332 RESPIRATION 



tendency to oedema of the lungs. The indication for bleeding is 

 evidently the distention of superficial veins. Bleeding was fre- 

 quently employed in the treatment of the chlorine cases, and with 

 great success. It is evident, however, that if there is no venous 

 distention, bleeding could not be expected to do anything but 

 harm. 



A more radical treatment is the continuous administration of 

 air enriched with oxygen. Unfortunately the problem of con- 

 tinuous administration of oxygen had never been attacked before 

 the war, and no suitable apparatus was available for the early 

 chlorine cases. But in the later stages of the war many cases of 

 lung oedema were successfully treated continuously with oxygen 

 by means of a nasal tube or the apparatus described in Chapter 

 VII. 



The next lung irritant gas used was phosgene (COC1 2 ). This 

 produces dangerous effects in considerably lower concentration 

 than chlorine, and its action is distinguished by the fact that it 

 has relatively less effect on the air passages and eyes and in the 

 end more on the alveolar walls. Thus a man exposed to a danger- 

 ous concentration of phosgene may notice but little irritant effect 

 at the time, or this effect may pass off rapidly, while the dangerous 

 effects on the alveoli only show themselves some hours later. 

 Phosgene was at first used as drift gas; but when drift gas was 

 abandoned as more or less ineffective against the protective 

 measures adopted, and also unmanageable owing to uncertain- 

 ties of wind, etc., phosgene was largely used in shells or bombs. 

 Various other substances with similar toxic properties were also 

 employed. 



A change in the type of the symptoms accompanying lung 

 oedema was now noticed. The deep plum-colored cyanosis and 

 venous distention were usually absent, and bleeding was useless. 

 The cyanosis was still very marked, but was of a pale or "gray" 

 type. The breathing was also shallower, and the pulse feeble and 

 rapid. Many slighter cases were also observed in which no defi- 

 nite lung symptoms were observed, but only general malaise with 

 cyanosis and fainting on any muscular exertion. 



In all these cases it seems evident that the rate of diffusion of 

 oxygen through the alveolar walls was diminished, but without 

 any marked interference with diffusion of CO 2 outwards, so that 

 owing to the hyperpnoea from want of oxygen there would be a 

 deficiency of CO 2 in the arterial blood. This is very intelligible 

 in view of the fact that on account of its greater solubility CO a 



