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Renal compensation of respiratory acidosis and alkalosis

Прочитайте:
  1. ACUTE RESPIRATORY DISTRESS-SYNDROME
  2. BREATHING AND THE RESPIRATORY SYSTEM
  3. Classification of acute respiratory failure
  4. CLINICAL PICTURE OF ACUTE RENAL FAILURE
  5. Devices for respiratory tracts
  6. ETIOLOGY, PATHOGENESIS AND CLASSIFICATION OF ACUTE RENAL FAILURE
  7. External nose. Nasal cavity (olfactory and respiratory regions). Paranasal sinuses.
  8. Metabolic alkalosis
  9. Preparations for acidosis correction

It is established that the degree of reabsorption of HC03~ by the cells of renal tubules is directly proportional to PC02 of blood. This reaction does not depend on blood pH. Mechanism of this process is associated with elevation of blood PC02 and increase of PC02 in tissues.

A process of hydration of carbon dioxide inside the cells of renal tubules increases, and the inflow of H+-ions into tubular urine intensifies in exchange for Na+-ions. Here, Na+ binds with HC03" and leaves for blood.

A) Compensation of respiratory alkalosis:

The essence of respiratory alkalosis lies in the decrease of PC02 and concentration of HCCyions in blood. A decrease of blood PC02 leads to inhibition of C02 hydrogenation in the cells of renal tubules and to a decrease of bicarbonate reabsorption from the urine. A lot of bicarbonate remains in the urine and it acquires an alkaline reaction. The concentration of bicarbonate in plasma drops.

B) Compensation of respiratory acidosis:

The process of development of respiratory acidosis is associated with elevation of PC02 and increase of the number of HC03"ions in blood. Carbon dioxide, entering inside the cells, is hydrogenized:

H+ ions are released into tubular urine in exchange for Na+ that is being bound inside the cells with HC03~ and enters the blood. Retention of bicarbonate in blood leads to chlorine substitution that is excreted with urine.


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