PH 61log [ HCOif10030lftOj

It is obvious from this equation that any decrease in PaCO2, as observed in primary respiratory alkalosis, leads to a reduction in [H +] and a consequent increase in pH, but that a subsequent lowering of [HCO3-] will minimize the degree of alkalemia. The latter effect occurs in vivo by two different mechanisms which take place in two consecutive steps characterized by different time constants.

First, there is a rapid buffering whose maximum effect is attained after 10 min; [H +] leaves the intracellular compartment and combines with [HCO3-] in the extracellular fluid. Intracellular buffers (proteins, hemoglobin, etc.) are the main sources of [H +] which leave the cells and enter the extracellular fluid. This can be described by the following equations for the intracellular fluid (ICF) and the extracellular fluid (ECF) respectively:

H-bufTcrs^cK H+-I-buffers^ ' (H* +1 ICOj fa? - Ï LCD, GO* + ] [p.

In addition, there may be intracellular lactic acid production due to alkalemia, which may also represent a source of H + ions aimed at buffering extracellular HCO3-. However, this last finding is not consistent and is controversial, and lactic acid production does not seem to play a significant role here even though acute respiratory alkalosis decreases lactate clearance by the liver in humans. Pragmatically, whatever the mechanism(s) causing some degree of hyperlactatemia in hyperventilation, plasma lactate is only moderately increased in this setting, i.e. its value is rarely higher than 3 to 4 mmol/l. Finally, the level of plasma chloride ions increases in acute respiratory alkalosis as a result of the chloride shift mechanism, in which ions are transferred across the red blood cell membrane (plasma chloride levels increase whereas plasma bicarbonate levels decrease) and all the ionic concentrations equilibrate at this new steady state in the extracellular fluid compartment. This causes a small decrease in [HCO3-]. The following rule of thumb can be used by intensive care clinicians: for each decrease of 10 mmHg (about 1.3 kPa) in PaCO2, [HCO3-] in the blood decreases by about 2 mmol/l. This buffering effect, although rapid, is not very efficient; it is only observed in acute respiratory alkalosis and is poorly suited to correcting alkalemia.

Secondly, if hyperventilation persists, plasma [HCO 3-] decreases further due to renal compensation of the acid-base disorder. This mechanism begins to operate after 2 h of persistent hypocapnia and its maximum effect is attained after 2 to 3 days. Urinary [HCO3-] losses increase and simultaneously ammonium excretion in urine decreases, probably because of a signal mediated by the intracellular increase in [H +] being sent to the tubular cells. Both the proximal and the distal nephrons are affected by changes in peritubular and intracellular PCO2. For instance, bicarbonate recuperation in the proximal nephron dramatically decreases when peritubular

PCO2 is reduced in animal preparations. In addition, ammoniagenesis is inhibited by acute alkaline conditions in animals, although the exact sites of inhibition (proximal and/or distal tubules) and the ultimate regulation are incompletely understood at present. Taken together, these mechanisms promote a decrease in the daily [H+] elimination and the extrapolation to humans seems to be valid.

Finally, the combined buffering processes lead to an average decrease of about 5 mmol/l of [HCO 3-] for each reduction of 10 mmHg (1.3 kPa) in PCO2 due to hyperventilation. This is another rule of thumb that may be useful for the clinician. Therefore, in chronic respiratory alkalosis, this combined buffering is more efficient for correcting the pH disturbance and reducing the magnitude of alkalemia. The occurrence of a mixed and more complicated acid-base disorder should be suspected when the observed reduction in plasma [HCO3-] is not consistent with the change in PCO2.

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