152 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



cent. In no case did there occur an increase in aortic pressure or in heart rate. It 

 therefore follows that at a heart temperature of 20° C. there is no functional 

 cardiac abnormality directly attributable to diminished coronary flow. 



A more important consideration in the assessment of the adequacy of the coronary 

 circulation in hypothermia is the question of release of oxygen by cold blood to cold 

 tissues. The displacement of the oxygen dissociation curve to the left by cold is well 

 known. At a given partial pressure of oxygen, a greater per cent of oxygen satura- 

 tion obtains in cold blood than in normal blood. This has been shown to be true 

 in vitro by Brown and HilP and in vivo by Penrod.* Does this phenomenon prevent 

 cardiac tissue from getting an adequate supply of oxygen even though blood flow 

 is abundant ? 



Penrod* measured coronary arterio-venous oxygen differences in dogs at normal 

 temperature and at blood temperatures of 20° C. His results are summarized in 

 table II. The average coronary A-V oxygen difference in ten normal dogs was almost 

 identical with that found in fifteen dogs at 20° C. A drastic reduction in the partial 

 pressure of oxygen in coronary venous blood and presumably in cardiac tissue made 

 this possible. It must be emphasized however that the coronary A-\' oxygen differ- 

 ence in deep hypothermia, i.e., at 20° C, is the same as that which obtains at normal 

 temperature. A similar situation exists in the dog at 17° C.^ Thus, per unit of blood, 

 hypothermic cardiac tissue can extract as much oxygen as it can at normal tempera- 

 ture. Since the volume of coronary blood flow is adequate for the conditions, it must 

 be concluded that an adequate volume of oxygen is taken up by cardiac tissue at 

 this low temperature. 



Cardiac output and work. In the early stages of hypothermia the volume of 

 blood put out by the heart varies with the oxygen consumption of the animal, which 

 in turn is directly related to the intensity of reflex shivering. When general anes- 

 thesia is light and shivering is violent, total oxygen consumption and cardiac output 

 are increased two, three, or even four-fold. When shivering is moderate, cardiac 

 output shows only a moderate increase over the non-shivering control state. When 

 general anesthesia is sufficiently deep to eliminate shivering, cardiac output is dimin- 

 ished. Thus, we have another example of a function modified by two opposing fac- 

 tors, reflex stimulation and direct depression. At temperatures of 20° C. to 18° C, 

 when shivering is absent, cardiac output is about 15 per cent of normal. 



The observation of Hegnauer and D'Amato,** summarized in table III. agree 

 closely with those of other workers. Nine dogs at normal temperature showed an 

 average cardiac output of 146 ml./kg./min. In eight of these dogs, at an average 



TABLE II 



Cardiac Oxygenation at Normal Temperature and in Hypothermia 



Normal 



temp. 



(n= 10) 



Coronary A-V O. diff . (vol. %) 12.3 



Coronary venous PO.. (mm. 1 Ir) 19 



Hematocrit (%) 41.9 



Heart rate (per minute) LS6 



Arterial prcs.sure (mm. Hg) 1^)3 



