664 CONDITIONS ACTING ON THE RESPIRATORY CENTRE. 



alveoli, occlusion of the capillaries of the alveoli, compression of the lungs, entrance of air into 

 the pleura, obstruction or compression of the windpipe. (2) Obstruction to the entrance of 

 the normal amount of air by strangulation, or enclosure in an insufficient space. (3) En- 

 feeblement of the circulation,* so that the medulla oblongata does not receive a sufficient amount 

 of blood ; in degeneration of the heart, valvular cardiac disease ; and artificially by ligature of 

 the carotid and vertebral arteries (Kussmaul and Tenner), or by preventing the free efflux of 

 venous blood from the skull, or by the injection of a large quantity of air or indifferent particles 

 into the right heart (4) Direct loss of blood, which acts by arresting the exchange of gases 

 in the medulla (J. Jiosaithul). This is the cause of the "biting or snapping at the air" mani- 

 fested by the decapitated heads of young animals, e.g., kittens. [The phenomenon is well marked 

 in the head of a tortoise separated from the body ( W. Stirling).] 



If we study the rapidly fatal effects of these factors on the respiratory activity, we observe 

 that at first the respirations become quicker and deeper, then after an attack of general con- 

 vulsions, ending in expiratory spasm, there follows a stage of complete cessation of respiration. 

 Before death takes place, there are usually a few "snapping" or gasping efforts at inspiration 

 .\S Sigm. Mayer 111). 



Condition of the Blood-Gases. As a general rule, in the production of dyspnoea, the want 

 of and the excess of C0 2 act simultaneously (PJiiiger and Dohmen), but each of these alone 

 may act as an efficient cause. According to Bernstein, blood containing a small amount of O 

 acts chiefly upon the inspiratory centre, and blood rich in CO* on the expiratory centre. (1) 

 Dyspnoea.' from want of O, occurs during respiration in a space of moderate size ( 133), in 

 spaces where the tension of the air is diminished, and by breathing indifferent gases or those 

 containing no free 0. When the blood is freely ventilated with N or H, the amount of C0 2 

 in the blood may even be diminished, and death occurs with all the signs of asphyxia (Pfliiger). 

 (2) Dyspnoea, from the blood being overcharged with C0 2 , occurs by breathing air containing 

 much C'Oo ( 133). Air containing much CO., may cause dyspnoea, even when the amount of 

 in the blood is greater than that in the atmosphere (Thiry). The blood may even contain more 

 than normal (PflUger). 



Heat Dyspnoea. An increased temperature increases the activity of the respiratory centre 

 ( 214, II., 3). This occurs when blood warmer than natural flows through the brain, as Fick 

 and Goldstein observed when they placed the exposed carotids in warm tubes, so as to heat the 

 blood passing through them. In this case the heated blood acts directly upon the brain, the 

 medulla, and the cerebral respiratory centres (Gad). Direct cooling diminishes the excitability 

 ( Fn<l- ricq). "When the temperature is increased, vigorous artificial respiration does not produce 

 apnoea, although the blood is highly arterialised (Ackermann). Emetics act in a similar manner 

 (Hermann and Grimm). 



Electrical stimulation of the medulla oblongata, after it is separated from the brain, 

 discharges respiratory movements or increases those already present (Kronecker and Marck- 

 icaUl). Langendorff' found that electrical, mechanical, or chemical (salts) stimulation usually 

 caused an expiratory effect, while stimulation of the cervical spinal cord (subordinate centre) 

 gave an inspiratory effect. According to Laborde, a superficial lesion in the region of the 

 calamus senptorius causes standstill of the respiration for a few minutes. If the peripheral 

 end of the vagus be stimulated, so as to arrest the action of the heart, the respirations also 

 cease after a tew seconds. Arrest of the heart's action causes a temporary anaemia of the 

 medulla, in consequence of which its excitability is lowered, so that the respirations cease for 

 a time (Langendorff). 



Action on the Centre. The respiratory centre, besides being capable of 

 being stimulated directly, may be influenced by the will, and also reflexly by 

 stimulation of a number of afferent nerves. 



1. By a voluntary impulse we may arrest the respiration for a short time, 

 but only until the blood becomes so venous as to excite the centre to increased 

 action. The number and depth of the respirations may be voluntarily increased for 

 a long time, and we may also voluntarily change the rhythm of respiration. 



2. The respiratory centre may be influenced reflexly both by fibres which excite 

 it to increased action and by others which inhibit its action, (a) The exciting 

 fibres lie in the pulmonary branches of the vagus, in the optic, auditory, and 

 cutaneous nerves; normally their action overcomes the action of the inhibitory 

 fibres. Thus, a cold bath deepens the respirations, and causes a moderate accelera- 

 tion of the pulmonary ventilation (Speck). 



8ection of both vagi causes slower and deeper respiratory movements, owing 

 to the cutting off of those impulses which under normal conditions pass from the 

 lungs to excite the respiratory centre (p. 661). The amount of air taken in the 





