Need help with Arterial Blood Gases

nurseprnRN, BSN, RN · Jan 29, 2013

Can someone please explain how:
head trauma causes respiratory acidosis
anemia causes respiratory alkalosis
fever/sepsis causes metabolic acidosis
The way I memorized ABGs is that CO2 (carbon dioxide) is toxic to the lungs. "Acids are toxic." So, if there's too much CO2, i know that the patient is in an acidotic state.
HC03 (bicarb) is a base or a pH buffer. So, if there's too much HC03, i know that the patient will be in an alkalotic state.
Right?
and this: when a patient is hyperventilating (breathing fast), they are blowing out lots of CO2, therefore decreasing PaCO2 levels in the body and increasing the pH of arterial blood thus putting the body in alkalosis. What do the kidneys do to compensate? Do they release HCO3 or retain HCO3?
and in hypercarbic resp failure, is the patient breathing fast or slow? Wait---if they have too much CO2 in them, that means their hypoventilating. Right? Cuz when you're breathing slow, you're retaining CO2.
I think i'm confusing myself

You're doing fine. Think of acid-base compensation as a seesaw or a balance scale. The body tries to compensate by bringing things back into balance. Too much CO2? Retain bicarb. Not enough bicarb? Blow off CO2.

So, think. Chronic lungers retain CO2 because their lungs do a lousy job of blowing it off. So what's their compensation? Right, their kidneys, over time, retain more bicarb.

That's how you can tell if your hypercarbic (high CO2) patient is acute (inadequate ventilation, bicarb hasn't had time to compensate- takes about 24hours) or chronic (bicarb is already up).

nurseprnRN, BSN, RN · Jan 29, 2013

Head trauma causes respiratory acidosis (too much CO2 on board, a respiratory problem) if it results in lousy breathing.

Anemia causes respiratory alkalosis because the body being short on oxygen wants to breathe faster, and that blows off the CO2 (too little acid, bicarb hasn't been excreted yet). (Remember, your lungs' first job is NOT bringing O2 in, it's getting CO2 out. If you don't know why, ask me.)

Fever/sepsis can cause metabolic acidosis in lots of ways, but the easiest (and most deadly) is if there is so much oxygen being consumed by the tissues working all that fever up that the tissues go into anaerobic metabolism from lack of oxygen. The main byproduct of anaerobic metabolism is...lactic ACID.

I LOVE physiology. This is a really short and dirty explanation of these, but I can expand if you like.

itsdebraanne, ASN, RN · Jan 30, 2013

when you say "blow off," this means low CO2 in the blood right? I've been saying blowing out, as in the body is exhaling CO2 and has low CO2 levels in the blood.

are hypercarbic and resp acidosis the same?

Head trauma causes respiratory acidosis (too much CO2 on board, a respiratory problem) if it results in lousy breathing.
Anemia causes respiratory alkalosis because the body being short on oxygen wants to breathe faster, and that blows off the CO2 (too little acid, bicarb hasn't been excreted yet). (Remember, your lungs' first job is NOT bringing O2 in, it's getting CO2 out. If you don't know why, ask me.)
Fever/sepsis can cause metabolic acidosis in lots of ways, but the easiest (and most deadly) is if there is so much oxygen being consumed by the tissues working all that fever up that the tissues go into anaerobic metabolism from lack of oxygen. The main byproduct of anaerobic metabolism is...lactic ACID.
I LOVE physiology. This is a really short and dirty explanation of these, but I can expand if you like.

Resp acidosis happens with head trauma because they're respirations are slow; slow rests retain CO2 and that puts them in an acidotic state. i get it :)

The fever part… I had an idea about O2 being used up by the tissues when the person gets the chills and shivers. their muscles are being overworked and lactic acid build up. glad to know i was thinking in the right direction :)

Anemia happens because they're low on blood and therefore low on O2 and high in CO2. to compensate, the body breathes faster to blow out CO2 putting the pt in reps alkalosis.

This can also relate to anxiety (also in my notes but i forgot to ask why). But I figured it out when you told me about how anemia can put a patient in resp alkalosis because anxious people are worried/stressed. stress, from my experience, can cause hyperventilation. breathing fast blows off CO2 and puts them in alkalosis.

but why is the lungs' first job to getting CO2 rather than bringing O2 in?

KelRN215, BSN, RN · Jan 30, 2013

The way I memorized ABGs is that CO2 (carbon dioxide) is toxic to the lungs. "Acids are toxic." So, if there's too much CO2, i know that the patient is in an acidotic state.
HC03 (bicarb) is a base or a pH buffer. So, if there's too much HC03, i know that the patient will be in an alkalotic state.
Right?

Sort of... CO2 is an acid and HCO3 is a base but you have to look at your pH to know if you're dealing with acidosis or alkalosis. Remember compensation? Acidosis can be respiratory (too much CO2) or metabolic (too little HCO3) just as alkalosis can be respiratory (too little CO2) or metabolic (too much HCO3).

So if you're looking at a pH of 7.30, an HCO3 of 18 and a PaCO2 of 35- what's your problem?

and this: when a patient is hyperventilating (breathing fast), they are blowing out lots of CO2, therefore decreasing PaCO2 levels in the body and increasing the pH of arterial blood thus putting the body in alkalosis. What do the kidneys do to compensate? Do they release HCO3 or retain HCO3?

This is how I learned it and have always remembered it despite never actually having to interpret ABGs on the job:

CO2 is an acid. If you lose acid (as in blowing off CO2 and lowering the level in the body), you're dealing with an alkalotic state. If you gain acid, you raise the level of acid making it an acidotic state.

HCO3 is a base. Losing base = acidosis and gaining base = alkalosis.

On to your question. If you have an alkalotic state, what SHOULD the kidneys do to compensate? Do they retain base? That makes more base and raises the pH even more, doesn't it? Or do they lose base and try to balance out the excessive base from the lungs?

I think you're on the right track.

nurseprnRN, BSN, RN · Jan 30, 2013

when you say "blow off," this means low CO2 in the blood right? I've been saying blowing out, as in the body is exhaling CO2 and has low CO2 levels in the blood.
are hypercarbic and resp acidosis the same?
Resp acidosis happens with head trauma because they're respirations are slow; slow rests retain CO2 and that puts them in an acidotic state. i get it :)
The fever part… I had an idea about O2 being used up by the tissues when the person gets the chills and shivers. their muscles are being overworked and lactic acid build up. glad to know i was thinking in the right direction :)
Anemia happens because they're low on blood and therefore low on O2 and high in CO2. to compensate, the body breathes faster to blow out CO2 putting the pt in reps alkalosis.
This can also relate to anxiety (also in my notes but i forgot to ask why). But I figured it out when you told me about how anemia can put a patient in resp alkalosis because anxious people are worried/stressed. stress, from my experience, can cause hyperventilation. breathing fast blows off CO2 and puts them in alkalosis.
but why is the lungs' first job to getting CO2 rather than bringing O2 in?

Almost. Hypercarbic means "high CO2" and since this is a respiratory thing, hypercarbic and respiratory acidoses are the same.

Anemia isn't "low on blood." You can have plenty of circulating blood volume but be anemic, because anemia means "lack of blood cells," most commonly red cells, the ones that carry oxygen. ("Pancytopenia" means low levels of all cells.) Anemia won't in and of itself make you high in CO2. The reason really anemic people are short of breath is because they have low oxygen-carrying capacity, so any kind of exercise that wants to pull oxygen off the red cells gets a "tank empty" signal really fast, and they get short of breath to allow the red cells they have to catch up.

(This is also why just looking at SpO2, the percentage of red cells carrying oxygen, gives you an incomplete assessment of cellular oxygenation-- somebody with a crit of 15 and an SpO2 of 98% is carrying one third of the amount of oxygen to his body cells as someone with a crit of 45 and an SpO2 of 98%. Look at the whole picture.)

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 because it's called on all the time.

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.

I LOOOOVE physiology.

Devon Rex, ADN, BSN · Feb 3, 2013

Hello! This is how I memorized the ABGs...

Think of ROME:

R = repiratory

O = opposite directions

M = metabolic

E = equal directions

Normal Values:

pH 7.35 - 7.45

CO2 35 - 45 mmHg

HCO3 22 - 26 mEq/L

* To determine acidosis or alkalosis, look at the pH value in your problem. Then determine if it's respiratory or metabolic. Is the question talking about a respiratory issue? If not, it's metabolic.

* In order to be respiratory alkalosis, pH must be greater than 7.45, and CO2 running opposite to below 35 mmHg.

* In order to be respiratory acidosis, pH must be less than 7.35, and CO2 running opposite to above 45 mmHg.

* In order to be metabolic alkalosis, pH and HCO3 would both be greater than their normal value range.

* In order to be metabolic acidosis, pH and HCO3 would both be lower than their normal value range.

* Lungs are located higher in the human body than the kidneys, right? So the higher values (35-45 mmHg) pertain to the lungs. The lower values pertain to the kidneys (22-26 mEq/L). (This was the only way I was able to make it stick to my mind, LOL)

** If all three values are out of normal range, look at pH first (for acidosis or alkalosis), then at the CO2 or HCO3 value that is furthest away from its normal range to call it resp/alk, resp/acid, metb/alk, or metb/acid. The closest to the the normal range (CO2 or HCO3) is said to be "compensating" to fix the imbalance.

Disclaimer: This trick only helps you answer some questions. It does not teach you how to think critically. So you must also learn the "why" behind every situation to fully understand what is going on in real life and know what to do about it.

Hope this helps! :headphone:

Esme12, ASN, BSN, RN · Feb 3, 2013

GrnTea has given you great information......I also know of a website that is very helpful icufaq's.org they have a section on Vents and ABGs go to the AGB's section 17- What are the ideal ABG values, and why do we use them?

NurseRies, BSN, RN · Feb 3, 2013

Head trauma causes respiratory acidosis (too much CO2 on board, a respiratory problem) if it results in lousy breathing.
Anemia causes respiratory alkalosis because the body being short on oxygen wants to breathe faster, and that blows off the CO2 (too little acid, bicarb hasn't been excreted yet). (Remember, your lungs' first job is NOT bringing O2 in, it's getting CO2 out. If you don't know why, ask me.)
Fever/sepsis can cause metabolic acidosis in lots of ways, but the easiest (and most deadly) is if there is so much oxygen being consumed by the tissues working all that fever up that the tissues go into anaerobic metabolism from lack of oxygen. The main byproduct of anaerobic metabolism is...lactic ACID.
I LOVE physiology. This is a really short and dirty explanation of these, but I can expand if you like.

Now, if you could just write a book about physiology eplaining things like the way you just did, it would be a lot less difficult!! The way you explained it sounds makes it easy to comprehend. I think it's so important to understand the physiology and the "why" of disease process because then we don't forget! Thanks.

SleeepyRN · Feb 3, 2013

Head trauma causes respiratory acidosis (too much CO2 on board, a respiratory problem) if it results in lousy breathing. Anemia causes respiratory alkalosis because the body being short on oxygen wants to breathe faster, and that blows off the CO2 (too little acid, bicarb hasn't been excreted yet). (Remember, your lungs' first job is NOT bringing O2 in, it's getting CO2 out. If you don't know why, ask me.)Fever/sepsis can cause metabolic acidosis in lots of ways, but the easiest (and most deadly) is if there is so much oxygen being consumed by the tissues working all that fever up that the tissues go into anaerobic metabolism from lack of oxygen. The main byproduct of anaerobic metabolism is...lactic ACID. I LOVE physiology. This is a really short and dirty explanation of these, but I can expand if you like.

I LOVE physiology as well. What a wonderful explanation. Thanks for posting it. Having a GREAT base in A&P led to sooo much less headache in nursing school, because I understood the entire picture. (Double major in Bio)