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Acid-base homeostasis exists when the following balances are maintained:

1. (H+ addition or production) - (HCO3- addition or production) = (H+ excretion) - (HCO3-excretion) ~ 60 mmol/day (diet-dependent).

2. (CO2 production) = (CO2 excretion) ~ 15 000-20 000 mmol/day.

H+ production (HCl, H2SO4, lactic acid, H3PO4, etc.) and adequate renal H+ excretion (^ p. 174ff.) are the main factors that influence the first balance. A vegetarian diet can lead to a considerable addition of HCO3- (metabolism: OH- + CO2 ^ HCO3-; ^ p. 138). HCO3- is excreted in the urine to compensate for the added supply (the urine of vegetarians therefore tends to be alkaline).

Acid-base disturbances. Alkalosis occurs when the pH of the blood rises above the normal range (see table), and acidosis occurs when it falls below the lower limits of normal. Respiratory acid-base disturbances occur due to primary changes in PCO2 (^ p. 144), whereas non-respiratory (metabolic) disturbances occur due to a primary change in [HCO3-]. Acid-base disturbances can be partially or almost completely compensated.

Nonrespiratory (Metabolic) Acid-Base Disturbances

Nonrespiratory acidosis is most commonly caused by (1) renal failure or isolated renal tubular H+ secretion defect resulting in inability to eliminate normal quantities of H+ ions (renal acidosis); (2) hyperkalemia (^ p. 180); (3) increased p-hydroxybutyric acid and ace-toacetic acid production (diabetes mellitus, starvation); (4) increased anaerobic conversion of glucose to lactic acid (^ lactate- + H+), e.g., due to strenuous physical work (^ p. 74) or hypoxia; (5) increased metabolic production of HCl and H2SO4 in individuals with a high intake of dietary proteins; and (6) loss of HCO3-through renal excretion (proximal renal tubular acidosis, use of carbonic anhydrase inhibitors) or diarrhea.

Buffering (^ A1) of excess hydrogen ions occurs in the first stage of non-respiratory acidosis (every HCO3- lost results in an H+ gained). Two-thirds and one-third of the buffering is achieved by HCO3- and non-bicarbonate buffer bases (NBB ), respectively, and the CO2 arising from HCO3- buffering is eliminated from the body by the lungs (open system; ^ p. 140). The standard bicarbonate concentration [HCO3 ]St, the actual bicarbonate concentration [HCO3-]Act and the buffer base concentration [BB] decrease (negative base excess; ^ p. 146).

Respiratory compensation of nonrespiratory acidosis (^ A2) occurs in the second stage. The total ventilation rises in response to the reduced pH levels (via central chemosen-sors), leading to a decrease in the alveolar and arterial PCO2 (hyperventilation; ^ A2a). This notonly helps to return the [HCO3-]/[CO2] ratio towards normal (20:1), but also converts NBB-H back to NBB- (due to the increasing pH) (^ A2b).The latter process also requires HCO3-and, thus, further compensatory pulmonary elimination of CO2 (^ A2c). If the cause of aci-dosis persists, respiratory compensation will eventually become insufficient, and increased renal excretion of H+ ions will occur (^ p. 174ff.), provided that the acidosis is not of renal origin (see above, cause 1).

Nonrespiratory (metabolic) alkalosis is caused by (1) the administration of bases (e.g., HCO3- infusion); (2) increased breakdown of r- A. Metabolic acidosis

Bicarbonate buffer y v

Non-bicarbonate buffer (NBB)

r- A. Metabolic acidosis

Bicarbonate buffer y v

Non-bicarbonate buffer (NBB)

Renal Respiratory And Blood Buffers

Stimulation of chemosensors

Non-respiratory (metabolic) acidosis: pH \

Stimulation of chemosensors

Increased pulmonary ço elimination of CO2 2 /

Total ventilation increases

2 Respiratory compensation

Increased pulmonary ço elimination of CO2 2 /

2 Respiratory compensation

Respiratory compensation i—HT]

of acidosis is achieved: p

But: [HCO3 ]act und Pco2 are decreased

Respiratory compensation i—HT]

of acidosis is achieved: p

But: [HCO3 ]act und Pco2 are decreased

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