Diagnostic approach to metabolic acidosis

The approach to the management of metabolic acidosis is based on correcting underlying pathogenic processes.

Metabolic acidosis is the consequence of bicarbonate (HCO 3-) loss or hydrogen ion (H+) gain. The normal respiratory compensation decreases carbon dioxide (CO2) tension in the arterial blood (PaCO2), such that it falls by 0.134 kPa (1 mmHg) for every 1 mmol/l decrease in HCO3- concentration. If PaCO2 is not appropriate for the HCO3- concentration, another primary respiratory acidosis or alkalosis is diagnosed. Inadequate respiratory compensation (so that PaCO2 is higher than expected) indicates respiratory acidosis, which is usually indicative of patient fatigue or interference with ventilatory drive. Because of the critical importance of respiratory compensation in the mitigation of changes to systemic pH, impairment of ventilation heralds marked worsening of acidemia, may indicate impending respiratory collapse, and requires prompt correction.

Metabolic acidoses can be classified as increased or normal anion gap ( Table 1). The anion gap ([Na+] - {[Cl-] + [HCO3-]}) should always be determined to direct appropriate management. The normal anion gap is 12 ± 2 mmol/l. However, the normal anion gap may be lower in critically ill patients because of hypoalbuminemia. The normal range of the anion gap is reduced by 3 mmol/l for every 10 g/l reduction in albumin. Other causes of a lowered normal anion gap (e.g. increased unmeasured cations with myeloma, lithium poisoning, or severe hypermagnesemia) are unusual in the critically ill ( Emmett etal 1992).

Table 1 Different forms of metabolic acidosis

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