ALTERATION IN THE ATMOSPHERIC PRESSURE 



to allow the blood of the pulmonary capillaries to combine with its usual 

 quantity of oxygen. There is enough oxygen absorbed, however, to 

 satisfy the amount used by the tissues under ordinary circumstances. 

 It is only when an extra amount of activity is called for that stress is 

 observed at this level. At still greater altitudes the oxygen of the arterial 

 blood is further reduced until a level is reached at which the total amount 

 of oxygen absorbed by the pulmonary blood is less than that normally 

 lost in the tissues. This produces a real tissue oxygen want. The con- 

 condition receives the technical name anoxemia. 



Progressive anoxemia sets into activity a number of physiological 

 mechanisms which aid the body to absorb its maximum of oxygen from the 

 alveolar air. These reactions are called compensatory. They have been 

 described by a number of workers in the Medical Division of the United 

 States Army who developed a technique for testing the ability of the 



FIG. 2410. The progressive increase of the amount of hemoglobin in the blood 

 during a journey from England to the high Andes (Richards). 



human body to withstand low atmospheric pressures in aviation. The 

 compensatory factors lead to great increase in respiratory rate, an increase 

 in the tidal air, therefore, a great increase in the respiratory minute 

 volume of air breathed. The heart rate is also greatly increased thus 

 maintaining a higher systolic blood pressure notwithstanding the fact 

 that there is vascular dilation, therefore, increased volume of blood flow. 

 Also, the percentage of hemoglobin in the blood is increased if the low 

 oxygen pressure acts through sufficient time, as in mountain residence, figure 

 2410. When the limit of compensation is reached, then the body quickly 

 succumbs through the following symptoms. Respiration decreases in rate 

 and in amplitude and stops. The blood pressure at first becomes high, 

 then falls slowly at first, but more rapidly later to a final low level. The 

 heart rate, which is greatly accelerated in the early stage of anoxemia, is 

 enormously slowed in the late stages and especially at the time of and 

 following the stopping of respiration. It would seem that the lack of 

 oxygen at first strongly stimulates the medullary centers of respiration, of 

 cardiac acceleration, and of vaso constriction. But in extreme anoxemia 



