Learning ABGs as simple as learning ABC’s

img_0153In nursing school, we learned how to correctly interpret ABGs. But, have you ever taken a step further to wonder why it is so important? What does it mean? What type of diseases which reflect that ABGs? What is an “okay” ABG? What is a “very bad” ABG that require immediate intervention? What kind of treatment do we do to bring the patient’s ABG back to normal? In this article, we will have a chance to review how to interpret ABGs as well as answering all these questions. We also will review some case studies which I hope will solidify what you already know about ABGs. So, let’s learn about ABGs and start saving lives.

Before we move on to how to interpret an ABG, let’s review some basic stuff about ABGs. There are four components in the ABGs:

  • pH – A normal pH is 7.35 to 7.45. If your patient’s pH <7.35, your patient is acidotic. If your patient’s pH>7.45, your patient is alkalotic
  • CO2 –A normal CO2 is 3545. If your patient’s CO2 <35, it’s alkalosis. If your patient’s CO2>45, it’s acidosis. Remember, CO2 makes your patient become more acidotic. The more CO2, the more acidosis.
  • HCO3 (bicarb) – A normal bicarb is 22-26. If your patient’s bicarb <22, it is acidosis. If your patient’s bicarb >26, it is alkalosis. Remember, HCO3 (bicarb) makes your patient become more alkalotic. The more bicarb, the more alkalosis
  • pO2 (partial pressure of Oxygen) – A normal is 80%. If your patient’s pO2 is less than 80%, your patient is hypoxic. If your patient’s pO2 is greater than 100%, your patient may receive too much oxygen. Therefore, pay attention to the FiO2 (Fraction of inspire Oxygen). Let’s say if your patient has pO2 of 150% on a vent with FiO2 of 100%, its time to decrease FiO2.

Now that we already familiar with the ABGs value. Let’s interpret an ABG.

There are several steps you should follow so that you can always get it right. Here is an example of an ABG

pH -7.18

pCO2 – 65

HCO3 – 35

pO2  – 45

Whenever I interpret an ABG, I always make a table like this below. I find it easier that way

pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45


  • Step 1: Before you start to interpret anything, look at the first three values of the ABG. If they are all normal, you have a normal ABG. If not, move on to the second step
  • Step 2: Looking at the pH. Although a normal pH is 7.35 to 7.45, you want to compare your pH value with 7.40
  • If your patient’s pH >7.40, its alkalosis (Yes, I said it 7.40 not 7.45. Therefore, if it’s 7.42, its alkalosis. In that scenario, because it is within normal range of 7.35-7.45, write down “full” for fully compensated. If not, just write down alkalosis).
  • If your patient’s pH <7.40, its acidosis. And again, if pH is within 7.35-7.45, write down “full” for fully compensated. If not, just write acidosis.
pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45
Since the pH < 7.40



  • Step 3: Looking at the CO2.
  • If CO2 >45, it is acidosis
  • If CO2<35, it is alkalosis
  • If CO2 is within 35-45, it is a normal limit, write uncompensated
pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45
Since the pH < 7.40


Since the CO2 >45



  • Step 4: Looking at HCO3.
  • If HCO3 >26, it is alkalosis
  • If HCO3 <22, it is acidosis
  • If HCO3 is within 22-26, it is a normal limit, write uncompensated
pH-7.18 CO2 – 65 HCO3 – 35 pO2 – 45
Since the pH < 7.40


Since the CO2 >45


Since HCO3 >26



  • Step 5: As you can see, both pH and CO2 have acidosis, your patient has Respiratory Acidosis. In addition, because the HCO3 is not within normal limit, we see a compensation which the kidney tries to bring the pH back to normal that has not been achieved. So your patient has Partially compensated Respiratory Acidosis.

With the same token, let’s say that your patient has the same pH, same CO2, but HCO3 is 24 which is within normal limit. What do you think your patient have? Yes, it is Uncompensated Respiratory Acidosis which means that even though your patient is in respiratory failure, his/her kidney did not increase HCO3 (bicarb) to bring the pH back to normal.


Here are some more examples you can practice on

Ex 1

pH-7.32 CO2-39 HCO3 -17 pO2-60

Ex 2

pH-7.24 CO2-74 HCO3 -33 pO2-17


Ex 3

pH-7.43 CO2-20 HCO3 -16 pO2-45


Answer Keys

Ex 1

pH-7.31 CO2-39 HCO3 -17 pO2-60
Acidosis Uncompensated Acidosis

-Uncompensated Metabolic Acidosis


Ex 2

pH-7.24 CO2-74 HCO3 -33 pO2-17
Acidosis Acidosis Alkalosis

-Partially Compensated Respiratory Acidosis


Ex 3

pH-7.43 CO2-20 HCO3 -16 pO2-45
Alkalosis and Full Alkalosis Acidosis

-Fully Compensated Respiratory Alkalosis


Now that you have mastered ABGs, Let’s move on to more in-depth topic, the pathology and modalities for each condition. So far we have Respiratory Acidosis, Respiratory Alkalosis, Metabolic Acidosis, and Metabolic Alkalosis.


I find it is very difficult to have a good understanding of those conditions by just memorize the diseases with each condition. So I have created some case study scenario, although I have changed much of the story details to keep patients’ confidentiality to comply with HIPPA regulation, these case studies could be very much true.

  • Let’s imagine. You have a patient who has hx of smoking and diagnosed with COPD several years ago. The patient was admitted to your unit because of shortness of breath, his O2 Sat was 84% on room air. The doctor ordered a Stat ABGs. What do you think his ABGs will look like?


Your patient has hx of COPD, in respiratory distress, bad O2 Sat, what do you think the problem come from? Is it respiratory or metabolic? If it is respiratory origin, is the CO2 going to be high or low? Think about that, if your patient can not breathe, there is probably a decrease in gas exchange resulting in an increased CO2 in the body. So, your patient probably has high CO2 and thus respiratory acidosis. Noted that your patient is breathing fast because he is trying to get some air for gas exchange, what do you think his pO2 going to be? Probably low, right?


  • That is totally different than having a patient who has normal pulmonary and kidney function, coming to the hospital because he failed and fractured his wrist. This patient may have a fast breathing too, but it is because he has pain. So his ABGs probably normal or Respiratory Alkalosis because he blew off too much CO2. This patient will have a low CO2 and normal or high pO2 (which is different than the guy with COPD). The doctor probably does not even bother to get the ABGs because it just a waste of time and resource. What he needs is an X ray and some pain medications. Patients with pneumothorax or pulmonary embolism usually show respiratory alkalosis on ABGs because they hyperventilate.


  • Let’s have another scenario. You have a patient admitted to the hospital because his daughter found him laid unresponsive in the bathroom. He is very altered. Blood test shows that he has a BUN of 110 and Creatinine of 5.5. His total CK is 1,700. His glucose is 900. He is currently breathing fast, respiratory rate of 32, and his O2Sat is 96% on room air. What do you think his ABGs going to look like?

Well, he has some kidney damage probably acute tubular necrosis (ATN) which evident by elevated BUN and Creatinine. Because his kidney is already damage, do you think his bicarb going to high or low? Remember, kidneys conserve and produce bicarb. If the kidney does not work, his bicarb is probably low. What is the condition that involves the kidney and low bicarb? Metabolic Acidosis, right? So, why does the patient is still breathing very fast when we say that he does not have any pulmonary issue? Remember, both lungs and kidneys are working together to compensate to the imbalance to neutralize the pH. If the patient has metabolic acidosis, the lungs will try to get rid of the acidosis part, right? How do the lungs decrease the acidosis? Probably by getting rid of CO2 because it makes the body acidic, right? So that’s why the patient is breathing fast. Also, noted that the patient has a blood sugar of 900, he is probably having a DKA on top of what is going on. Look at his total CK also. It is very high, greater than 1000. He probably has rhambdomyolysis which resulting in release of myoglobin into the blood stream. The myoglobin is a large protein which could cause an obstruction in the nephrons of the kidneys resulting in kidney failure.


  • Another case study? Yeah? You have a patient who has hx of CHF, the patient was admitted to the hospital because of shortness of breath. Blood test showed his BNP was 2,000 and he seemed edematous. So the doctor prescribed Lasix 40mg every 4 hours and 1500mL fluid restriction. Three days later, you the nurse who is assigned to the patient. Upon assessment, you noted that the patient edema had completely gone. The patient became pretty skinny, poor skin turgor. What do you think his ABGs will look like? The patient will have Metabolic Alkalosis. Due to overuse of diuretic, your patient is probably dehydrated. As a result, the kidney increases the HCO3 reabsorption that causes increased bicarb. In general, any volume depletion (including vomiting and diarrhea) could cause Metabolic Alkalosis.

So far we have reviewed how to interpret ABGs and the kinds of disease which reflect each condition. Let’s move on to the next several questions:

What is an “okay” ABG?  What is a “very bad” ABG that require immediate intervention?  What kind of treatment do we do to bring the patient’s ABG back to normal?


  • When we try to figure if an ABG is “okay” or “very bad”, we should think ABCs. Technically, if you have a patient with respiratory problem, you need to be more aggressive to treat the patient. Pt with metabolic problem requires appropriate treatments too, yet it is not as urgent as respiratory issue. In general, patient with respiratory acidosis requires our immediate attention because if your patient is in respiratory distress, he/she could get to respiratory failure at any moment, so the sooner you treat the patient, the better outcome.


  • Treatment usually goes as order, or the physician could jump right into intubation if the ABG result looks bad enough (how bad is bad enough, it’s up to the physician who decides the course of treatment based on the patient’s condition)
    • nasal cannula (1L-6L of oxygen with FiO2 of 24%-44%)
    • then venture mask (which FiO2 could get as high as 50%)
    • then non-rebreather ( which FiO2 could get as high as 100%)
    • then BiPAP (in addition to be able to provide 100% FiO2, the mask creates positive pressure upon inspiration and expiration to enhance air flow to facilitate gas exchange)
    • then intubation with mechanical ventilation support as the last resource


  • For patients with metabolic problems, the treatment is usually more straight-forward. In patient with metabolic acidosis, sodium bicarb is the primary treatment to increase the base to bring pH back to normal (sodium bicarb IV push first then continuous infusion). Bicarb is only used when pH <7.1 and HCO3< 6 mEq/L (Ellis, 2015) . According to Myra Ellis, there are two causes of metabolic acidosis, a real HCO3 deficit (which usually caused by kidney failure) or a net addition of strong acids (such as toxins, lactic acid in sepsis, or ketone in DKA) (Ellis, 2015). Bicarb replacement is only used for patient with true bicarb deficit (Ellis, 2015). In addition for patients with kidney injury, fluid challenge and diuretic therapy for patient with pre-renal kidney injury, hemodialysis for patient with intrarenal kidney injury or acute tubular necrosis (ATN). In patient with metabolic alkalosis caused by dehydration, fluid resuscitation is the primary treatment.

So far, we have learned how to correctly interpret ABGs as well as being able to understand their pathology and modalities. I hope that you find this helpful as you studying or working on the floor. If there is any discrepancy between what you read in my article and your text book, please don’t hesitate to leave me a comment below. I would love to hear from you.

Best Regards,



Ellis, M. F. (2015). Use of Bicarbonate in Patients With Metabolic Acidosis [Abstract]. Critical Care Nurse, 35, 5, 73-75. doi:10.4037/ccn2015502



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