COLD THERAPY IN BACTEREMIC SHOCK 



deeper and deeper into hypoxia and finally succumbed from cardio- 

 pulmonary failure. The increased ventilatory work required in 

 septic shock is demonstrated in Figure 18. To provide 80 cc of 

 oxygen, normally the dog must breathe 2,8 liters/min, (Curve B). 

 In septic shock (Curve S.S.) an equivalent oxygen availability 

 required 6.2 liters/min. The dog's breathing apparatus had to 

 work 120 per cent harder. When cooled (Curve S.S. + H.), 80 cc 

 of oxygen was obtained with 4.5 liters/ min., reducing work load 

 in septic shock by one-half, but still 60 per cent above normal. 

 Failure of circulation with reduced tissue perfusion has been 

 most often pin-pointed as the main mechanical breakdown leading 

 to death (Spink, 1960; Altmeier and Cole, 1958), These studies 

 are in agreement. Figure 19 demonstrates the relationship be- 

 tween X^Oo ^^^ ^ ^^ the normal. A and A' represent the approx- 

 imate range of normal flow required for a given Vq-, In Fig- 

 ure 20 the effects of septic shock with and without hypothermia 

 are illustrated. Normally, to maintain adequate tissue oxygen- 

 ation, 100 cc of oxygen is delivered by a minimal flow of 1.1 liters/ 

 min. In septic shock, the equivalent oxygen is supplied by a markedly 

 reduced flow of 0.4 liters/min., a flow deficit of 65 per cent. 

 Induction of hypothermia returned the relationship toward nor- 

 mal. This was achieved primarily by reducing MRO2 with likely 

 little alteration in perfusion. This represents the single most 

 important benefit of hypothermia in this condition. Metabolic 

 environment was brought to a level more commensurate with 

 the sharply compromised capabilities of the physiologic apparatus. 

 The pathophysiologic picture of death in the hypothermic dogs 

 was similar to that in the non-cooled group. The difference is 

 primarily a temporal one. The shock state is due primarily to 

 reduced cardiac output, as is also reported to occur in the human 

 (Gilbert et al., 1955) and in experimental endotoxemia (Maxwell 

 et al., 1960). This is attributed to reduced venous return, secondary 

 to hypovolemia and to pooling (Gilbert, 1960; Ebert and Abernathy, 

 1961), with the latter occurring primarily in the liver and the 

 splanchnic beds. 



The physiologic picture of septic shock in the human and in 

 the dog are similar. Hj^othermic effects, however, differ principally 

 in failure to raise ABP in the dog. This may be due to anesthesia 

 or to species difference response. The criteria of septic shock in 



437 



