1130 PHYSIOLOGY 



abolished. The pauses between the inspirations become longer and longer, 

 until at the end of four or five minutes the animal takes its last breath. 



If we increase the activity of the centre and therefore its gaseous inter- 

 changes, by warming the blood in the carotid arteries, there may be a 

 considerable quickening of respiration unaccompanied by any deepening, a 

 condition which is spoken of as tachypncea. On the other hand, we may slow 

 the respiratory movements by placing a small piece of ice on the floor of the 

 fourth ventricle. 



In the production of the phenomena of asphyxia two factors must be at 

 work. In the first place, there is an accumulation of carbon dioxide in the 

 blood bathing the centre, or an increased tension of this gas in the centres 

 themselves, either as a result of deficient excretion or increased production. 

 On the other hand, the centre is deprived of oxygen, either by failure of 

 renewal of the oxygen supply or by increased using up of this gas in the 

 metabolism of the centre. The question arises, which of these two changes 

 is responsible for the different physiological events which characterise 

 asphyxia ? At various times these phenomena have been ascribed either to 

 the increased tension of carbon dioxide or to the diminished tension of 

 oxygen in the centre. The view, that the normal stimulus to the respiratory 

 centre in asphyxia was the lack of sufficient oxygen and that the normal 

 activity of this centre was determined by the tension of oxygen in the blood 

 circulating through the brain, was first put forward by Rosenthal. When 

 sufficient oxygen was present, the centre, according to this observer, would 

 cease to act, so that a condition of apncea would be produced. According 

 to Traube, on the other hand, the special respiratory stimulus was the 

 excess of carbon dioxide in the blood, and this view was supported strongly 

 by Miescher. The tendency of recent work, especially by Haldane and 

 his pupils, has been to show that there is an element of truth in both views 

 that indeed the respiratory centre can be excited either by excess of 

 carbon dioxide or by lack of oxygen, but that its sensitivity to carbon 

 dioxide is by far the more important factor in the determination of the 

 increased respiratory movements in asphyxia, and is the only chemical 

 factor which can be regarded as playing any part in the regulation of the 

 respiratory movements under normal conditions. This factor is well brought 

 out if we investigate the effect on the respiratory movements of altering the 

 tensions of the two gases in the air breathed. If by this means we succeed 

 in altering the tension of the two gases in the alveolar air, we may assume that 

 the tensions of the gases in the arterial blood leaving the lungs are altered in 

 the same ratio. The results of such experiments are very striking. Even 

 a slight increase in the percentage of carbon dioxide in the air causes an 

 increase first in the depth and later on in the rhythm of respiration (Fig. 518). 

 This is shown in the following Table by Haldane, which represents the average 

 depth and frequency of the respirations when the subject was breathing 

 normal air and air charged with varying percentages of carbon dioxide. 

 A rise of carbon dioxide in the atmosphere to 2 per cent, increases the depth 

 of respirations by 30 per cent., and the total alveolar ventilation by 50 per 



