Acid Base balance disturbances

The pH of the ECF is determined by the rate of conju­gate base to their weak acids. The total amount of buffer base in whole blood including HCO₃, Hb and other bases of lesser importance is called buffer base (B.B). These bases are known as metabolic components determining blood pH. Acid base disturbance involves either the gain or loss of strong acid or the gain or loss of base (Cl^– or HCO₃^–) by the ECF.

Metabolic acidosis

• The gain of strong acid or loss of base from the ECF is known as metabolic acidosis. Acidemia will be present in metabolic acidosis. It occurs in:
  • Ketosis.
  • Diabetes mellitus in which ß hydroxy butyric acid, acetone, aecto acetic acid are produced.
  • Renal acidosis in which there is failure of HCO₃^– reabsorption and loss in the urine.
  • Diarrhoea where pancreatic juice containing HCO₃ is not reabsorbed and is lost.
• In all these cases, HCO₃^– falls either as a result of a reaction with acid or due to direct loss from ECF and pH falls. This results in fall of all blood buffer bases. Usually there is no change in plasma PCO₂  . However, a fall in pH results in increased alveolar ventilation and therefore a fall in PCO₂. Decreased PCO₂ will bring the ratio of conju­gate base to weak acid back to normal. However, the total bases will be less than normal and this requires renal correction – the excretion of H⁺ and restoration of plasma HCO3^–.
• The acidemia stimulates secretion of H⁺ ion by the renal tubule. This ensures reabsorption of all HCO₃ ions from tubular fluid and the excess H⁺ ions will begin to acidify the urine. For each H⁺ ion secreted, one HCO₃ will be reabsorbed into the  plasma. This holds good for short-term stress and in severe conditions, therapeutic action is required.

Metabolic alkalosis

• This process involves the gain of base (OH or HCO₃ ions) or loss of strong acid by ECF.
• Metabolic alkalosis is present in
  • Persistent vomiting, in which gastric acid is lost from the body.
  • K⁺ deficiency in which renal tubules secretes large amount of H⁺ ions into urine.
  • Injection of HCO₃ solutions.
• In all these cases, there is an increase in HCO3^– in ECF, resulting in increased base content. The response of the body is opposite to the one observed in metabolic acidosis.  Alkalemia results in rise in pH which will depress pulmonary ventilation and PCO₂ will rise. This respiratory compensation thus will bring pH back to normal. Renal correction consists of decreased secretion of pH ions and so increased excretion of HCO₃^– ions.

Respiratory acidosis

• If excretion of CO₂ by the lungs falls below the rate of CO₂ production in the body, respiratory acidosis develops.
• There will be an increase in blood PCO₂ (hypercapnia) and the primary defect will be in the inability of lungs to expire CO₂ at a normal rate. This may be due to
  • Depression of respiratory centres in CNS.
  • Abnormality of chest wall or respiratory muscles which prevents enlargement of thorax.
  • Obstruction to gas movement in lungs.
• A rise in PCO₂ causes increase in H₂CO₃ and buffer reaction prevents the fall of pH caused by rise in H₂CO₃.
• Renal compensation then follows. Low pH stimulates secretion of H⁺ into urine with a rise in plasma HCO3^– .

Respiratory alkalosis

• When alveolar hyperventilation occurs, the expiration of CO₂ may exceed the rate of its production within the body and respiratory alkalosis develops.
• There will be low plasma PCO₂ (hypocapnia) and alkalemia.
• Hyperventilation is caused by abnormal stimulus to respiratory centres either directly as in NH₃ toxicity or through hypoxemia acting through peripheral chemoreceptors.
• Buffer reaction follows:

HHb + HCO_3^– → HB^– + H₂CO₃ → CO₂

• Thus HCO₃ falls and Hb rises. The renal compensation begins,  alkalemia depresses H⁺ ion secretion by renal tubules and excretion of filtered HCO₃ rises. This results in further fall of plasma HCO₃ and the ratio of HCO₃ to H₂CO₃ moves back to normal.