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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



monary blood flow were just twice the systemic flow, 

 the reduced hemoglobin would increase only to 2.5 g 

 per 100 ml. If, however, pulmonary and systemic flows 

 were equal, the mixed blood in the arteries would con- 

 tain 3.4 g oi reduced hemoglobin per 100 ml, and well 

 over 5 g per 100 ml at the capillary level, assuming 

 that capillary blood has 3.5 more grams of unsaturated 

 hemoglobin per 100 ml than arterial blood. As a rule, 

 then, if pulmonary blood flow exceeds the systemic 

 flow by more than twofold, cyanosis when at rest is 

 not likely even with complete mixing of the total 

 systemic and pulmonary venous return. 



An increase in oxvgen consumption (an increase in 

 the amount of oxygen extracted by the tissues) re- 

 sults in a decrease in the oxygen saturation of venous 

 blood and, as has been pointed out, a decrease in the 

 arterial oxygen saturation. Exercise, for example, in- 

 creases the metabolic rate and thus decreases the ar- 

 terial oxygen saturation. 



It would be a useful adaptation to a state of chronic 

 hypoxemia if the body would find a means of carrying 

 on its basal activities with a diminished consumption 

 of oxygen. That such an adaptation may actually 

 occur was suggested by Bing et al. (31), who reported 

 that in 28 of 30 patients with tetralogy of Fallot who 

 were chronically hypoxemic from congenital heart 

 disease the ba.sal metabolism was either significantly 

 below or at the lower limits of normal. Values as low 

 as —48 per cent for the basal metabolic rate were re- 

 corded, and the average for the group was —23. 



In contrast to these results, normal or slightly ele- 

 vated values for basal oxygen consumption in con- 

 genital cyanotic heart disease have been obtained by 

 Holling & Zak (133), Burchell and co-workers (49), 

 Ernsting & Shephard (95), Davison and colleagues 

 (77) and Husson & Otis (139). Thus most of the evi- 

 dence indicates that no diminution in basal oxygen re- 

 quirement occurs in chronic hypoxia resulting from 

 congenital cyanotic heart disease. 



COMPENSATORY EFFECTS RESULTING FROM ARTERIAL 



HYPOXEMIA. It is well known that individuals who are 

 chronically hypoxemic tend to develop a polycy- 

 themia with a concomitant increase in the oxygen- 

 carrying capacity of the blood. The mechanism by 

 which the increase in concentration of blood hemo- 

 globin is brought about is still oijscure, nor is there 

 general agreement as to its importance in the over-all 

 picture of acclimatization (122). 



Data showing the magnitude of the increase in oxy- 

 gen-carrying capacity of the blood in man residing at 

 various altitudes have been summarized bv Hurtado 



(137). Husson cS: Otis (139), in an excellent discussion 

 of this subject, have suggested the possibility that 

 hypoxia more severe than that represented by an ar- 

 terial saturation of 70 per cent fails to stimulate any 

 further increase in hemoglobin. 



The mountain dweller gains from an increased oxy- 

 gen capacity because remo\'al of a given amount of 

 oxygen from the blood by the tissues produces less of a 

 drop in the saturation, and hence the tension of oxygen 

 supplied to the tissues as well as the oxygen saturation 

 of venous blood returning to the heart is increased. 

 The arterial oxygen saturation, since it is determined 

 almost solely by the ventilation, will not be affected 

 by an increased o.wgen-combining power of the 

 blood. The individual with hypoxemia resulting from 

 a venoarterial shunt will gain e\'en more than the al- 

 titude dweller from an increased oxygen capacity, 

 since in effect this increases his pulmonary blood flow 

 which, if the rate of oxvgen consumption is constant, 

 is tiie major determinant of his arterial oxygen satura- 

 tion. 



A normal individual who is exposed to an altitude 

 that produces an arterial saturation of 75 per cent, 

 whose oxygen-carrying capacity is 20 volumes per 

 cent, and whose oxygen consumption and cardiac out- 

 put are such that his arteriovenous oxygen difference 

 is 5 volumes per cent will have a mixed venous satura- 

 tion of 50 per cent. If his oxygen capacity were in- 

 creased to 30 volumes per cent, leaving other variables 

 as before, his arterial saturation would remain at 75 

 per cent and the mixed venous saturation would be 

 increa.sed to 58 per ceitt. 



However, consider an indi\idual who lives at sea 

 level has an oxygen capacity of 20 Noluines per cent 

 but who has a right-to-left shunt of such magnitude 

 that his arterial blood consists of a mixture of eqtial 

 parts of blood that has passed through the lungs and 

 mixed venous blood and who has an arteriovenous 

 difference of 5 volumes per cent. With normally 

 saturated blood leaving the lungs, the saturations of 

 arterial and mixed venous blood would be 75 and 50 

 per cent, the same as in the case of the normal indi- 

 \'idual at altitude. If the oxygen capacity of the indi- 

 \idual with the shunt is then increased to 30 \'olumes 

 per cent, the arterial oxygen saturation would increase 

 to 83 per cent and mixed venous saturation to 67 per 

 cent. 



Adaptations are, by their nature, compromises in 

 that concessions must be made in return for the ad- 

 vantages gained. In this respect, there is evidence that 

 polycythemia is a predisposing factor in the fonnation 

 of pulmonary and cerebral thrombi (27, 199). The 



