HEMORRHAGIC SHOCK— FRH:DAIAN, DAVIDOFF and FINE 375 



TABLE IV 



Cardiovascular and Respiratokv Dynamics in Dogs Cooled Akter Induction of 



Hemorrhagic Shock 



tt 





c ^• 



; 3 o. 





r b ■=. "^ « !=. 



-I Si-1 "H giJ 



i>CO «* 



K*' -< "■ P-( U° < < 0. O 



Prior to cooling or 

 shock 38-39 130 150 2920 19.2 6.3 19.6 164.4 12 34 



During shock 38-39 30 166 724 17.0 13.2 18.6 99.5 18 ^2 



During hvpotlicrniia 

 and shock 24 30 84 366 17.6 14.2 15.5 68.8 30 21 



After transfusion and 

 rise in bodv tem- 

 perature ..." 33.2 106 90 4572 19.1 4.2 22.7 193.4 13.8 21 



Number of experi- 

 ments for each value 

 listed (10) (10) (10) (4) (4) (4) (4) (4) (4) (10) 



kind of protection as prophylactic antil)iotic therapy, thou^di hy a cHfferent action 

 npon the offending hacteria. 



The effect of hypothermia on the cardiovascular dynamics of hemorrhagic 

 shock {tables III and IV.) In the unanesthetized dog hypothermia (28° C. ) 

 lowers the blood pressnre, pulse rate and cardiac output, but the pulmonary ven- 

 tilation is adequate to sustain the oxygen content of the arterial blood. The con- 

 siderable increase in oxygen consumption and in the A-\' oxygen difference are due 

 to muscular activity, for when shivering is prevented by ether the oxygen con- 

 sumption is considerably reduced rather than increased, and the A-V oxygen dif- 

 ference is unchanged. Hence the rise in the \-\ difference in the unanesthetized 

 dogs appears to result from the increased extraction of oxygen by muscle. 



After the induction of shock the pulse rate continues to fall instead of rising as 

 it does in the normothermic dog. The precipitous further decline in cardiac output 

 is such as to reduce the stroke volume to less than 3 ml. With an oxygen consump- 

 tion only 20 per cent of normal during shock, the sharp rise in the A-V oxygen 

 difference must signifv an almost static peripheral circulation. For this reason, to- 

 gether with the feeble eft'ect upon caval flow of the much reduced respiration, re- 

 turn flow to the heart is extremely small. The resultant slow flow through the pul- 

 monary circuit allows the very low ventilatory exchange to provide enough oxygen 

 to maintain an adequate arterial oxygen content. Because of the low level of tissue 

 metabolism, hypercapnia does not develop in the face of a depressed respiration, as 

 indicated 1)V the fact that no significant shift in blood ^jH occurred in our experi- 

 ments (table \). Therefore, we were not obliged to employ hyperventilation.^ 



Following transfusion and warming there is a return to normal or nearly normal 

 values in all categories. The notable increase abt)ve normal in oxygen consumption 



§ The death of hypothermic dogs in shock cannut be explained as due to the effects of hypo- 

 thermia upon pulmonary efficiency because such a death would not be prevented by an antibiotic, 

 unless it could be shown that the primary effect of deficient ventilation is pulmonary infection. 



