RESPIRATION 23 



of CO2 is breathed, the alveolar CO2 percentage naturally be- 

 comes constant after a few minutes ; but with forced breathing of 

 ordinary air it is not possible to maintain an alveolar COg per- 

 centage which is below the normal by some required small amount. 



To get over this difficulty we employed forced breathing with 

 air to which CO2 had been added, and found that on successive 

 trials with increasing percentages of CO2 in the inspired air 

 the duration of apnoea following forced breathing diminished 

 until, when there was more than about 4.7 per cent of CO2 in the 

 inspired air, no apnoea at all was produced. It was thus evident/ 

 that a very small diminution in the alveolar CO2 percentage/ 

 produces apnoea. The actual composition of the alveolar air at the 

 end of forced breathing in similar experiments was determined 

 later by Douglas and myself.^ It was found that with more than 

 4.7 per cent of CO2 in the inspired air no apnoea could be produced 

 by forced breathing, however hard, in a person whose normal 

 alveolar CO2 percentage was about 5.6, and that apnoea was only 

 produced if the alveolar CO2 was reduced by more than 0.2 per 

 cent below the normal. When, however, the CO2 in the inspired 

 air was lower, so that the alveolar CO2 percentage was reduced 

 by more than 0.2 per cent, apnoea was produced. 



Itis thus clear that the cause of the apnoea following forced 

 bre athing is reduction in the CO2 percentage in the alveolar air, 

 and that a reduction of as little as 0.2 per cent is sufficient to cause_ 

 apnoea. The astounding sensitiveness of the respiratory center to 

 CO2 is thus clearly established in both an upward and a downward 

 direction. A mean increase or diminution of .01 per cent in the 

 alveolar CO2 will evidently produce an increase or diminution of % 

 5 per cent in the alveolar ventilation, or of about 400 cc. per minute «* 

 in the lung ventilation. 



It may be useful to review briefly the sources of error in the 

 views current until recently with regard to the causes of the apnoea 

 produced by excessive ventilation of the lungs. One view was 

 that the excess of oxygen in the arterial blood causes the apnoea. 

 This theory had so little evidence to support it that it is very 

 surprising that it should have remained current so long. It is 

 true that during excessive artificial respiration the arterial blood 

 contains slightly more oxygen than usual; but there is a still 

 greater excess during the quiet normal breathing of pure oxygen, 

 which causes not the smallest sign of apnoea. Rosenthal^ laid great 



' Campbell, Douglas, Haldane, and Hobson, Journ. of Physiol., XLVI, p. 312, 

 1913- 



* Rosenthal in Hermann's Handbuch der Physiologie, IV, 2, p. 266. 



