Macklin and Macklin 341 



ones. Clinically the effect is general. Airblock strikes at two vital functions, 

 circulation and respiration. More thought might well be given to the physical 

 nature of the air bubbles which do the damage. Their stnface tension derives 

 from the natuie of the connective-tissue fluid. The bubbles, as they emerge 

 from the alveoli, and press upon the terminal pulmonic vascular branches, 

 must be very tiny. Their tendency to meige is irresistible. In the mediastinum 

 they are large and conspicuous, and in the retroperitoneum may be inches 

 across. It may take some hours for any given case of airblock to develop. With 

 conditions favorable for the continuance of air leakage the air tends to move 

 on into the mediastinum. 



The air accumidates in the mediastinum and the cmious condition may 

 arise in which its pressure there is even greater than that of the atmosphere. 

 Situated thus it is in the position of a strong invading army in a vital center. 

 It is placed where it can do the greatest possible damage. All the mediastinal 

 contents are pressed upon. The filling of the ventricular, and particularly the 

 atrial, chambers would be hampered, and, in extreme cases, actually prevented. 

 The great vessels, too, would be pressed upon. Systemic venous return would 

 be slowed and even halted. Generation of pressure in the mediastinum would 

 reflect back on the lung, and the aberrant air pressure there would also rise. 

 Relief would be instantly afforded by air breaking out of the mediastinum, 

 so that, in some ways, such things as subctitaneous emphysema and retroperi- 

 toneum are favorable signs in that they indicate at least a temporary surcease 

 for the oppressed mediastinal contents. Pneumothorax is of the same order, 

 and, in addition, if on the affected side, it tends to stop the leakage. The pro- 

 gressively weakened circulation is less and less able to take care of the task 

 of absorbing the air, so that there is little or no assuagement from that quarter. 

 The importance of a serious case of pneumomediastinum can hardly be over- 

 emphasized. It constitutes a dramatic crisis. Yet until recently many physicians 

 have been blind to a realization of what was going on, and how the condition 

 might be relieved. It has, no doubt, been occurring for ages, in the dark. 



It may be that there are many relatively slight cases of PIE w^hich clear up 

 without producing serious airblock, but there are undoubtedly many cases 

 where the interstitial emphysema rapidly advances from local to general as the 

 bubbles, swarming toward the lung root, hamper the circulation in the entire 

 lung rather than in a part; then, invading the mediastinum"""^ they proceed 

 to evoke the circulatory crisis there, already described. Physicians are urged to 

 visualize the effects on the mediastinal contents when the pressure of medi- 

 astinal air rises above atmospheric pressure. Doubtless many of these cases were 

 thought by the attending physicians to be hopeless, when but a needle prick 

 would have saved their lives! Many were probably set down to a failing myo- 

 cardium. In view of the hidden nature of the malady it is not surprising that 

 there has been failure in diagnosis. Some have been mistaken for angina pec- 

 toris,"' ^' and the symptoms were presumably due to pressure upon the gieat 

 vessels, heart, or perhaps specifically upon the coronaries themselves. Here is 



