24 RESPIRATION 



stress on an experiment in which on slightly raising the pres- 

 sure in a spirometer from which an animal is breathing, the an- 

 imal stops breathing; and he attributed this to increase in the 

 partial pressure of the oxygen in the spirometer. The real cause 

 was quite evidently the distention of the animal's lungs by the 

 pressure, as in the experiments of Hering and Breuer. When a 

 man or animal has been rendered hyperpnoeic from want of oxy- 

 gen, and the hyperpnoea has reduced the normal percentage of 

 CO2 in the alveolar air and blood, apnoea is produced by supply- 

 ing more oxygen; but this apnoea is of course dependent on de- 

 ficiency of CO2, and cannot, therefore, be cited in support of the 

 oxygen theory of ordinary apnoea. 



The other erroneous theory — that apnoea following forced 

 breathing is due to a summation of inhibitory vagus stimuli aris- 

 ing from distention of the lungs in the forced breathing — 

 was based on two fallacies. The first was that intact vagi are 

 necessary for the production of apnoea by artificial respira- 

 tion. This is certainly not the case; for apnoea can be produced 

 quite promptly and easily after section of the vagi. It is necessary, 

 however, to make sure that the excessive artificial ventilation is 

 really effective in ventilating the lungs, since after section of the 

 vagi the natural breathing does not follow the rhythm of the 

 artificial respiration, and may thus partly annul the effects of 

 the latter. 



The other fallacy connected with the vagus theory of ordinary 

 apnoea was that when air containing little or no oxygen is used 

 for artificial respiration an apnoea due to excessive aeration of 

 the blood is impossible. Advocates of the vagus theory wrongly 

 thought only of oxygen want in connection with aeration of the 

 blood. They thus attributed to vagus excitation any apnoea which 

 was produced in presence of defective oxygenation of the blood, 

 ignoring the fact that deficiency of CO2 was present along with 

 defective oxygenation, and that this fact explained the observed 

 apnoea. Provided that the alveolar CO2 percentage is sufficiently 

 reduced, apnoea can be produced readily in spite of great defi- 

 ciency of oxygen in the alveolar air. 



The fact that apnoea is produced when forced breathing reduces 

 the alveolar CO2 percentage by as little as 0.2 per cent (with the 

 alveolar oxygen percentage not abnormally low), and that if this 

 reduction is prevented no amount of excessive lung ventilation 

 1 will produce apnoea, affords, in conjunction with the other facts 

 already referred to, conclusive evidence that the apnoea following 



