344 Pulmonic Interstitial Emphysema 



tected against air invasion, the alveolar bases being competent to hold the air 

 in the alveoli against not only the normal hyperatmospheric pressures of ex- 

 piration, but the still higher ones of coughing, straining, forcible expiration, 

 etc. But we have seen that when these bases are ruptured the tendency is for 

 air to continue to leak into the interstitial tissue and for pressure to rise in the 

 accumidated air pools. Once in the interstitial tissue the air apparently cannot 

 go back into the alveoli. There is a sort of valve action here, and bubbles move 

 toward the mediastinum in natural course. The augmented pressure head in 

 the alveoli during covighing, straining, etc., is carried over into the bubbles 

 and, in part, held therein. The effect is cumulative. It extends along the train 

 of bubbles into the mediastinum. The potential raised in the elastic tissue of 

 the broncho-vascular rays and other parts of the lung in inspiration, particu- 

 larly when forced, is expended in the expiratory phase to pack the bubbles 

 and move them onward, as we have seen in the discussion of the mechanism 

 of transpulmonic air-bubble movement. It seems that air can in this way get 

 into the mediastinum more easily than it can break out. It is thus compressed 

 by the recoil of the chest, particularly after the inspiratory movements are 

 forced, as in dyspnea. We have here something analogous to the intake and 

 compression strokes of the internal combustion engine. The greater the air- 

 block the greater the dyspnea; and the severer the dyspnea becomes, the more 

 likely is the tension in the mediastinum to increase. It is to be noted that, as 

 with tension pneumothorax, aberrant air can enter the mediastinum only 

 during the expiratory phase, once the pressure in it has reached that of the 

 atmosphere, for only at that period is a pressure in excess of atmospheric gen- 

 erated in the lung; and not (as most authors erroneously state for tension 

 pneumothorax) during inspiration. Therefore, when a patient, in whom 

 atelectasis may be present, is making or has just made forced expiratory efforts 

 of any kind, as in coughing, the clinician should be alive to the ever-present 

 menace of PIE and particularly of its sequel— air in the mediastinum under 

 pressure— which will certainly establish an airblock. If the leakage continues 

 imder such conditions, ruptiue from the mediastinum into the pleural cavity 

 is likely to set up a tension pneumothorax. 



Animal Experiments 



The interpretation of PIE and its sequels just given has a broad foundation of 

 data from animal experiments. Without the information gained from these 

 we should not understand how air breaks out from the lungs; is moved in a 

 definite way to distant points, and exerts its pernicious, even lethal, effects; 

 nor should we be able to visualize the tissue mechanics of inspiratory swelling 

 of the pulmonic blood vessels. Functional anatomy and, through it, pathology 

 and clinical medicine are incalculably indebted to the experimental method. 

 Through it the connective tissue of the lung is seen in a new light. As has so 

 often happened in research work, the experiments were started with quite 

 another objective— information on the nature of the pulmonic alveolar walls— 



