IN the normal subject, an increment in the partial pressure of carbon dioxide (Pco2) in arterial blood of only a few millimeters of mercury suffices to double or even triple minute and alveolar ventilation. However, analysis of this relation in terms of a simple stimulus-response pattern is complicated by several factors: changes in blood pH accompany the changes in blood Pco2; intracellular buffers are interposed between the arterial blood and the respiratory center; and the magnitude of the ventilatory response seems to be conditioned, in some obscure way, by factors such as the level of total-body . . .
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Richter et al. (1957) studied this question.