ACIDOSIS 75 



(partial compensation) and thence over to Area 4 (complete compensa- 

 tion). 



The compensatory increment of blood alkali probably comes from 

 two sources: (1) The increased excretion of ammonia and titratable acid 

 through the kidneys tends to raise the bicarbonate content of the entire 

 body, and the blood plasma bicarbonate would normally rise with that of 

 the other fluids. (2) HC1 may, perhaps, leave the blood plasma and enter 

 the tissue cells, as it has been shown to leave the plasma and enter the 

 blood cells when the pH rises (Reaction 1 of the diagram on p. 61). 

 The rate of blood alkali rise observed by Henderson and Haggard appears 

 too rapid to be accounted for by acid excretion alone, and these authors 

 attribute the increase to alkali drawn from the tissues. The effect would 

 be the same if acid passes from the blood into the tissues, a process which 

 from analogy with the shift between plasma and blood cells seems 

 more probable. The relative parts that these two factors, acid excretion 

 and shift of acid to the tissues (or of alkali in the reverse direction), play 

 in the compensatory rise of blood bicarbonate during CO 2 retention is 

 uncertain. That accelerated acid excretion occurs has been shown. That 

 acid shift from blood to tissues also occurs seems probable. 



Increased blood bicarbonate due to compensation of CO 2 retention 

 may, it appears, be clinically differentiated from that due primarily to 

 alkali excess by the fact that CO 2 retention is accompanied by cyanosis 

 (see also discussion of Area 4). This has been observed by Means, Bock, 

 and Woodwell in the cases cited above. 



Area 9. Uncompensated Alkali Deficit. This is the condition de- 

 fined by Hasselbalch and Gammeltoft (1915) as "uncompensated acidosis." 

 It has been most frequently observed in cases of nephritic and diabetic 

 acidosis in the premortal period. Means, Bock, and Woodwell (1921) 

 describe most completely both the symptoms and blood changes in such 

 a nephritic case. The blood bicarbonate is extremely low. Respiration, 

 which up to the terminal stage has kept the H 2 CO 3 sufficiently low to 

 maintain a normal H 2 CO 3 :BHCO 3 ratio, now fails to do so, and the 

 blood condition shifts from that represented by Area 6 over into that 

 represented by Area 9. 



In deep ether anesthesia, according to the results of Van Slyke, Austin, 

 and Cullen (1920) and in certain cardiac patients (Peters and Barr, 

 1921), the blood state is represented by Area 9, and both alkali deficit and 

 carbonic acid retention occur. 



