Role of respiratory system in Acid–base balance

Blood PCO₂ can be varied extensively because the partial pressure of CO₂ in alveoli determines the amount of CO₂ dissolved in blood.

The respiratory mechanism depends upon the sensitivity of respiratory control systems to change in blood PCO₂ and pH.

A small increase in PCO₂ or decrease in pH stimulates pulmonary ventilation, so that CO₂ expiration increases.

If an acid is added to body fluids, chemical buffering results in formation of additional H₂CO₃ and leading to a depletion of HCO₃

H⁺ + HCO₃^– → H₂CO₃ → CO₂ + H₂O

When the production of CO₂ is increased or pulmonary hypoventilation occurs, it leads to the accumulation of CO₂ in blood Therefore, the pH falls slightly.

However, the increase in CO₂ and decrease in pH stimulate respiration, causing a rapid expiration of extra CO₂. Then blood PCO₂ decreases and pH returns to normal.

When an alkali is added to blood or pulmonary hyperventilation occurs, this causes a decrease in H₂CO₃ {CO₂} level in blood. The respiratory system is inhibited and additional CO₂ is retained in ECF. These increase PCO₂ to balance the increased HCO₃ resulted from added alkali.

Metabolic acidosis

In metabolic acidosis, (ketosis, diabetes mellitus, renal acidosis and diarrhoea) blood 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 the blood buffer bases.

Usually no change in plasma PCO₂ because of buffer action can be detected. However, a fall in pH results in increased alveolar ventilation and 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 academia stimulates secretion of H⁺ ion by the renal tubule. This ensures reabsorption of all HCO₃ from tubular fluid and the excess H⁺ will begin to acidify the urine. For each H⁺ ion secreted one HCO₃ will be reabsorbed in to plasma.

Metabolic alkalosis

Metabolic alkalosis, (vomiting, K⁺ deficiency) involves the gain of base (OH^– or HCO₃^–) or loss of strong acid by ECF. In these conditions, 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 HCO₂.

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 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
  1. Depression of respiratory centres in CNS.
  2. Abnormality of chest wall or respiratory muscles, which prevents enlargement of thorax.
  3. Obstruction to gas movement in lungs

A rise in PCO₂ cause 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 occur 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 + HCO₃ →Hb^– + H₂CO₃ → CO₂ + H₂O

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