1030 



PHYSIOLOGY 



B.P. 



therefore be detected in the blood whenever violent exercise is taken sufficient 

 to produce dyspnoea, or when the access of oxygen is diminished by poisoning 

 with carbon monoxide, or by reducing the tension of this gas in the air 

 breathed. Oxygen lack can be regarded therefore as synonymous with the 



production of lactic acid. Lactic acid 

 introduced into the blood stream, as 

 is shown in the curve in Fig. 464, B, 

 is equally efficacious with oxygen lack 

 \lnf. Vol. or with carbon dioxide excess in the 

 production of a rise of blood pressure 

 indistinguishable from the asphyxial 

 rise. It seems therefore that the 

 common factor in asphyxia is the 

 increased acidity or H' ion concen- 

 tration of the blood. We shall have 

 occasion to return to this question in 

 dealing with the regulation of the 

 respiratory movements. 



If in the dog, and to a less extent 

 in other animals, the vagi be left 

 intact, the blood pressure tracing 

 during asphyxia has quite another 

 appearance. At the point of the 

 tracing, corresponding to the rapid 

 rise in the previous experiment, there 

 is in this case only a slight rise of 

 pressure, but the heart begins to beat 

 very slowly. At each beat it neces- 

 sarily sends out a greater volume of 

 blood than when it is beating more 



frequently, and hence the oscillations on the blood pressure curve caused by 

 the heart beats become very large. This slow beat is due to the action of the 

 vagus centre, and is at once abolished by section of the two vagi. The sparing 

 of the heart by means of this vagus action enables it to last longer, and 

 the final fatal fall of blood pressure due to heart failure comes on rather 

 later than when the vagi are divided. In the increased vagus action, which 

 occurs during asphyxia, two factors are probably involved. The cardio- 

 inhibitory centre in the medulla probably partakes of the general excita- 

 tion of the medullary centres due in the first place to carbon dioxide excess, 

 in the second to oxygen lack. More important is the direct action of the 

 rise of blood pressure on the medullary centre. The rise of arterial pressure 

 causes increased intracranial tension, and any increase of the latter excites 

 the vagus centre and produces slowing of the pulse. The vagus slowing 

 is therefore absent in asphyxia if the arterial blood be allowed to escape 

 through a mercury valve so as to prevent any rise of pressure in the brain 

 cavity. 



Fia. 466. Tracing of arterial blood 

 pressure and of intestinal volume, 

 to show the influence of a moder- 

 ate increase in the CO, tension of 

 the blood. (MATHISON.) 



