the ABGs... the CO2 can indicate that the lungs are adequately exchanging CO2 and O2.. and PCO2 can be an indicator of respiratory portion of acid-base balance regulation.

Not exactly. Your lungs preferentially excrete CO2 much better than they take in O2. Plenty of people with pulmonary disorders (like pneumocystis pneumonia or big pulmonary emboli) have normal (or even low) CO2s due to hyperpnea, but subnormal O2.

The short answer is in the physiology of acid-base, because breathing is 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.

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?

Here's another cool thing, with a little repetition:

OK, as to why the lungs do CO2 first, a little background. Your CO2 levels vary considerably over the course of a day, whether you are sitting quietly (not generating a lot of CO2 in muscle work) or running up the stairs with a big bag of heavy laundry (lots of CO2 manufacture going on). Why do you breathe heavily when exercising? To blow off that new CO2 load, that's why. Yes, you use the oxygen, too. However, there are two sensors in your respiratory controls that tell your body when to breathe. One, the primary one, is an acid/base sensor. When it sees increasing acid levels of whatever origin, it makes you breathe faster and more deeply to engage that compensatory mechanism for acidosis: Blow off CO2. It's fast, it's effective, and it's a great bit of engineering. This is why you breathe fast and deep with exercise OR, if, for example, you have diabetic ketoACIDosis or eat a bottle of acetylsalicylic ACID. The respiratory drive is primarily CO2-driven.

If your CO2 level is chronically elevated, as in, oh, lung disease, that sensor kinda feeps out. Fortunately, you have a back-up. It's an oxygen sensor, and in chronic lungers, low oxygen levels are what drives their respiration. Increased CO2 doesn't do it anymore.

This all makes for some interesting clinical things. But first, a brief chemistry review. Remember semipermeable membranes? A substance diffuses from the area of higher concentration to an area of lower concentration? Diffusion pressure, that's called.

Think about your alveolus-- blood on one side of the membrane, air on the other. The air you have in your alveolus has an oxygen pressure (at sea level) of about 80-100 torr (mmHg). So if the blood on the other side of it has less oxygen than that, which of course venous blood does, oxygen will slide over there to be picked up by red cells. Good so far? What that means is that you can NEVER have a higher blood oxygen than what's being inhaled, else how would it get there? You can breathe as fast and as deep as you want but the PaO2 (pressure of arterial oxygen) will never exceed that of the air you breathe. (As a quick-and-dirty estimate, PaO2 should be roughly 4-5x inspired oxygen concentration in a healthy lung-- at 21% O2 for room air, that's...80-100. Neat. If you breathe 50% oxygen, your arterial oxygen should be 200-250; you never see it that high in hospitals because people in hospitals getting oxygen DON'T HAVE NORMAL LUNGS. The difference between what it ought to be and what it is is called the "arterial-alveolar gradient," A-a gradient

OK, now the CO2 part. Remember the diffusion gradient, the difference between one side of the membrane and the other. Well, for practical intent and purpose, there's not much CO2 in your alveolus if you are breathing, so ANY CO2 on the other side will leap at the chance to leave the RBCs and fly out there. This is why you can hyperventilate yourself into dizziness (respiratory alkalosis)...and why we give people who are hyperventilating a paper bag to rebreathe their exhaled air; its higher CO2 level makes it harder for them to keep blowing off more and more, and eventually it all equilibrates.

The architecture of your lungs makes it easier to lose CO2 than to take in O2, because it's more important in the greater scheme of things to regulate your body pH rapidly. So... you can have crappy lungs, giving you a very low PaO2 even on supplementation, and still have the CO2-excreting thing working relatively well. This is why you see people with pneumocystis pneumonia (blessedly not as prevalent as it was in past years) with ABGs showing PaO2 of 50 and CO2 of 30. They're breathing hard, not because their CO2 drive demands it, but because their hypoxic drive demands it. The CO2 loss is the result.

Last: This whole thing is why kids drown in pools all the time having thought they'd play a joke on their buddies and go hide in the deep end. They intentionally hyperventilate, thus driving down their CO2 levels but not, as we saw above, loading themselves with extra oxygen. Then they go down to the deep end and sit. Alas, they pass out from lack of oxygen before their CO2 elevates enough to alert them to being literally short of breath, so by the time their CO2 drive kicks in they're already asleep, and they take a big breath of water. Finis.

GrannyRRT · Mar 28, 2015

This website will give you a synopsis of Acid Base and ABGs.

http://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: 10.1186/cc11475

Oxygen-induced hypercapnia in COPD: myths and facts

Quote from the above link:

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 O₂tension 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.

nurseprnRN, BSN, RN · Mar 30, 2015

I hope you are not getting the idea that I'm espousing some sort of "never give CO2 retainers oxygen" sentiment, because I'm not.

However, if you give that old bird 4 LPM, she will stop breathing. 1/2 to 1 LPM as prescribed (and don't mistake "3/4 LPM" for "3 or 4 LPM" as the new grad in my cautionary tale did) and watch the patient like a hawk, check sats, check other VS, and do not assume they'll be just fine for a few hours while you go do something else.

GrannyRRT · Mar 30, 2015

I am just saying it is time to put the correct reasoning behind statements like "if you give that old bird 4 L she will stop breathing" and understand not all COPD patients are retainers. The longer you leave a patient in a hypoxic state the more chance of CO2 rising once oxygen is administered. But, you must understand there is a difference between the hypoxic drive and the theory that was initiated in 1950 and circulated as the truth and only truth in nursing and past RT classes.

Have you ever heard the expression "chasing gases in the ICU"? Some doctors love to make rapid fire changes on the ventilator per the ABGs. Many COPD patients will "spike up" their PaCO2 once on a vent with adequate oxygenation and then trend down. If you know about pulmonary Vasconstriction, deadspace and V/Q mismatch, you don't make knee jerk changes.

The same for metabolic issues. Adjust the ventilator for pH only long enough for other therapies to start correcting and understand the vent is supportive; not the cure.

This is also why both the serum CO2 and the PaCO2 needs to be understood.

la_chica_suerte85, BSN, RN · Mar 30, 2015

So, the take home here is that in an acute exacerbation, a patient would be better off with titrated O2 and not just throwing at them as much as they will take? I'm still not clear on what the myth v. reality is concerning hypoxic drive. Is it not the case that a typically acidotic COPD pt who runs a baseline 88% sat has reduced hypercapnic drive and administering too much O2 can dampen the hypoxic drive? :confused: