346 Pulmonic Interstitial Emphysema 



ticles.'^ '* The alveolar bases about the finer pulmonary blood vessels of the 

 •overinflated region were implicated. The role of the pulmonic connective 

 tissue as an air conduit to the mediastinum was clearly demonstrated. 



Conditions here are not, of course, identical with those in the human sub- 

 ject. The air pressure was sometimes much higher, for instance, than that 

 under natural conditions, and the inflow was sudden and continuous. The 

 overdistended region, however, was comparable to a region of compensatory 

 emphysema such as frequently occurs in human lungs and where leakage of 

 air into the interstitium is known to happen at times.^' 



Forcible Overinflation of Entire Fresh Limgs.—The fresh excised lungs of 

 calves were overinflated n? toto"'' by blowing air into the tightly cannulated 

 trachea until the alveoli ruptured. As the pletira became taut and the air 

 escaped into the connective tissue and opened up runways therein, a striking 

 noise of coarse crepitation was heard. Soon air began to bubble out from 

 around the stumps of the great pulmonary vessels in the lung roots. It was a 

 dramatic sight to watch it emerging thus continuously as long as it was forced 

 into the trachea, and was an unforgettable lesson in the way air invades the 

 mediastinum from the lung tissue. When the trachea was again opened, part 

 of the air escaped through it, but the lungs did not resume their original size, 

 and their enlargement was due to retained air in the interstitial tissues. In 

 the lungs of cattle the partitions between lobule groups are very obvious, and 

 these became infiltrated with air, giving a characteristic pavement appearance 

 not only to the surface but to sections of the interior cut from intrabronchially 

 fixed material. It was easy to see why a patient in whom such a condition had 

 arisen should show a chest fixed in a state of inspiration, with little tidal flow 

 of air, and also why dyspnea and cyanosis shoidd be prominent features of the 

 airblock syndrome. Splinting of the lung and clamping down upon the blood 

 vessels combine to vitiate the patient's circulatory and respiratory systems. In 

 this material a few actual ruptures in alveolar bases not only of the vascular 

 sheaths but of the interlobular septa were demonstrated in microsections. 



Analogies in Human Chest Pathology 



The lessons learned from the animal experiments go far to explain how air 

 breaks into the pulmonic connective tissue, moves toward the mediastinum, 

 and exerts its evil influence in airblock. A number of common factors underlie 

 the animal and human phenomena. The human cases may be classified broadly 

 in accordance with the two experimental subdivisions, namely, as local and 

 general overstrain of the air-container system. 



Thus there is a large group which shows the result of local overstrain aris- 

 ing as a consequence of definite pathological change. There is a limit beyond 

 which the pleural cavity may not normally be reduced in capacity, and the 

 lung has to adapt itself to this minimal volume. Hence, if any part of the lung 

 is abnormally reduced in bulk, as it is in atelectasis, then other parts have to 

 overexpand to fill up the space. This overfilling of a part with air is known 



