REVIEW AND APPRAISAL OF PARTS I AND II— SEVERINGHAUS 281 



food at rectal temperatures of 28° C. A comment on this work suggested that 

 rectal temperature might be seriously in error in these dogs with neurologic lesions 

 since cervical vagotomy had been shown to cause marked differential cooling of 

 the rectum. 



The EEG is said to exhibit large delta waves at about 30° C, falling to elec- 

 trical silence at 18° C. Recovery of electrical activity may require several hours 

 after 20 minutes of ischemia at 28° C. (and about 1 hour after 6-8 minutes at 

 28° C. in the reviewer's experience). Cerebral seizures reported during hypo- 

 thermia are believed explained by brain hyper-reactivity and the larger and more 

 spread-out afferent volleys from the periphery. 



Cerebral hemodynamics have received considerable attention. Several workers 

 report increased cerebral blood flow in response to elevated pC02 in dogs at 25- 

 28°. A suggestion that elevated pC02 decreased cerebral oxygen consumption 

 seems unv^arranted in view of the scatter of experimental data and the possible 

 fall in brain temperature with increased perfusion rates during cooling. Even at 

 low temperatures cerebral blood flow regulates according to the brain's metabolic 

 needs. 



Hemodynamics. A curious observation is that, whereas pulse rate declines 

 linearly with fall in temperature, arterial pressure falls only gradually to about 

 24° C, and then considerably more rapidly at lower temperatures. The bradycardia 

 at low temperatures is not like vagal bradycardia, and is not altered (at 25° C.) 

 by atropine or vagotomy. Stroke volume is nearly normal down to 20-25° C, and 

 the ventricular filling pressure is not elevated. Coronary flow has been shown ade- 

 quate for the needs of the heart by a number of investigators, although the 

 coronary vascular resistance is highly dependent on arterial pressure at low tem- 

 peratures (reduced resistance resulting from high pressures). Although peripheral 

 capillary stasis has been noted, no evident oxygen debt occurs, so the consensus is 

 that peripheral circulation is also adequate while the heart continues to beat. 



Post-hypothermia circulatory insufficiency was noted by several authors and re- 

 mains an unsolved problem. Factors which seem' most prominent as possible causes 

 are two : the peripheral vasodilatation during rewarming, with resultant increased 

 tissue oxygen utilization, and possible adrenal insufficiency resulting from the lack 

 of adrenal response to trauma during hypothermia, perhaps augmented by renal 

 sodium loss. 



Hematology. A marked thrombocytopenia has been observed by many investi- 

 gators in dogs, and by one in monkeys. Reports in man were limited to two patients 

 who showed small decreases at moderate temperatures. This thrombocytopenia, it 

 was suggested, could be prevented by the ganglionic blocking drug, Arfonad, or 

 by blood stream cooling instead of surface cooling in dogs. The mechanism of 

 these interesting observations was not discussed. The platelets were shown to 

 sequester in the liver and spleen, and possibly the gut, and to reappear on re- 

 warming. 



Respiration. The errors and difficulties in correcting blood gas tensions for the 

 physico-chemical effects of low temperatures have been responsible for a number 

 of erroneous reports in this field. For example, the oxygen tension of blood in a 

 syringe falls 6% per degree temperature fall ; pK' was found not to be constant. 



