Acid-Base Explanation Needed

I think he's got compensated respiratory acidosis, but I do not quite grasp the understanding of whether it's true respiratory acidosis, why it's considered compensated, and if it is, does that mean it could potentially be metabolic alkalosis?

He's also on lactated ringer's, so I am also trying to figure out how that plays a role in what I am seeing in the lab values.

And I've had a VERY difficult time with lactated ringer's because it's not in ANY drug book I've looked at so far, and it's only mentioned very briefly once in my text books.

The PH is normal but is a little higher than acidotic range which means that there may be a compensated acid-base imbalance.

The PCO2 is a bit elevated which means there is respiratory problem.

Remember ROME - Respiratory Opposite Metabolic Equal

(Example: PH high and bicarb (HCO3) high = metabolic alkalosis OR PH high and co2 low = respiratory alkalosis)

The PO2 is high indicating that this patient is receiving oxygen. (possibly vented or on BIPAP)

The HCO3 is borderline high = alkalosis and in this case - probable compensation

The formula to determine anion gap is as follows:

Sodium - (Chloride + CO2)

The anion gap is normal.

The other lab values are normal as well except for the calcium which is a bit low.

The patient has a compensated respiratory acidosis

IMO, it's not an acidosis at all. The pH is normal. Also, reporting values as PCO2 or PO2 is not useful; is the sample arterial or venous? Interpretation needs to be based, first and foremost, on the source of the blood sample as normal ranges will depend on type of blood being analyzed.

IMO, it's not an acidosis at all. The pH is normal. Also, reporting values as PCO2 or PO2 is not useful; is the sample arterial or venous? Interpretation needs to be based, first and foremost, on the source of the blood sample as normal ranges will depend on type of blood being analyzed.

It's compensated, so it still is compensated respiratory acidosis.

I think he's got compensated respiratory acidosis, but I do not quite grasp the understanding of whether it's true respiratory acidosis, why it's considered compensated, and if it is, does that mean it could potentially be metabolic alkalosis?

You are correct! Good job! It is a compensated respiratory acidosis. The easiest way I have found to break down ABGs is to label each value.

The first thing you look at is the pH. If it is in the normal range, then you know that either 1. It's normal or 2. It's compensated.

If it is out of range then it is either uncompensated or partially compensated.

Below .35 = acidosis

Above .45 = alkalosis

So right away, you label your pH as either Acid or Base

Next, you label your CO2 and HCO3

CO2 is an acid. If it's high, you label it acid, if it is low, then you label it Base.

HCO3 is a base. If it's high, you label it base, if low, then you label it Acid.

Then you match them. You should either have 2 acids or 2 bases. That will tell you the type of acid-base imbalance that you have.

So what if it is compensated? How do you know what type you have? Well, if it is below .40 then it is a compensated acidosis, and if it is above .40 then it is compensated alkalosis. The body will not overcompensate. Some nursing interventions can cause overcompensation (such as administering bicarb), but the body itself will not overcompensate.

So, for your listed scenario:

pH: 7.36 (ACID)

CO2: 48 (ACID)

HCO3: 27.1 (high end of normal = BASE)

The 2 that match tell you that you have a Respiratory Acidosis. The fact that pH is WNL and HCO3 is on the high end of normal tells you that it is compensated.

Now, what if you had?

pH: 7.36

CO2: 44

HCO3: 27.1

It would just be WNL. No calculations needed. You must have either CO2 or HCO3 out of the normal range for it to be an acid-base imbalance. Could the patient be starting to go acidotic? Yes. And if their trend showed a huge jump (like from 7.42 and 35 yesterday), then I'd probably call the doc and ask if he wanted to change the vent settings to increase the RR and blow off some of that CO2 before it even had a chance to reach the acidotic level. That is why trends are so important.

As far as the PO2, the clients FiO2 probably needs to be decreased. High FiO2 is related to pulmonary damage anyway, so turning that down as soon as the patient can tolerate will always be the goal anyway.

I hope all that made sense. If not, I'd be happy to help clarify. I'm weird and I really enjoy interpreting ABGs.

Not to throw a monkey wrench in here, but I disagree with your characterization of 7.36 as acidotic and your bicarb of 27 as normal. All the references I have show normals as

pH 7.35 - 7.45

PaCO2 35 - 45

Bicarb 22 - 26

You are correct in that compensation rarely gets people into the normal pH range, so knowing pH is a good place to start looking, because if it's acidotic, the problem has to be either too much C02 (respiratory acidosis) or not enough bicarb (metabolic acidosis).

In my opinion, if you assume that 7.36 is on the acidotic side of normal and the CO2 is high, you have to be looking at a respiratory acidosis. Since the bicarb is also elevated, it can't be the cause of an acidosis, so it has to be compensatory for a respiratory acidosis.

It's compensated, so it still is compensated respiratory acidosis.

I'm sticking with my original opinion (opinion being the key word here), assuming the results are from an arterial blood gas: there is no compensatory mechanism at work if the bicarb is normal. Of course, I realize that different facilities use slightly different reference ranges for lab values, so I can understand that opinions on a borderline gas like this might vary. I am basing my opinion on using a normal HCO3 reference range of 22-28. If, for example, that facility or school used a bicarb reference range with a high normal of 26 (as someone mentions in another post), then I would agree with the interpretation of compensated respiratory acidosis.

Thank you for all the explanations! I turned my assignment in before seeing any of these. I tried to explain what I thought was going on with the patient the best I could, but learning these ABGs is a hard concept to grasp. This particular patient was actually not on O2 therapy... I think that some of the meds he is taking are effecting the values, and that's making it harder for me to really grasp what is happening at a cellular level in his body. For example, he is on a lot of strong pain meds, and because of his reason for treatment (trauma injury), I do think he is at risk for fluid imbalance. Plus, he's on lactated ringer's which is really where I got confused because I know it contains sodium, chloride, potassium, calcium and lactate which is metabolized into bicarbonate. Combining those factors, I also think the meds he was taking were having an effect on respiratory depression, and if so, could that have an effect in the lab values too? Please correct me if I'm totally wrong.

I'm working on my next patient's labs now for a different assignment... HTN and cirrhosis!!

Respiratory depression can cause a patient to become acidotic due to build up of CO2. However, the patient would also be hypoxic, he certainly wouldn't have a paO2 over 100. I am honestly stumped at to how he could possibly have a level of 141 without O2 administration. I've only ever seen those types of levels on vented patients.

Can anyone provide any info on that???? I'm super curious.

Respiratory depression can cause a patient to become acidotic due to build up of CO2. However, the patient would also be hypoxic, he certainly wouldn't have a paO2 over 100. I am honestly stumped at to how he could possibly have a level of 141 without O2 administration. I've only ever seen those types of levels on vented patients.

Can anyone provide any info on that???? I'm super curious.

Completely agree that at sea level, nobody will have a PaO2 > about 100 without supplemental oxygen. I won't bore you with the equation, even though it's actually not that complicated to understand, but the rule of thumb is that normal lungs will give you a PaO2 of 4-5x FIO2, meaning for room air (.21, 21%), PaO2 = about 80-100 torr; for .50 (50%), 200-250torr, and for 1.0 (100%), 400-500torr. The difference between those ideal numbers and the actual ones your patient achieves gives you a rough idea of how lousy his lungs are. So, for example, somebody on 40% O2 who has a PaO2 of 100 isn't doing great, because he should have a PaO2 of around 160-200. Somebody on 80% 02 who has a PaO2 of 100 is really in trouble, because his should be like 320-400.

So. This example was a lady who was a chronic lunger who a new grad on night shift didn't know that the new doc had ordered "3/4 LPM" and so put the old bird on 3 LPM, and when she didn't do so hot on that, cranked her up to 4 LPM. This lady hadn't seen this much oxygen in her blood since the Eisenhower administration, so she pretty much stopped breathing. So that caused her CO2 rose to near-lethal levels before her O2 dropped far enough to make her breathe. Remember that in normal people, elevated CO2 increases resps, but in chronic CO2 retainers that reflex is dead and gone, so it's hypoxia that drives their resp rate.

So what happened is that an old experienced nurse came in at 0700, saw this (and knew the patient from many previous admissions), ripped off the O2 and bagged the heck out of her. And delivered an on-the-spot ABG lesson to the new grad.

And THAT's why I used to teach ABGs to students and new grads.