The use of artificial respiration in pulmonary emphysema accompanied by high carbon dioxide levels.

Abstract

A syndrome resembling carbon dioxide narcosis, which may be precipitated by the administration of oxygen to patients with advanced emphysema, has attracted increasing attention in recent years, although few reports on this subject have appeared in the literature (1-7). A similar response to oxygen has been described by Marshall and Rosenfeld (8) in experimental animals anesthetized with barbiturates or morphine. Marshall and Rosenfeld's analysis provides a basis for understanding the phenomenon in man; in the presence of an increased level of carbon dioxide in the alveolar air and arterial blood, the respiratory center becomes adjusted to the high carbon dioxide pressure, so that carbon dioxide no longer dominates the chemical control of respiration. Such a loss of sensitivity to carbon dioxide in patients with advanced emphysema was demonstrated in 1920 by Scott (9). In the presence of high levels of carbon dioxide and diminished responsiveness of the respiratory center, the principal stimulus to breathing arises from the effects of hypoxia on the carotid body and aortic chemoreceptors. When the stimulus is removed by relief of the hypoxia through oxygen administration, the driving mechanism is weakened or absent, and pulmonary ventilation falls.