REVIEW AXn APPRAISAT. OE PART III— BROOKS axd HOFFMAN 359 



l)alance of the animal during the entire experiment. It is quite possihle that, due to 

 l)oor perfusion, the tissue levels of L\)j are not accurately reilected l)y blood pH. 

 The studies of ( jollau. in which die circulation is maintained by a immp-oxygenator 

 (hu-ing cooling, suggest that perfusion may indeed be inadequate. Thus, he was 

 able to cut off all coronary How tcj cooled hearts (25° ) for 20 minutes without 

 fibrillation, and when perfusion was resumed cardiac ])0., returned to normal. This 

 period of anoxia can be repeated. On the other liand, if the coronaries were re- 

 occluded too soon after the first period of anoxia. irreversil)le filjrillatiou su])er- 

 venecb 



In this respect, the use of a pump-oxygenator. anfl independent control of H and 

 COo seems indicated in intact animals. In addition, further study of isolated 

 cardiac tissues is certainly suggested. It is perhaps significant that in isolated 

 preparations (where perfusion is presumably adequate) arrhythmias are not seen 

 during slow cooling. 



Cardiac efficiency in hypothermia and rewarwing. Although it is generally 

 agreed (D'Amato, Berne, Adolph, Kao. etc.) that the heart's need for oxygen is 

 satisfied during hypothermia some inefticiency is reported (AIcMillan, Swan). The 

 reduction in cardiac and body metabolism permits the heart to supply itself and 

 other tissues with needed oxygen (Horvath and Spurr ; Rosomofif). No oxygen debt 

 is incurred during hypothermia. The increase or decrease of cardiac efficiency ap- 

 pears to be of little significance in hypothermia but on rewarming (Swan) an effi- 

 ciency of cardiac action capable of meeting the increased body needs is not im- 

 mediately developed and rewarming may entail its own specific hazards. 



GENERAL SUMMARY AND DISCUSSION 



The first and most important observation which emerges from the Symposium 

 is that different investigators have had markedly different results. Most workers 

 (Hegnauer, Kay, Swan, etc.) have obtained fibrillation at 26-19° C. but Gollan 

 (who uses a pump-oxygenator) and Lewis (who does not) have cooled animals to 

 much lower levels without trouble. Similar discrepancies are apparent with respect 

 to production of alkalosis-vs. -acidosis. It is doubted that hypothermia, itself, in- 

 creases the tendency toward fibrillation (Dammann and ^Nluller). A review of the 

 contributions indicates that the entire story can be put together some\\hat as follows. 



With cooling of the whole body metabolic requirements decrease in all organs, 

 and Oo use and CO2 production drop. This decrease in metabolic activity is accom- 

 panied by a decrease in cardiac output roughly proportional to the requirement for 

 O2 transport. There is no evidence that the contractility of the myocardium is im- 

 paired (IMcMillan) . If the heart rate is not artificially high or exceptionally low there 

 is no evidence that the cardiovascular dynamics are abnormal (D'Amato). High 

 driven rates, however, will impair filling of the heart, due to prolonged contraction 

 time (D'Amato) and (when Q-T begins to equal cycle length) will also influence 

 apparent diastolic thresholds (Brooks), causing a spurious increase. The change in 

 total and absolute refractory periods are those that would be expected from the 

 combined eft'ects of temperature and rate ( 1' rooks. Hegnauer) and thus will vary 

 unless changes in rate are eliminated. With fairly severe cooling, asystole is the 



