RESPIRATION I 4 I 



mixed alveolar air at the end of the apnoea produced by two 

 minutes of forced breathing, and the results are plotted in Figure 

 46. 6 It will be seen that the CO 2 pressure (and of course also the 

 length of the apnoea) rises with the alveolar oxygen pressure 

 until the latter reaches about 120 mm. (corresponding to about 

 17 per cent of oxygen in the dry alveolar air), beyond which a 

 further rise in alveolar oxygen pressure has no effect. In this case 

 the oxygen pressure in all the lung alveoli would be at a more or 

 less equal high level at the beginning of an apnoea, but would 

 fall at unequal rates in the different alveoli. Accordingly at the 

 end of apnoea the mixed arterial blood would' be getting venous 

 unless the average alveolar air contained more than 17 per cent 

 of oxygen. And yet as little as 8 per cent would be enough to 

 prevent this effect if the air was evenly distributed in relation to 

 the blood supply of the alveoli, or if respiratory movements pre- 

 vented anything more than comparatively slight variations in 

 the oxygen percentages in different alveoli. 



Judging from aerotonometer experiments on normal animals, 

 and from direct determinations on human arterial blood, the hae- 

 moglobin of average human arterial blood is only about 94 to 96 

 per cent saturated with oxygen about 2 per cent less than if the 

 whole arterial blood was saturated to the oxygen pressure of the 

 mixed alveolar air. A very accurate series of determinations 

 described by Meakins and Davies in the paper just quoted showed 

 that in different healthy persons the saturation varies from 94 to 

 96 per cent. The slight variations seem to be due to the variations 

 which Barcroft described in the oxyhaemoglobin dissociation 

 curves of different individuals. 



The periodic breathing produced by shallow breathing differs 

 strikingly from the periodic breathing produced by anoxaemia 

 in normal persons. As will be seen from Figure 44, the periods 

 are much longer, and in this respect bear a striking resemblance 

 to ordinary clinical Cheyne-Stokes breathing. The reason why 

 the periods are longer is evident enough : for the shallow breath- 

 ing is very ineffective in raising the oxygen percentage in the 

 badly ventilated parts of the lungs and so relieving the anox- 

 aemia. The relief thus comes slowly. The breathing, therefore, 

 "waxes and wanes" gradually, as in clinical Cheyne-Stokes 

 breathing. In hibernating animals similar breathing is often ob- 

 served and can be explained in the same way, as, owing to the 

 small production of CO 2 , the breathing is very shallow. 



9 Douglas and Haldane, Journ. of Physiol., XXXVIII, p. 401, 1909. 



