Tutorial to help answer this question

A slowing of the respiration rate compensates for chronic metabolic alkalosis by allowing blood CO₂ to rise. By mass action, this increase in CO₂ triggers an increase in the H₂CO₃ intermediate, which, in turn, dissociates to bicarbonate and H⁺, thus lowering pH.

As one would expect, pH is near normal in compensated cases of metabolic alkalosis. The causal defect for metabolic alkalosis, increase in [HCO₃^-], remains, and pCO₂ is elevated as compensation.

	respiratory					metabolic
	acidosis		alkalosis			acidosis		alkalosis
	U	C	U	C		U	C	U	C
pH
HCO3-:CO2 ratio
[HCO3-]
pCO2
total CO2

= increased = decreased = no major change

U = uncompensated C = compensated = Red arrows indicate the primary defect. = Green arrows indicate compensation mechanisms.

As seen in the table above, metabolic alkalosis always shows a rise in blood pH which is accompanied by a corresponding rise in blood HCO₃^-. Since compensation may or may not occur (but usually does), the pH itself is not the "primary" cue to a metabolic alkalosis, rather the elevated HCO₃^- is a better indication of what is going on.

To explain why this is so, one must consider two consequences of alkalosis:

1. In the simplest case, ingestion of alkali will instantaneously change pH by consuming H⁺. The same thing can be accomplished, however, by removal of acid from the body, such as might occur during prolonged vomiting.
2. A drop in [H⁺] will pull the bicarbonate equation to the right, thus raising [HCO₃^-]:

CO2

+

H2O

[H2CO3]

H+

+

HCO3-

The main compensatory response to this is respiratory (indicated by a green arrow in the table), and is perhaps is a bit confusing in that the body tries to further push the reaction to the right (in the same direction it is being pulled already by the loss of H⁺!). However, recall that what the body is trying to do here is correct pH, so by pushing the reaction further to the right by retaining CO₂ in the lungs, the [H⁺] is raised, hence lowering pH back toward the normal range.