THE METABOLISM OF TRAUMATIC SHOCK 257 



ami found that the alkali reserve began to fall below normal, only when 

 the blood pressure fell below the critical level of 80 mm. Hg. Henderson 

 in 15)10 suggested that the probable explanation for this diminished alkali 

 reserve lies in the inadequate supply of oxygen to the tissues, and in the 

 resulting abnormal metabolism. The actual explanation is still under dis- 

 cussion. Henderson believes that the decreased alkali reserve is not due 

 to an accumulation of acid bodies, but rather is due to the disappearance 

 of the reserve alkali into the tissues. According to this theory, shock is 

 due to marked hyperpnea and a resulting loss of too much carbon dioxid, 

 thus causing an accumulation in the blood of an extra amount of reserve 

 alkali. He believes that this excessive alkali* leaves the blood stream and 

 migrates into the tissues, or is excreted by the kidney. As a result, a 

 diminished alkali reserve is found. Many investigators, however, believe 

 that the diminished alkali reserve is due to an accumulation in the blood 

 stream of acids formed because of an inadequate oxygen supply during 

 the metabolism of body tissues, and recently Macleod has shown the 

 presence of abnormal quantities of lactic acid in the blood plasma of cases 

 of shock. 



Basal Metabolism in Shock 



It might well be expected that, with the decreased oxygen available 

 for tissues, the normal rate of metabolism could not be maintained. The 

 marked loss of body temperature seen in shock suggests likewise that 

 the metabolism is not adequate to maintain the normal body heat. No 

 work on this subject has been possible in man. Henderson, Prince and 

 Haggard mention that there is a' marked drop in metabolism in shock. 

 Aub, working on cats, found that with the development of shock there 

 was a marked fall in the rate of the basal metabolism as studied by the 

 respiratory gas exchange. The temperature in these experiments was 

 kept as constant as possible, so that the .change in metabolism was not 

 due to a drop in temperature. In mild cases of shock the metabolism 

 fell to a level averaging 19 per cent below that found before shock was 

 induced; and in severe cases of shock the metabolism fell 30 per cent 

 below that found in the intact anesthetized animal. This drop in metab- 

 olism was roughly parallel to the severity of the shock, and usually did 

 not appear until the blood pressure had fallen to 80 mm. Hg or below. 



That the fall in metabolism was dependent upon the inadequate blood 

 flow was readily shown by experimentally producing slow blood flow by 

 increasing pericardial tension. This method, which does not induce a 

 true shock, but mechanically lowers the blood pressure, caused a similar 

 drop of about 30 per cent in the basal metabolism of the experimental 

 animal. The fall in basal metabolism, therefore, seems to be due to an 



