Metabolic acidosis is indicated by a decrease in the plasma bicarbonate level and/or a marked increase in the serum anion gap (AG). Arterial pH <7.35 defines acidosis. The presence of metabolic acidosis is a clue to the possible existence of several underlying medical conditions.
Metabolic acidosis may occur due to:
- Addition of strong acid that is buffered by and consumes bicarbonate ion
- Loss of bicarbonate ion from the body fluids, usually through the GI tract or kidneys
- Rapid addition to the extracellular fluid of a nonbicarbonate solution.
Calculating serum AG helps to differentiate the cause. Serum AG is calculated by subtracting the sum of major measured anions, chloride (Cl¯) and bicarbonate (HCO₃¯), from the major measured cation, sodium (Na⁺).
- AG = Na⁺ - (Cl¯ + HCO₃¯)
Normal serum AG is due to the difference between unmeasured anions such as sulfate (SO₄²¯), phosphate (PO₄¯), albumin, and organic anions, and unmeasured cations such as potassium (K⁺), magnesium (Mg⁺), and calcium (Ca²⁺). Plasma proteins also play a role in maintaining normal serum AG.[1]
Acute metabolic acidosis, lasting minutes to several days, is relatively common among critically ill patients with reported incidence varying from 6% for more severe acidosis (plasma pH <7.20) to up to 64%.[1] [2] [3] [4] In one multicenter, retrospective study, 14% of intensive care unit (ICU) patients had metabolic acidosis (median incidence at a study ICU 172.5 patients per year), suggesting identification and management is a relevant issue in the critically ill.[5]
