Evaluating Acid-Base Disorders

pH of the human blood is very tightly controlled, usually between 7.38-7.42. Two major organs help regulate the pH: the lung and the kidney. The lung does so by controlling the CO2, which as some soda drinkers would know, is involved in the following equilibrium:

CO2 + H2O = H2CO3 = H+ + HCO3-

The kidney is the site of major filtration of the blood, and the kidney can secrete and reabsorb H+ as well as HCO3- into the urine, thereby having an effect on acid-base balance.

In evaluating an acid-base disorder, the first step is to look at the blood pH, which will tell you if the patient has acidemia (acidic blood) or alkalemia (alkaline blood).

The second step is to classify the the process into either respiratory (originating from the lung, e.g. change in CO2 intake) or metabolic (originating from other metabolic processes). To classify, look at the pCO2 and HCO3- in the blood. Example: respiratory acidosis can result from hypoventilation (e.g. lung disease or chronic obstructive pulmonary disease [COPD]), leading to an increase in pCO2 as CO2 exchange is not happening quickly enough. The equilibrium is shifted to the right, producing more H+ (strong acid) and HCO3- (weak base), thus lowering the pH. Because HCO3- is also generated, HCO3- levels in the blood may be higher than normal. In contrast, metabolic acidosis results from some process (many causes are possible) that increase H+ and/or decrease HCO3-, thus acidifying the blood. Measured HCO3- is lower than normal, and pCO2 can be low as the lung tries to compensate for the acidemia by hyperventilating.

The third step is to further classify metabolic acidosis into anion gap metabolic acidosis or non-anion gap metabolic acidosis. Anion gap is defined as Na-(Cl+HCO3-). These are the major clinically-measured cation (Na) and anions (Cl and HCO3) in the blood. In certain metabolic processes (e.g. lactic acidosis, diabetic ketoacidosis), large amounts of anions (lactic acid, ketoacids) are generated. The presence of these acids (H+A-) leads to acidic blood, which HCO3- buffers by combining with H+. In effect then, HCO3- levels are decreased and are replaced by A-. This results in an increase in anion gap. The reason for classifying metabolic acidosis into anion gap and non-anion gap subclasses is to aid in differential diagnosis. Anion gap metabolic acidoses usually result from processes that generate anions, while non-anion gap metabolic acidoses may be a result of abnormal secretion or reabsorption of H+ and HCO3- by the kidney.

This is actually a simplification of the evaluation process, as many patients will have mixed acid-base disorders (e.g. respiratory alkalosis on top of metabolic acidosis), and 2 more steps can be undertaken to evaluate mixed acid-based disorders, but it is beyond the scope of this blog.

Presented here is only a flowchart of how to approach acid-base disorders. The job does not end at arriving at a classification of the disorder. The classification only aids the clinician in narrowing down the list of possible diagnoses. More needs to be done to pinpoint the pathological process that is leading to the acid-base abnormality, and arrive at an appropriate treatment.