Advanced Pathophysiology

The concepts in this section will be used to further expand on Steps 3 and 4 of the diagnostic algorithm shown in Figure 28-1. Under normal circumstances the serum is in the isoelectric state. This means that the positively charged entities reported in a standard chemistry panel (cations: sodium and potassium) should be exactly balanced by the negatively charged entities (anions: chloride and bicarbonate). However, this relationship is consistently incorrect, as the measured cations are higher than the measured anions by 10 to 12 mEq/L (mmol/L). This discrepancy results from the presence of unmeasured anions (e.g., circulating proteins, phosphates, and sulfates). This apparent difference in charges, the serum anion gap, is calculated as follows:

Because the serum potassium content is relatively small and is very tightly regulated, it is generally omitted from the calculation.10

It is important to realize that the serum 1 3 concentration may be affected by the presence of unmeasured endogenous acids (lactic acid or ketoacids). Bicarbonate will attempt to buffer these acids, resulting in a 1 mEq loss of serum HCO-for each 1 mEq of acid titrated. Because the cation side of the equation is not affected by this

HCO-

transaction, the loss of serum 1 1 - -- 3 results in an increase in the calculated anion gap. Identification of an increased anion gap is very important as a limited number of clinical scenarios lead to this unique acid-base disorder. A mnemonic to recall the differential diagnosis for an anion gap acidosis is shown in Table 28-3. The concept of the increased anion gap will be applied later in Patient Encounters 6 through 10.

Step 3 in Figure 28-1 suggests that any time an ABG is analyzed it is wise to concurrently inspect the serum chemistry values and to calculate the anion gap. The body does not generate an anion gap to compensate for a primary disorder. As such, if the calculated anion gap exceeds 12 mEq/L (mmol/L) there is a primary metabolic

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