THE NERVOUS MECHANISM OF RESPIRATION. 385 



tioned above as possible after unusual ventilation of the lungs may be re- 

 garded as a brief apnoea. 



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

 tory centre was brought about by the more than necessarily 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 vigor of the 

 artificial respiratory movements the haemoglobin of the arterial blood, which 

 in normal breathing is not quite saturated with oxygen, became almost com- 

 pletely 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 reasons which render such a view untenable. In the first 

 place there is no direct and satisfactory proof that in apnoea the arterial 

 blood is overloaded with oxygen as supposed ; indeed, during the course of 

 apnoea before it has come to an end the blood becomes distinctly less arterial, 

 more venous than usual. In the second place apnoea if not entirely impossi- 

 ble, 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 cha- 

 racters as ordinary apncea. 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 apnoea by generating potent inhibitory im- 

 pulses, which by a kind of summation of their effects in the medulla stop for 

 a while the generation of respiratory impulses in the respiratory centre. 

 This conclusion, moreover, is strongly supported by the fact that an apnoea 

 may be produced, so long as the vagus nerves are intact, by forcible artificial 

 respiration with hydrogen instead of atmospheric air ; in other words, the 

 inhibitory impulses generated in the vagus nerves by the inflation are suffi- 

 cient wholly to neutralize the development of respiratory impulses which 

 the deficient arterialization of the blood would otherwise have produced. 

 The exact nature and development of such a summation of inhibitory im- 

 pulses, especially in the presence of correlative augmentative impulses called 

 forth by the corresponding successive collapses of the lungs, is too complex a 

 matter to be dwelt on here. Moreover, an apnoea may be produced, though, 

 as we have said, with difficulty after section of both vagus nerves ; but in 

 this case air and not hydrogen must be used for inflation, the use of the 

 latter, in contrast to the result when the nerves are intact, leading to dysp- 

 noea. The subject cannot as yet be considered as fully cleared up. That 

 apnoea as ordinarily produced is in some way the result of inhibitory im- 

 pulses generated by the inflations can, however, hardly be doubted. 



318. Secondary respiratory rhythm Cheyne-Stokes respiration. A re- 

 markable abnormal rhythm of respiration, first observed by Cheyne but 

 afterward more fully studied by Stokes, and hence called by their combined 

 names, occurs in certain pathological cases. The respiratory movements 

 gradually decrease both in extent and rapidity until they cease altogether, 

 and a condition of apnoea, lasting it may be for several seconds, ensues. 

 This is followed by a feeble respiration, succeeded in turn by a somewhat 

 stronger one, and thus the respiration returns gradually to the normal, or 

 may even rise to hyperpncea or slight dyspnoea, after which it again declines 



25 



