RESPIRATION 149 



acute anoxaemia due to imperfect oxygenation of the arterial 

 blood. There were the ordinary chlorine symptoms of acute bron- 

 chitis, alveolar inflammation, and oedema of the lungs. The faces 

 of the patients were deeply cyanosed, in spite of considerably in- 

 creased breathing of adequate depth. At first it was suspected that 

 the cyanosis was due to "toxaemia," causing the formation in the 

 blood of methaemoglobin or some similar dark-colored decompo- 

 sition product; but on diluting a drop of the blood, saturating 

 with CO, and comparing the solution with the tint of similarly 

 treated normal blood, I found that there was no abnormal pigment 

 present, so that the blue color was due simply to anoxaemia. That 

 this anoxaemia was, in the main at least, due to delay in the pas- 

 sage of oxygen into the arterial blood was then confirmed by the 

 fact that on administering oxygen the blue color changed to red, 

 and the patients improved in other respects. It was evident that 

 with the greatly increased partial pressure of oxygen in the al- 

 veolar air, the oxygen was able to pass into the blood at a sufficient 

 rate to saturate or nearly saturate the blood, and thus maintain 

 life. The delayed passage was probably due mainly to the fact 

 that the alveolar walls were swollen and oedematous, so that they 

 did not allow oxygen to pass inwards at a normal rate. As will be 

 pointed out in Chapter IX, this condition was produced experi- 

 mentally in animals by Lorrain Smith. The distribution of air in 

 the lung alveoli was doubtless also gravely interfered with by the 

 bronchitis and emphysema caused by the actions of chlorine, 

 though at the time I was ignorant of the importance of this cause. 

 To judge by the increased breathing there was also much dis- 

 turbance in the excretion of CO2 by the lungs; and the great dis- 

 tention of the veins and other signs in the chlorine cases pointed 

 in this direction also. 



In the cases of poisoning by phosgene and other lung irritants 

 used later, the symptoms of irritation of the air passages were 

 much less prominent. The general symptoms corresponded more 

 closely with those of pure anoxaemia. This was particularly true 

 in the earlier seen, or less severe, cases, when there was no evi- 

 dent oedema of the lungs. Thus, at first, the symptoms of acute 

 anoxaemia were shown only on muscular exertion sufficient to 

 cause a greatly increased need for oxygen ; and some of the men 

 who were apparently at the time only slightly affected lost con- 

 sciousness or died as a result of muscular exertion. Others suf- 

 fered only from general malaise or symptoms similar to those of 

 mountain sickness, and apparently due to slight anoxaemia. In 



