Metabolic acidosis is a commonly presenting feature and is often caused by diabetes, renal failure or poisoning. However, it can cause diagnostic difficulties, particularly in the acute situation when patients can be seriously ill and where the aetiology is not obvious. It is vital that its diagnosis is considered in the clinical context with attention given to history (especially of drugs) and physical signs.
Metabolic acidosis is characterised by a raised [H+] and a low / normal PCO2 (in contrast with respiratory acidosis where the PCO2 is high). A low derived bicarbonate or low plasma total CO2 accompanies the raised [H+].
The raised [H+] stimulates the respiratory centre and hyperventilation occurs with a consequent rise in PO2. Hyperventilation reduces PCO2 and hence some of the potential acid burden on the body and acts to compensate for the metabolic acidosis. Complete compensation does not occur (ie the [H+] remains elevated) and the extent of the compensation will be limited in patients with an underlying diminution in respiratory function.
Some confusion may occur in patients admitted with 'collapse' and in extremis. Cardio respiratory collapse will result in a mixed acidosis due to a peripheral metabolic acidosis due to poor perfusion and a respiratory acidosis due to poor ventilation resulting in a raised [H+] and raised PCO2
Anion gap = [Na+ + K+] - [Cl- + HCO3-] = usual reference range 12-20 mmol/L
Type A - tissue hypoxia
shock, haemorrhage, hypotension,
Type B - no evident tissue hypoxia
Ethanol, methanol, ethylene glycol
glucose 6 phosphatase deficiency,
fructose 1,6 diphosphatase deficiency
Plasma lactate does not always indicate lactic acidosis
Plasma lactate may be a consequence of alkalosis since there is:
increased oxygen demand due to lactate induced vasodilatation
impaired mitochondrial respiration
These factors are exacerbated by increasing oxygen debt due to:
reduced oxygen delivery due to the shift in the dissociation curve
further anaerobic lactate production