G04 APNOEA. [BOOK n. 



carried on very vigorously for a while, and then suddenly stopped, 

 the animal does not immediately begin to breathe. For a variable 

 period no respiratory movements at all take place, and breathing 

 when it does begin occurs gently and normally, only passing into 

 Ivspncea if the animal is unable to breathe of itself; and even 

 then the transition is quite gradual. Evidently during this period 

 the respiratory centre is in a state of complete rest, no explosions 

 are taking place, no respiratory impulses are being generated, and 

 the quiet transition from this condition to that of normal respira- 

 tion shews that the subsequent generation of impulses is attended 

 by no great disturbance. Not only is the centre at rest, but it 

 is less irritable than the normal; impulses along the vagus or 

 other nerves which otherwise would produce respiratory explosions 

 are now ineffectual. This state of things is known as that of 

 apncwi, the converse of dysjnm-a ; and the longer pause in breathing 

 mentioned above as possible after unusual ventilation of the lungs 

 may be regarded as a brief apncea. 



Now it seemed natural to suppose that such a state of rest of 

 the respiratory centre was brought about by the more than neces- 

 sarily ample supply of oxygen afforded by the previous increased 

 inspiratory movements; and indeed it was maintained that apnoea 

 was the result of too great, just as dyspnoea is the result of too 

 little arterialization of the blood reaching the respiratory centre. 

 It was argued that owing to the increased vigour of the artificial 

 respiratory movements the haemoglobin of the arterial blood, 

 which in normal breathing is not quite saturated with oxygen, 

 became almost completely so, and that at the same time the 

 quantity of oxygen simply dissolved in the blood became largely 

 increased and its tension largely augmented. But there are 

 "easons which render such a view untenable. In the first place 

 there is no direct and satisfactory proof that in apncea the arterial 

 blood is overloaded with oxygen as supposed ; indeed during the 

 course of apncea before it has come to an end the blood becomes 

 distinctly less arterial, more venous than usual. In the second 

 place apncea if not entirely impossible, is much more difficult to 

 bring about when both vagus nerves are divided, and if it does 

 occur after section of the vagus nerves has not the same characters 

 as ordinary apnoea. Now, when artificial respiration is being 

 carried on section of the vagus nerves can have no effect on the 

 quantity of oxygen taken up by the blood in the lungs. But 

 the vagus nerves are the channel of impulses affecting the 

 respiratory centre, and this relation of the apnoea to the vagus 

 nerves suggests another and different interpretation of apnoea. 

 As we have seen, expansion of the lung by acting in some way 

 or other on the pulmonary terminations of the vagus nerve 

 sends up along that nerve impulses which inhibit inspiration. 

 And it is argued that repeated forcible inflations of the lungs 

 produce apncea by generating potent inhibitory impulses, which 



