344 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



direct vision, using hypothermia, 11 (23 per cent) had ventricular fibrillation. By 

 using 5 per cent carbon dioxide in oxygen and an artificial respirator, we have had 

 only one case of ventricular fibrillation in twelve operations. All except one of the 

 fibrillators in which blood chemistries were measured had pH's above 7.45 during 

 cooling. 



Profound cooling has also been successfully carried out in monkeys. Using car- 

 bon dioxide, it has been possible to cool monkeys to temperatures below 10° C. 

 without ventricular fibrillation and successfully resuscitate them. So far we have 

 cooled five monkeys and lost only one. One of them had his cardiac action arrested 

 for 56 minutes and was perfectly normal after he recovered. 



Dr. B. F. Hodman: Several other people who have studied hypothermia have 

 noticed this same electrocardiographic change which Dr. Hegnauer mentioned. The 

 electrocardiogram reveals an elevated junction, J, and ST primarily below the base 

 line.* I am impressed by the potassium and calcium interrelationships which Dr. 

 Hegnauer has mentioned, and I think that we could account for this type of ECG 

 on the basis of the electrolyte abnormalities which he has found. The normal 

 cardiac action potential reveals a prominent plateau prior to repolarization. In the 

 ventricle the effect of increased extracellular calcium is to change the configuration 

 of the action potential so that the plateau is abolished. 



If we assume that some of the fibers in the ventricular myocardium are more 

 strongly influenced by calcium than others and thus have some fibers repolarizing 

 along the normal time course and others along a "high calcium" time course, and 

 we take an electrocardiogram from that ventricle, we will get a tracing exactly like 

 the ones which he has recorded. This is a known effect of high calcium on the ven- 

 tricular muscle. I don't think we should imply, on the other hand, that this ECG 

 configuration would result only from high extracellular calcium, because localized 

 anoxia also abolishes the plateau from the ventricular action potential, and with 

 anoxia of 15 or 20 minutes' duration one sees an action potential configuration 

 similar to that produced by Ca excess. With some areas of the heart more anoxic 

 than others, we would again have a situation obtaining in the cells which would 

 result in an elevated J, a depressed ST segment and very deep T wave which tends 

 to stay on one side of the base line. 



I think that if this tracing recorded from dogs prior to fibrillation has any gen- 

 eral significance, it is probably that some influence, either anoxia or change in 

 calcium and potassium fluxes across the cell, has progressed further in some 

 localized area than in other parts of the heart. 



I might emphasize that whenever we do not have a uniform condition obtaining 

 in the ventricle, the heart is much more susceptible to fibrillation than when all of 

 the cells follow a similar time course of depolarization and repolarization. 



Dr. Gollan: We have heard from different investigators that a hypothermic heart 

 whose coronary circulation is perfused with oxygenated blood, does not lose potas- 

 sium, continues to heal at lower temperatures and is protected against ventricular 

 fibrillation. These phenomena, especially the remarkal)k' tolerance to myocardial 

 ischemia, can be observed in the dog wlinse venous blood is passed through a small 

 oxygenator and returned into the left subclaxian artt-ry. 



* Dr. Hoffman illustrated this and the following ECG contiguratiuns at tlie hlackhoard. 



