The accurate interpretation of arterial blood gases is crucial in critically ill patients. Clinicians, respiratory therapists, and nurses should be equipped with the appropriate knowledge for making the correct clinical decisions when interpreting blood gases. In this article, we describe 5 easy steps that guide the health care provider in making an accurate interpretation and diagnosis of different acid-base disorders. The attached infographic is available for download here.
The first step in the interpretation of blood gases is to determine if the arterial blood gases are valid. This is done by assessing the internal consistency of the values using the Henderseon-Hasselbach equation:
[H+] = 24 x (PCO2 / [HCO3 -]
There are different methods to interconvert pH to [H+], such as the "0.1 pH Change Rule" or the "Drop the 7 and Decimal Point Rule". However, our preferred method is to get the value of 10 to the power of (9-pH), which estimates the concentration of H+ in the blood. Once it is decided that the pH is valid, the next move is to determine whether we are dealing with acidemia (if pH is less than 7.35) or alkalemia (if pH is more than 7.45).
The second step is to determine the primary disorder by examining the relationship between the change in pH and the change of PaCO2. In respiratory acidosis, the pH decreases and the PaCO2 increases, whereas in respiratory alkalosis, the pH will be elevated and the PaCO2 will be decreased. In metabolic acidosis, the pH is decreased as well as the PaCO2. Whereas, in metabolic alkalosis, the pH is elevated along with PaCO2. In other words, in primary respiratory disorders, the pH and PaCO2 levels change in opposite directions; however, in metabolic disorders, the pH and PaCO2 change in the same direction.
The third step is to determine whether there is an appropriate compensation or not. If we are dealing with respiratory disturbance, it is critical to determine whether it is acute (within 3-5 days) or chronic, as the kidney compensation takes time before it reaches full compensation. The table in the infographic details the expected pH and HCO3 for each 10 mm Hg increase (respiratory acidosis) or decrease (respiratory alkalosis), and whether it is acute or chronic. In metabolic acidosis, the respiratory compensation is instantaneous and the expected PCO2 can be calculated from Winter's formula. Any variation in the actual PCO2 or HCO3 from the expected values indicates a combined abnormality.
The fourth step is to determine whether there is an added acid or not. This step is essential, even if the initial abnormality does not indicate metabolic acidosis as there may be a mixed disorder. The increased anion gap (AG) from the normal value (12 mEq/L) indicates the amount of added acid to the serum in mEq/L. When calculating the AG (Na -[Cl+HCO2]), it is necessary to account for any decrease in the albumin value, as every 1 mg/dL drop in albumin causes a 2.5 mEq/L decrease in the AG. A high AG indicates the presence of an acid such as lactic acid or ketones. The acronym (MUDPILES) is used for the differential diagnosis of different acids that may account for the increased AG (detailed in the infographic). It is important to note that the concentration of the added acid should equal the difference of the AG (∆ AG) from its normal value. Any other acids must be searched for in the serum until the AG (±2) is filled. If the ∆ AG was 12 and the concentration of lactic acid was only 5 mmol/L, search for another acid at a concentration of 7 mmol/L–ketones, for example. On the other hand, a normal AG indicates bicarbonate loss through the kidneys or the gastrointestinal tract or a dilution of bicarbonate due to excessive normal saline resuscitation.
The fifth step is to compare the change in AG (∆ AG) to the change of bicarbonate from its normal value (∆ HCO3). Normally, for each 1 mEq/L of added acid, the bicarbonate will decrease by 1 mEg/L. If there is a concomitant non AG metabolic acidosis, the decrease in bicarbonate will be greater. On the other hand, if there is a concomitant metabolic alkalosis, the decrease in bicarbonate will be less than the change in AG.
REFERENCES
Rose, B.D. and T.W. Post. Clinical physiology of acid-base and electrolyte disorders, 5th ed. New York: McGraw Hill Medical Publishing Division, c2001.
Fidkowski, C And J. Helstrom. Diagnosing metabolic acidosis in the critically ill: bridging the anion gap, Stewart and base excess methods. Can J Anesth 2009;56:247-256.
Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—first of two parts. N Engl J Med 1998;338:26-34.
Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—second of two parts. N Engl J Med 1998;338:107-111.
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