RESPIRATION 95 



all. We are also familiar with instructions to increase the breathing 

 so as to "improve the oxygenation of the blood" and with quack 

 advertisements based on the same idea. How does it come about 

 that although the regulation is so exact on the average, yet 

 temporary deviations from this average exactitude do not cause 

 any discomfort? How is it, also, that when the production of CO2 

 is suddenly increased to perhaps ten times the normal, as on a 

 sudden muscular exertion, yet the breathing responds gradually 

 and easily to the new conditions? 



The answer to this question is that there are physiological buf- 

 fers between the stimulus of increased production of CO2, or 

 increase in the alveolar CO2 pressure, and stimulation of the 

 respiratory center, and that if it were not so the respiratory center 

 would work in a jerky, irregular, and extremely inconvenient 

 manner. The first of these buffers is the large volume of air always 

 present in the lungs. Thus in my own case the mean volume of air 

 in the lungs at the end of inspiration during rest is 3650 cc, 

 measured dry at o°C., including about 3000 cc. of saccular al- 

 veolar air containing about 5.6 per cent -of CO2. Let us assume 

 that the breath is held at the end of inspiration during rest, and 

 consider what happens. About 250 cc. of CO2 would be normally 

 given off per minute, or 20 cc. in 5 seconds; and if the latter 

 quantity were given off with the breath held the mean CO2 pres- 

 sure in the lung air would rise by 0.6 per cent in 5 seconds. But, 

 as will be shown later, about 700 cc. of blood will pass through the 

 lungs in 5 seconds, and as the arterial blood will be more highly 

 saturated with CO2 if the alveolar CO2 percentage rises, some of 

 the CO2 which would ordinarily have been given off will be 

 dammed back in the blood. Figure 25 shows that for every rise of 

 2.5 mm. or .36 per cent in the alveolar CO2 pressure the blood will 

 take up, or hold back, i volume per cent of CO2. Hence the actual 

 rise in the mean CO2 pressure within the lungs cannot be more 

 than about 0.4 per cent in the 5 seconds during which the breath 

 is held. The net result is that about two-thirds of the COg which 

 the suspension of the breathing prevents from escaping from the 

 body is temporarily accommodated in the lung air, which thus 

 acts as a first buffer for preventing too sudden a change in the 

 arterial CO2 pressure. 



A second buffer is provided by the tissues and lymph in and 

 around the respiratory center itself. So far as we know the re- 

 action in all parts of the body is slightly alkaline, just as in the 

 blood; and the tissues and lymph have, like the blood, a con- 



