In the previous post, the physiology of the acid-base system was discussed. This post will focus on the practical interpretation of arterial blood gases for clinical diagnosis. The arterial blood gas (ABG) is usually the quickest lab test to obtain in a critically ill patient. In the emergency department, in the ICU, in the operating room, and during cardiopulmonary resuscitation, the ABG often leads to a correct diagnosis and directs initial treatment. There are four steps in interpreting the acid-base components of an ABG:
- Determine if the primary process is an acidosis or alkalosis
- Determine if the primary process is respiratory or metabolic
- Determine if the primary process is appropriately compensated
- Check the anion gap
This post will focus on the acid-base components of the ABG and will not discuss oxygenation.
Steps 1 &2: Determine the main acid-base disorder
Although normal values for pH, PCO2, and HCO3 are in reality a range, it is much easier to assume a single normal numeric values for each when interpreting an acid-base disturbance. Therefore, assume normal values of:
- pH = 7.40
- PCO2 = 40
- HCO3 = 24
If the ABG shows a pH < 7.40, then there is an acidosis; if the PCO2 is elevated, then it is a respiratory acidosis and if the HCO3 is reduced, then it is a metabolic acidosis.
On the other hand, if the ABG shows a pH > 7.40, then there is an alkalosis; if the PCO2 is reduced, then it is a respiratory alkalosis and if the HCO3 is elevated, then it is a metabolic alkalosis. Therefore, each of the four primary acid-base disturbances can be defined as follows:
Respiratory acidoses can be divided into those that are acute (duration of minutes to hours) and those that are chronic (duration of days, weeks, or years). The patient’s clinical history will dictate whether the condition is acute or chronic. For example, a newly unconscious patient with a fentanyl ingestion 45 minutes ago will typically have an acute respiratory acidosis whereas a smoker with long-standing, stable COPD will typically have a chronic respiratory acidosis. There are six main causes of respiratory acidosis:
Respiratory alkaloses can also be divided into those that are acute and those that are chronic. Once again, the patient’s clinical history will dictate whether the condition is acute or chronic. There are eight main causes of a respiratory alkalosis:
There are two subcategories of metabolic acidosis: (1) increased anion gap metabolic acidosis and (2) normal anion gap metabolic acidosis. The anion gap can be calculated using the equation:
Anion Gap = Na – (Cl + HCO3)
The anion gap is normally composed of miscellaneous anionic molecules in the blood such as albumin and phosphate. When the anion gap is increased, then there are abnormal anions in the blood that will result in a lowering of the HCO3 level. The anion gap is often reported from the lab when ordering an electrolyte panel but for general ABG calculation purposes, a normal value of up to 12 mEq/L can be assumed (normal range = 6-12 mEq). However, when the pH is very high (> 7.50), the anion gap will increase to 15-16 by uncovering anionic sites on albumin. Therefore, a slightly elevated anion gap is normal when the pH is very high. The anion gap can be decreased in conditions such as hypoproteinemia, hypophosphatemia, and multiple myeloma (the latter due to an increase in cationic monoclonal IgG levels).
There are five common causes of an increased anion gap metabolic acidosis and two common causes of a normal anion gap metabolic acidosis:
Note that aspirin overdose can cause both a respiratory alkalosis (by direct stimulation of the brain’s respiratory drive center) and a metabolic acidosis (by accumulation of acetylsalicylic acid in the blood).
Increased anion gap metabolic acidoses can be further subdivided into those that cause an increased osmolar gap (> 10 mOsm/L) and those with a normal osmolar gap (< 10 mOsm/L). The osmolar gap is the difference between the measured and the calculated osmolality of the blood and this is normally reported out by the lab when a plasma osmolality test is ordered. The two most common causes of an increased osmolar gap are (1) methanol poisoning and (2) ethylene glycol poisoning. These are critical diagnoses to make because neither ethylene glycol nor methanol blood levels are able to measured quickly and so the arterial blood gas is usually the only way to establish an early diagnosis in order to direct life-saving treatment. All of the other causes of metabolic acidosis result in a normal osmolar gap.
There are two subcategories of metabolic alkalosis: (1) chloride responsive metabolic alkaloses and (2) chloride unresponsive metabolic alkaloses. Chloride responsiveness is defined by the urine chloride level: if the urine chloride is < 10 mEq/L, the metabolic alkalosis is chloride responsive and if the urine chloride is > 10 mEq/L, the metabolic alkalosis is chloride unresponsive. There are three common causes of a chloride responsive metabolic alkalosis. Although there are also three causes of a chloride unresponsive metabolic alkalosis listed below, the most common is corticosteroid medication.
Step 3: Determine if the main acid-base disturbance is compensated
Very frequently, there will be more than once acid-base disturbance simultaneously. For example, a patient with pneumonia can have both a respiratory acidosis (from respiratory failure) and a metabolic acidosis (from lactic acidosis due to sepsis). To determine if there is more than than one acid-base disturbance, there are compensation rules. If a patient meets the criteria for these rules, then there is a simple acid-base disturbance (i.e., only one acid-base disturbance). Many of these rules are cumbersome and involve using nomograms or complex formulas. The following are the compensation rules that I have used throughout my career that are simple, require minimal calculations, and easy to use:
- Metabolic acidosis: The last 2 digits of the pH will equal the PCO2
- Metabolic alkalosis: For every 10 mEq increase in the HCO3, there will be a 6 mm increase in the PCO2
- Respiratory acidosis:
- Acute: For every 10 mm increase in the PCO2, there will be a 1 mEq increase in the HCO3
- Chronic: For every 10 mm increase in the PCO2, there will be a 3.5 mEq increase in the HCO3
- Respiratory alkalosis:
- Acute: For every 10 mm decrease in the PCO2, there will be a 2 mEq decrease in the HCO3
- Chronic: For every 10 mm decrease in the PCO2, there will be a 5 mEq decrease in the HCO3
If the patient fails the simple acid-base disorder compensation rule, then there is more than one acid-base disturbance. The direction of change from the expected compensation in PCO2 (metabolic disorders) or HCO3 (respiratory disorders) will indicate what that second acid-base disorder is.
Although patients can rarely have three or even four different acid-base disorders occurring at the same time, most patients will only have one or have two occurring simultaneously. The table below describes the findings when there are two acid base disturbances:
Step 4: Check the anion gap
Always, always, always calculate the anion gap! If the anion gap is elevated, then there is an increased anion gap metabolic acidosis, even if the pH, PCO2, and HCO3 are all normal. The combination of a metabolic acidosis plus a metabolic alkalosis can cause the ABG to appear normal and the only clue that the patient has acid base disorders will be the increased anion gap.
The “delta-delta” rule. The Greek letter delta (Δ)is often used in medical shorthand to mean ‘change in’. In a simple, compensated increased anion gap metabolic acidosis, the Δ anion gap should always be equal to the Δ bicarbonate. In other words, the increase in the anion gap in mEq/L from normal should equal the decrease in the HCO3 in mEq/L from normal. Once again, assume that the normal anion gap is 12 mEq/L and the normal HCO3 is 24 mEq/L. If these two values for Δ are not equal, then there is a second acid-base disturbance. For example, if the anion gap is 20 mEq/L (8 mEq/L above normal), then the bicarbonate should be 16 mEq (8 mEq/L below normal). If the change in bicarbonate is larger than the change in the anion gap, then there is a concurrent metabolic acidosis. On the other hand, if the change in bicarbonate is smaller than the change in anion gap, then there is a concurrent metabolic alkalosis.
Questions containing a completely normal ABG with an increased anion gap are a favorite of those who write questions for board examinations, and with good reason. A common scenario where this occurs is the patient with diabetic ketoacidosis (causing an increased anion gap metabolic acidosis) who is vomiting (causing a chloride responsive metabolic alkalosis). In this case, the decrease in the HCO3 from the metabolic acidosis can be offset by the increase in the HCO3 from the metabolic alkalosis – the ABG can look normal but the patient will still be very sick. The Δ bicarbonate will be less than the Δ anion gap. In this situation, the increased anion gap will be the only prompt for the emergency room physician to immediately start the patient on IV fluids and insulin.
There is a wealth of information contained in those four numbers: the pH, PCO2, HCO3, and anion gap. During emergent situations, such as during a cardiopulmonary arrest, there is not time to look up ABG interpretation in a book or on-line reference. By being able to rapidly analyze the acid-base status, the clinician can use that information to direct life-saving treatments. Memorization of the differential diagnosis of each of the four primary acid-base disturbances and memorization of the compensation rules is essential to the practice of emergency medicine, anesthesia, and critical care medicine.
May 9, 2022