548 FKANCIS W. PEABODY AND EDNA H. TOMPKINS 



low carbon dioxid tension of the blood in cardiac cases with dyspnea and 

 the elevation of the tension upon improvement, as well as the normal 

 tension in those cases without dyspnea, They explained the normal or 

 elevated tension that they found in pulmonary cases on the basis of simul- 

 taneous occurrence of acid products due to incomplete combustion, and 

 an accumulation of carbon dioxid due to the pulmonary involvement. In 

 patients with heart disease, Peters made determinations of the carbon 

 dioxid tension of both alveolar air and blood. The ratio between the two 

 was normal in cases without dyspnea, but in those with dyspnea it was low. 

 In individual patients it approached normal as the clinical condition im- 

 proved, and fell again as they became worse. This low ratio is regarded 

 as due to a retention of carbon dioxid, with the production of a carbon 

 dioxid acidosis, which is a factor in the causation of dyspnea. In severely 

 decompensated cardiac patients the plasma readings, which were slightly 

 low, indicate an acidosis apart from that which would be implied by 

 the observations on the alveolar air. Fitzgerald found low alveolar carbon 

 dioxid in one case each of bronchitis, asthma, mitral stenosis, and con- 

 genital heart disease, while a normal tension was found in tuberculosis, 

 pleurisy and emphysema, and a high tension in one case of mitral insuf- 

 ficiency with asthma and cyanosis, and in one of pulmonary stenosis. In 

 Peabody's cases of decompensated heart disease, the alveolar carbon dioxid 

 tension was usually normal or a little decreased, but the hydrogen-ion 

 concentration of the blood, determined electrochemically, was normal. 

 Beddard and Pembrey also found the carbon dioxid of the alveolar air 

 reduced in decompensated cardiac patients. In none of these cases, 

 however, were the evidences of acidosis, as judged by the alveolar air, of 

 marked degree. On the other hand, Scott obtained a high blood and 

 Hoover a high alveolar carbon dioxid in emphysema, while Friedman and 

 Jackson found an elevated carbon dioxid content of the alveolar air in ex- 

 periments upon dogs with mechanical obstruction to the expiration. 



It is difficult to evaluate these results on the blood and alveolar air in 

 their relation to the metabolism. It is clear that moderate circulatory or 

 pulmonary lesions do not affect the oxygen content of the blood, but that 

 with severe processes, usually associated with cyanosis, the oxygen content 

 may be decreased. It is not at all certain that a moderate decrease in the 

 oxygen content of the arterial blood will affect the metabolism in the 

 tissues, but if the disease progresses actual asphyxia in all probability 

 takes place and death results. Even if, however, the oxygen content of 

 the arterial blood does not fall so low during life as to produce complete 

 asphyxia of the tissues, it is quite possible that the moderate decrease, 

 such as has been described in severe circulatory and pulmonary disease, 

 may be sufficient to alter the metabolic processes in the tissues, without 

 stopping them entirely. If this is so one may seek the evidence of it in 

 alterations of the intermediary metabolism. The normal respiratory 



