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Metabolic acid–base disorders are caused by an increase in H⁺ production or a loss of H⁺ triggering compensatory mechanisms that result in the loss or gain of HCO₃⁻. Direct loss or gain of HCO₃⁻ will also cause metabolic acid-base disorders. Primary metabolic acid–base disorders are recognized by inspecting the bicarbonate concentration (Fig 21.1). Respiratory compensation takes place quickly so patients with metabolic acid–base disorders will usually show some change in blood PCO₂ because of hyperventilation or hypoventilation (Fig 21.2).

Metabolic acidosis

In a metabolic acidosis the primary problem is a reduction in the bicarbonate concentration of the extracellular fluid. The main causes of a metabolic acidosis are shown in Figure 21.3. These are:

Fig 21.3 Reasons for metabolic acidosis and alkalosis.

 increased production of hydrogen ions

 ingestion of hydrogen ions, or of drugs that are metabolized to acids

 impaired excretion of hydrogen ions by the kidneys

 loss of bicarbonate from the gastrointestinal tract or in the urine.

The anion gap

The cause of a metabolic acidosis will nearly always be apparent from the clinical history of the patient, but occasionally knowledge of the anion gap may be helpful. This can be assessed by looking at the serum electrolyte results and calculating the difference between the sum of the two main cations, sodium and potassium, and the sum of the two main anions, chloride and bicarbonate. There is no real gap, of course, as plasma proteins are negatively charged at normal [H⁺]. These negatively charged amino acid side chains on the proteins account for most of the apparent discrepancy when the measured electrolytes are compared. The anion gap is thus a biochemical tool that is sometimes of help in assessing acid–base problems. It is not a physiological reality.

In practice, because the potassium concentration is so small and will vary by so little, it is generally excluded when calculating the anion gap. Thus:

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