Nephrology – Acid-Base Abnormalities: By Bernard Unikowsky M.D.

The concentration of H+ in the extracellular fluid is kept constant at 40 nmol/L. Our bodies produce two types of acid Volatile acid and non-volatile acid. Volatile acid forms when carbon dioxide produced by cellular respiration combines with water and forms carbonic acid. Pulmonary alveolar ventilation eliminates carbon dioxide from our body and prevents the accumulation of roughly 15,000 millimoles of carbonic acid produced daily.

Respiratory acidosis develops when alveolar ventilation is impaired and can be caused by disorders of the lung, or a failure of ventilation from depression of the central respiratory centre or neuromuscular disease. In acute respiratory acidosis, an abrupt failure of ventilation causes the PaCO2 to be elevated with an accompanying acidemia. In chronic respiratory acidosis, the PaCO2 is elevated with a near-normal pH, secondary to renal compensation and elevated serum HCO3– levels. Acute respiratory alkalosis results from an acute increase in ventilation secondary to disorders of the lung or due to direct stimulation of the respiratory centre.

Chronic respiratory alkalosis allows for renal compensation and decreased HCO3– levels. Metabolism of proteins generates non-volatile acids which are buffered by both intracellular and extracellular buffers including HCO3–. The HCO3– used up in the daily buffering of non-volatile acid is regenerated by the kidney. Metabolic acidosis associated with an increased anion gap may be caused by the accumulation of endogenous acids such as lactic acid and ketones, the metabolism of exogenous ingestions including methanol and ethylene glycol, or the inability of the kidney to regenerate HCO3– because of renal failure.  Loss of HCO3– in diarrhea or loss of HCO3– by the kidney seen with renal tubular acidosis causes a non-anion hyperchloremic metabolic acidosis.

Metabolic acidosis stimulates ventilation, with an associated decrease in the PaCO2 and improvement in serum pH. Metabolic alkalosis is caused by loss of H+ in gastric fluid which occurs with vomiting, or the loss of H+ from the kidney seen with either primary hyperaldosteronism or secondary hyperaldosteronism associated with diuretic use.