64 



D. V. Bates and R. V. Christie 



Lastly, is tlierc any change in the abihty of the inspired 

 air to make proper contact with the pulmonary blood? It 

 nii^ht seem that the obvious way to settle this point would 

 be to analyse the arterial blood and find out just what has 

 happened to the blood as it passed through the lungs. To do 

 this with any accuracy it is not enough to measure the Og 

 saturation of the arterial blood; both the alveolar and arterial 



YOUNG 



80 



60 



emphysema) 40 



20 



20 



40 60 ao /i"*^*" 



MEAN " 31 



sot 6-4 

 NO 72 



% 



<J 20 40 60 80 



Fig. 7. The percentage of CO removed from the hispired air when 

 breathing 0- 1 per cent CO in air is shown on the al)seissa. 



O2 tensions have to be measured, the technique of which is 

 difficult and laborious. More straightforward is the use of 

 carbon monoxide. As you all know, haemoglobin has a great 

 affinity for carbon monoxide. In fact if a healthy individual 

 breathes a low concentration of CO most of the gas which 

 reaches the alveoli will be taken up by the blood (Bates, 1952). 

 The expired air will therefore contain very much less CO than 

 was inspired. If, however, some of the inspired air were wasted 

 in ventilating avascular areas a very different result might be 

 expected. In these bloodless areas the CO would not be ab- 

 sorbed and therefore the concentration of CO in tlie expired 



