Analysis of the respiratory response to carbon dioxide inhalation in varying clinical states of hypercapnia, anoxia, and acid-base derangement.

Individuals with cor pulmonale secondary to chronic pulmonary emphysema tend to have pulmonary ventilation which is less than normal both at rest and during exercise, despite the presence of factors ordinarily making for increased ventilation such as anoxemia and acidosis (1), and despite the fact that these ventilatory levels may be appreciably less than the observed maximum breathing capacity. Moreover, the ventilatory response to increased CO2 in the inspired air may be less than normal in certain patients with pulmonary emphysema (2-5). These observations have been interpreted as indicating a disorder of the chemical regulation of respiration associated with emphysema. The present study was undertaken to define more specifically the nature of this disorder in terms of the sensitivity of the neural regulatory mechanism to the carbon dioxide-hydrogen ion stimulus, and to characterize the conditions under which such a disorder might exist. Sensitivity of the neural regulatory mechanism to CO2 and/or hydrogen ion has been evaluated quantitatively by correlation of arterial blood hydrogen ion concentration and CO2 tension with effective alveolar ventilation when changes are brought about by varying amounts of carbon dioxide in the inspired air. In the present investigation, the effects of CO2 inhalation in normal subjects have been compared