Part 1 of this post will cover the physiology behind arterial blood gases and part 2 will cover clinical interpretation of arterial blood gases. Arterial blood gases (ABGs) are an essential part of the evaluation of unstable patients. In unconscious patients who are unable to give a history, the blood gas can provide key data that can lead to a diagnosis long before other test results come back. In the intensive care unit and in the operating room, the ABG can provide critical results that can direct life-saving treatment. But optimal use of the arterial blood gas requires the physician to be able to rapidly interpret the results of the ABG. The two main components of the arterial blood gas are (1) oxygenation and (2) acid-base status. This post will focus on the background physiology of the acid-base components of the ABG. If you are primarily interested in the use of ABGs in clinical decision making of acid-base disorders, skip ahead to the next post.
Components of the ABG
Fundamentally, there are 5 main results in an arterial blood gas report: pH, PO2, PCO2, HCO3, and O2%. The pH is measured directly and indicates whether the patient is acidemic (pH < 7.40) or alkalemic (pH > 7.40). The PO2 is the partial pressure of dissolved oxygen in the blood. The PCO2 is the partial pressure of dissolved carbon dioxide in the blood. The HCO3 is the bicarbonate concentration which is very similar to the serum CO2 reported in an electrolyte panel (the serum CO2 is the total of everything that can be converted into CO2 in the blood including bicarbonate, carbonic acid, and dissolved carbon dioxide – it should not be confused with the PCO2 from the arterial blood gas which is a completely different value). The O2% is the oxygen saturation which is the percentage of hemoglobin binding sites that contain bound oxygen molecules. The normal values for each of these results are usually listed as a range of normal but for the purposes of analyzing the acid-base status, consider normal to be single numbers: pH = 7.40, PCO2 = 40 mm Hg, and HCO3 = 24 mEq/L.
Many ABG analyzer machines can also measure other values such as methemoglobin, carboxyhemoglobin, potassium, lactate, hemoglobin, etc. However, these tests usually need to be ordered separately and if only an ABG is ordered, then you will just get the 5 results as described above.
Our bodies try to keep the pH as close to 7.40 as possible. The two ways that we regulate the pH are by (1) increasing or decreasing carbon dioxide excretion by the lungs and (2) increasing or decreasing bicarbonate excretion by the kidneys. When the carbon dioxide level of the blood is too high or too low, the kidneys compensate by increasing or decreasing the bicarbonate level of the blood by altering bicarbonate excretion in the urine. On the other hand, when the bicarbonate level is too high or too low, the lungs compensate by increasing the carbon dioxide level using hypoventilation or by decreasing the carbon dioxide level using hyperventilation.
Our tissues are constantly producing acids (in the form of hydrogen ions) and acid production can increase very rapidly with exercise. Therefore, there has to be an efficient way to get rid of acid as quickly as it is produced. This is done by converting hydrogen ions into carbon dioxide. In the blood, this is done by the enzyme carbonic anhydrase that first converts hydrogen ions into carbonic acid and then converts carbonic acid into carbon dioxide and water. The carbon dioxide is then excreted by the lungs in the form of exhaled carbon dioxide. When more acid (and thus carbon dioxide) is produced, for example, during exercise, the lungs can immediately dispose of that carbon dioxide by hyperventilation. In order to keep the pH at 7.40, we have to maintain a constant ratio of bicarbonate:dissolved carbon dioxide, as dictated by the Henderson-Hassalbach equation.
During conditions resulting in hyperventilation, the lungs get rid of more carbon dioxide and as a consequence, the blood PCO2 can become lower. Conversely, during conditions resulting in hypoventilation, the lungs are not able to get rid of carbon dioxide adequately and the blood PCO2 will rise.
There are other acids that are produced by metabolism that cannot be converted into carbon dioxide. These are called non-volatile acids and must be excreted by the kidneys. The kidneys can also excrete bicarbonate into the urine and can thus respond to a change in the blood carbon dioxide level by either eliminating or retaining bicarbonate. Unlike the lungs which can respond to increased carbon dioxide within seconds, it takes the kidneys 2-3 days to raise or lower bicarbonate levels with the result that the kidney’s full compensatory response to an acid-base disorder takes several days. However, the blood does have the ability to have a small but immediate effect on a changing carbon dioxide level by a chemical buffering mechanism. The result of this is that there are two responses to a high or a low carbon dioxide level: an acute compensation by chemical buffering and a chronic compensation from excretion of bicarbonate by the kidney. The buffering mechanism of the blood is fairly limited and can only result in a mild/limited degree of compensation compared to kidney excretion of bicarbonate.
Base deficit and base excess
In some situations, the ABG report will be resulted as “base deficit” or “base excess”. This is commonly used in the operating room by anesthesiologists. A base deficit refers to the amount that the bicarbonate level is too low and a base excess refers to the amount that the bicarbonate is too high. For practical purposes, base excess can be used synonymously with metabolic alkalosis and base deficit can be used synonymously with metabolic acidosis.
Acid-base disorders can be divided into those that make the pH go up (alkaloses) or make the pH go down (acidosis). Each of these can be dividing into respiratory disorders that affect the carbon dioxide level and metabolic disorders that affect the bicarbonate level. Thus, there are 4 main groups of acid-based disturbances:
In a respiratory acidosis, the primary problem is that the blood carbon dioxide level is too high and the kidneys compensate by retaining bicarbonate. In a respiratory alkalosis, the primary problem is that the blood carbon dioxide level is too low and the kidneys compensate by increasing bicarbonate excretion into the urine. In a metabolic acidosis, the primary problem is that the blood bicarbonate level is too low and the lungs compensate by hyperventilating to reduce the blood carbon dioxide level. In a metabolic alkalosis, the primary problem is that the blood bicarbonate level is too high and the lungs compensate by hypoventilating to increase the blood carbon dioxide level.
As noted previously, the lungs can compensate to a metabolic acidosis or alkalosis within seconds but the kidneys take 2-3 days to fully compensate for a respiratory acidosis or alkalosis. However, there is a partial compensation to a respiratory acidosis or alkalosis by the buffering chemistry within the blood that happens immediately. For this reason, metabolic acidoses and alkaloses can be divided into those that are acute (occurring in minutes to hours) that are partially compensated by buffering and those that are chronic (occurring more than 2-3 days previously) that are more fully compensated by renal bicarbonate excretion.
It is important to note that a person can have more than one acid base disturbance at the same time. For example, a person can have a condition causing a metabolic acidosis and also simultaneously have another condition causing a metabolic alkalosis. Or, a person can have both a metabolic acidosis and simultaneously have a respiratory acidosis. If there is a single acid-base disturbance, it is called a simple acid base disorder and if there are more than one acid-base disturbances, it is called a complex acid base disorder.
The next post will review the causes of acid-base disturbances and how interpretation of the arterial blood gas can be used to diagnose these disorders.
May 9, 2022