376 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



TABLE V 



Blood pH in Nine Dogs Prior to and During Hemorrhagic Shock 

 Plus Hypothermia (24° C.)' 



During 

 shock 

 Dog plus 



no. Control hypothermia 



1 7.20 7.20 



2 7.20 7.18 



3 I.'il 7.30 



4 7.40 7.40 



5 7.45 7.45 



6 7.4 7.4 



7 7.44 7.48 



8 7.28 7.40" 



9 7.52 7.60" 



» Produced by surface cooling. 

 ■> Shock induced prior to cooling. 



may be due to resumption of greater muscular activity than occurred during the 

 control period under morphine. 



Comparison of the foregoing data with those from dogs which are cooled after 

 the induction of shock reveals several points of interest. The fall in oxygen con- 

 sumption and cardiac output is appreciably less than in the precooled dog, and the 

 respiratory depression is not nearly so steep. The higher level of metabolic activity, 

 as reflected in the higher oxygen consumption, suggests that when the circulation is 

 already defective external cooling may fail to reduce the temperature of some of the 

 deeper tissues to the same level as in the precooled animal. 



That hypothermia reduces bleeding volume is evident from the data in table II. 

 One cannot attribute the greater tolerance to shock in precooled dogs (Group I and 

 II) to this effect of hypothermia because dogs bled prior to cooling (Group III) 

 suffered a greater than average blood loss and also showed a greater tolerance to 

 shock. Since the antibiotic therapy alone cannot account for the difference in sur- 

 vival rates in these three groups of dogs, we conclude that some property of hypo- 

 thermia other than its effect of bleeding volume must account for its influence upon 

 the course of the shock state. 



COMMENTS 



Deterling et al.^° observed ventricular fibrillation in 40 per cent of 16 normal 

 dogs under barbiturate anesthesia at temperatures below 23° C. Spurr et a/.^^ ob- 

 served this complication in 33 per cent of normal dogs cooled to 20-26° C. for four 

 hours. In a series of 34 shocked dogs at temperatures ranging from 22-28° C, we 

 encountered fibrillation in only 6 per cent. Bigelow et al.^~ lowered the incidence of 

 fibrillation by a 50 per cent reduction in blood volume, and attributed the cause of 

 filirillation to an increase in venous pressure. Our own observations are consistent 

 with this view, for we found that rapid transfusion via the femoral vein is well tol- 

 erated by normothermic dogs in hemorrhagic shock, but precipitates ventricular 

 fibrillation in hypothermic shocked dogs. The lowered irritability of cardiac muscle 

 during shock may contriliute to the lower incidence of fibrillation in our series of 

 shocked dogs. 



