3 20 



RESPIRATION 



the respiratory center is no longer supported in activity, and the cardiac 

 inhibitory center is stimulated to inhibitory spasm. This is shown in 

 figure 2416. This figure represents only the terminal effect of anoxemia 

 in the dog under chloretone anesthesia. The stopping of respiration is 

 shown in the top trace. The blood pressure tracing shows an enormous 

 slowing of the heart rate by anoxemial stimulation of the vagus medullary 

 center. The proof is found in the rapid heart rate after the vagus nerves 

 are both cut. 



' 





FIG. 2416. The effects of extreme anoxemia in the dog. 



The compensatory increase in respiratory rate and volume during 

 oxygen want disturbs the factor of carbon dioxide balance in the blood. 

 The carbon dioxide is lost more rapidly than usual, hence its concentration 

 in the blood is diminished, often from twenty to fifty per cent. That 

 carbon dioxide is the chemical stimulator of the respiratory center has 

 long been known, but Henderson has more recently given evidence of the 

 stimulating effect of carbon dioxide on certain other functions of the 

 nervous and muscular mechanisms. He has called the condition of reduced 

 carbon dioxide acapnia, and offers the suggestion that lack of sufficient 

 carbon dioxide may contribute to the complex of symptoms associated 

 with coincident lack of oxygen. 



Men are often subjected to higher than normal barometric pressures in 

 caisson work, diving, etc. Paul Bert has found in experimenting with 

 animals that the oxygen pressures may be gradually increased to a con- 

 siderable extent without marked effect, even to the extent of 8 or 10 atmos- 

 pheres, but when the oxygen pressure is increased up to 20 atmospheres the 

 oxygen becomes poisonous and the animals experimented upon died with 



