328 THE RESPIRATION 



capacity of the air passages. As explained elsewhere (page 361), 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-Friestley method (see 

 page 357), and also for some of the clinical 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 respirations 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 entering the lungs, it 

 has a high CO 2 content, which results, when compared with the uniformly low CO 9 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 

 superventilated in order to compensate for the high CO 2 tension in the blood entering 

 the left heart from the diseased alveoli. However, the O 2 content of the blood leaving 

 the sound alveoli is practically normal (because superventilation can not cause it to 

 take up more), and can not compensate for the low O 2 content in the blood coming from 

 the diseased alveoli, the net effect being therefore a low tension of O 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- 

 sume a more inflated condition between breaths or, as it has been clum- 

 sily styled, a greater mid-capacity. These changes may serve as a 

 physiological method for increasing the efficiency of alveolar ventilation 

 so as to meet the greater needs of the body. This is partly because the 

 pulmonary vessels become dilated and the bloodflow through the lungs 

 is favored, and partly because of the influence of the reserve and sup- 

 plemental airs on the tension of the arterial blood gases during the res- 

 piratory cycle. For example, if the lungs were completely depleted 

 of air during expiration, the blood leaving them at the end of this act 



