Acid Base regulation

7.35 to 7.45

Potential of hydrogen

12-20 mEq/L

8-16 mEq/L

Maintains normal enzyme function, protein structure and cellular processes.

Around 2-3

Around 7

Around 8-9

Decreased heart contractility; altered neurological function; potassium shifts between cells and blood, potentially causing hyperkalaemia or hypokalaemia depending on the disturbance.

Effects on bone and stone formation; associated with progression of kidney disease.

Lungs

Kidneys

Aerobic respiration; Anaerobic respiration; Sulfuric acid production from sulfur-containing proteins; Acid production from ketone bodies; Phosphoric acid production from phosphate-containing compounds.

A weak acid and its conjugate base, or a weak base and its conjugate acid, that resist changes in pH when small amounts of acid or alkali are added.

Volatile acid is excreted as CO2 via the lungs, while non-volatile acids are excreted by the kidneys.

Strong acids and alkalis completely dissociate in solution whereas weak acids and alkalis partially dissociate in solution.

Bicarbonate buffer system; Haemoglobin buffer system; Protein and amino acid buffer systems; Phosphate buffer system.

An increase in bicarbonate relative to CO2 increases pH, while a decrease lowers pH.

The lungs remove volatile acid as CO2. Increased ventilation removes more CO2 and raises pH, while decreased ventilation retains CO2 and lowers pH.

Reabsorbs filtered bicarbonate; generates new bicarbonate; increases hydrogen ion secretion and excretion in urine, mainly buffered by phosphate and ammonia.

Predominantly in the proximal tubule.

Mainly in the proximal tubule and distal nephron, particularly the collecting ducts.

Hypoventilation causing CO2 retention

Hyperventilation causing excessive CO2 loss

Diarrhoea; Renal failure; Lactic acidosis; Ketoacidosis; Renal tubular acidosis; Certain toxins.

Metabolic acidosis due to accumulation of unmeasured anions, such as in renal failure, lactic acidosis, ketoacidosis or poisoning.

Metabolic acidosis commonly caused by bicarbonate loss or impaired renal acid excretion, such as in diarrhoea or renal tubular acidosis.

Vomiting; Nasogastric suction; Diuretic use; Excess mineralocorticoid activity; Alkali intake in susceptible individuals.

The difference between measured cations and measured anions, used to estimate the concentration of unmeasured ions in the blood.

Sodium and potassium ions.

Chloride and bicarbonate.

There is an increased concentration of unmeasured anions, which may indicate lactic acidosis, ketoacidosis, renal failure or poisoning.

Some patients with advanced COPD develop chronic CO2 retention and may have a reduced ventilatory response to CO2. Hypoxaemia can contribute to their respiratory drive. Excess oxygen can worsen hypercapnia through changes in ventilation-perfusion matching and the Haldane effect, as well as reduced ventilation in some patients. Oxygen should be carefully titrated, usually to a target saturation of 88–92% in patients at risk of hypercapnic respiratory failure, with blood gases monitored as indicated.