THE MECHANICS OF RESPIRATION 311 



capacity of the air passages. As, explained elsewhere (page 344), the pro- 

 longation of expiration required to obtain the sample of alveolar air by this 

 method gives figures that are too high even under normal conditions, 

 and it is plain that this error will be exaggerated in asthma, where the 

 expiration is greatly prolonged. An increase in the capacity of the 

 dead space must be accompanied by an increase in the respiratory vol- 

 ume if the alveoli are to be adequately ventilated. It has been thought 

 by some clinicians that the difficulty in asthma, emphysema and car- 

 diac decompensation may lie in part in an increase in the dead space. 

 Careful estimations of the dead space in these conditions, however, 

 fail to demonstrate any great variation. 



An explanation of the fact that the dead space in emphysematous 

 patients has been found to be generally large when determined by the 

 Haldane-Priestley method (see page 340), and also for some of the clin- 

 ical phenomena accompanying the condition, may be as follows: In 

 emphysema the walls of the alveoli, especially about the lateral and 

 lower borders of the lungs, have lost their elasticity and fail to expand 

 or relax properly during the respiratory cycle. As a result the air in 

 these alveoli remains relatively unchanged except when forced respira- 

 tions are made. When a sample of alveolar air is taken directly, this 

 dead air is pushed out of the distended and diseased alveoli by the 

 forced respiration required in the direct sampling of the alveolar air. 

 Since the air in these alveoli has been in contact with the blood enter- 

 ing the lungs, it has a high C0 2 content, which results, when compared 

 with the uniformly low C0 2 content found in the tidal air, in giving a 

 large figure for the dead space. Since the capacity of the dead space 

 is not increased, the blood in the normal alveoli is probably being super- 

 ventilated in order to compensate for the high C0 2 tension in the blood 

 entering the left heart from the diseased alveoli. However, the 2 

 content of the blood leaving the sound alveoli is practically normal (be- 

 cause superventilation can not cause it to take up more), and can not 

 compensate for the low 0, content in the blood coming from the dis- 

 eased alveoli, the net effect being therefore a low tension of 2 in the 

 blood leaving the heart, which accounts for the cyanosis often seen in 

 emphysema (Pearce). A somewhat similar explanation can be given 

 for the cyanosis present in pulmonary edema, if we assume that all the 

 alveoli in this condition do not share alike in the edema (Hoover). 



The Residual Air and Mid-capacity of the Lungs 



During muscular exercise the residual air of the lungs is increased, 

 and the vital capacity decreased (Bohr). This causes the lungs to as- 



