When interpreting an arterial blood gas result I like to take a systematic, yet contextual, approach. Other methods that I have seen on the internet focus on isolating parameters such as PaCO2 and HCO3 and using steadfast rules based on their behavior to classify the blood gas results. One such method that I have seen often on youtube asks the nurse to place parameters within boxes in an equation like matrix. While using approaches such as these, which are aided by tables like the one shown above, are valuable for quick classification of ABG’s, they tend to isolate the variables and fail to truly “interpret” the overall results.
I like to know why the ABG is behaving the way it is. What is it about the situation that is making all these values move? Without knowing, for example, that ketones from diabetic ketoacidosis are causing the blood to become acidic and that the respiratory centers are responding by offloading CO2 through hyperventilation, the nurse my still pass the test but may also fail to fully comprehend the interplay between compensatory mechanisms in the body.
- Respiratory Acidosis.
This situation arises when ventilation is insufficient to remove CO2 from the blood stream, across the alveolar-capillary membrane, and out of the lungs. This can be due to either an impediment to breathing, such as COPD or asthma, or because of a hypermetabolic state, like an infection, which increases the workload at the cellular level of the body, producing more byproducts in the form of carbonic acid (H2CO3). The lungs can become overwhelmed and unable to keep up with the excretion of the volatile fraction (CO2) through ventilation. With uncompensated respiratory acidosis, the PaCO2 will typically rise and the pH will fall. In chronic, or compensated, respiratory acidosis, the HCO3 will rise to counteract the acidic nature of the blood to restore equilibrium. Bicarbonate (HCO3) levels are influenced by the kidneys. When more HCO3 is present, acidic elements of the blood are bound and inactivated, neutralizing the acidic effects and restoring a pH between 7.35-7.45. The compensatory shift in HCO3 takes hours to days to occur so sometimes interventions such as ventilatory support through BiPAP may be necessary.
- Respiratory Alkalosis.
This situation can be caused by central nervous system derangements causing excessive ventilation, such as a brain injury. It may also be caused by hypoxemia or pain which are situations in which the drive to breath is rapidly increased. In any case, the lungs are expelling more CO2 than necessary, causing an increase in the pH as the blood becomes more alkalotic (basic) because of an excess of HCO3 in relation to CO2. This situation is usually remedied by eliminating the cause of hyperventilation. Supplying oxygen, reducing pain, relieving intracranial pressure, or simply turning down the respiratory rate on the ventilator can help. The ABG may appear compensated if the situation endures long enough for the HCO3 to drop. However, respiratory muscles usually fatigue by this point, causing respiratory failure and respiratory acidosis as a result.
- Metabolic Acidosis.
Metabolic acidosis occurs when excessive quantities of acids are present in the blood or when the kidneys fail to produce enough HCO3 to buffer the acids. My favorite acronym for the causes of metabolic acidosis is MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol, infection, lactic acidosis, ethylene glycol, and salicylates. This will usually be reflected on the ABG by a HCO3 less than 22. When this occurs, the balance of acids and bases causes the blood to become acidic and the pH to fall below 7.35. You will see the body react by an increase in ventilation, which removes acid or CO2 from the blood. In a compensated metabolic acidosis, the pH is within normal range but both the HCO3 and CO2 are decreased.
- Metabolic Alkalosis.
Metabolic alkalosis is usually caused by loss of hydrogen ions through nasogastric suctioning, vomiting, or diuretic use. Sometimes the body can gain HCO3 from external sources such as sodium bicarbonate administration. Either way, the HCO3 will rise disproportionate to the PaCO2. The ABG will reveal an increased pH which reflects alkalosis. The HCO3 will be increased. If the body compensates, which the respiratory center is capable of doing quickly, the patient will begin to hypoventilate, retaining CO2 and decreasing the pH back to normal levels.
Classifying, or labeling, ABG’s is a little bit easier but I still like to use an approach that takes into account the whole picture. It involves the following steps:
- Is the pH out of range? If so, acidosis or alkalosis.
- Which parameter, PaCO2 or HCO3, is behaving in the direction that the pH has shifted?
- If the pH is within normal limits, is erring toward acidosis or alkalosis?
- If it is, which parameter, PaCO2 or HCO3 is behaving in direction that the pH is erring?
- If a parameter, PaCO2 or HCO3, is out of range, did the other parameter help the situation?
7.3/50/24 – The pH is out of range. It is acidotic. The PaCO2 is out of range and behaving acidotically. Therefor, respiratory acidosis.
7.36/50/30 – The pH is in range but erring toward acidosis. The PaCO2 behaved acidotically. The HCO3 is also out of range. It behaved helped by increasing. Therefor, fully-compensated respiratory acidosis.
7.5/30/24 – The pH is out of range. It is alkalotic. The PaCO2 is out of range and behaving alkalotically. Therefor, respiratory alkalosis.
7.44/30/20 – The pH is in range but erring toward alkalosis. The PaCO2 behaved alkalotically. The HCO3 is also out of range. It helped by decreasing. Therefor, fully-compensated respiratory alkalosis.
Hopefully, this little tutorial helped you to understand both the causes of ABG derangements and how to label ABG’s. If you’d like to see my video over this topic, you can visit my channel at youtube.com/channel/nursemastery or check out my eBook with more than 75 tables just like the one above at amazon.com. My book is called “75 Nurse Cheat Sheets for Students and New Grad Nurses”. Thanks!
– Aaron Reed, CRNA, MSN, RT