HYPOTHERMIA AND EXPERIMENTAL MYOCARDIAL 



INFARCTION* 



CHARLES HUGGINS 



We have been interested in the effect of pre-existing pathology on the safety of 

 hypothermia, particularly within the range of temperatures employed clinically. As 

 ventricular fibrillation appears to be the greatest hazard of general body cooling we 

 thought it reasonable to investigate first the effect of hypothermia on dogs with 

 heart disease. In particular, we chose to study dogs with recent myocardial infarc- 

 tions. 



Healthy male mongrel dogs were cooled to 28.5° C. by immersion in ice-water. 

 They were allowed to equilibrate (usually between 24—25° C.) for one hour, and 

 then rapidly rewarmed. This initial cooling served as a control on the health of the 

 animal, and allowed us to obtain electrocardiograms for future comparison. One 

 week after control cooling a thoracotomy was performed and the anterior descend- 

 ing branch of the left coronary artery was occluded, either by direct ligation and 

 division, or by the insertion of a small polyethylene cannula into the artery at the 

 same level. Large areas of infarction were consistently produced. Three to five clays 

 following the thoracotomy, the animal was again cooled exactly as before. 



In the first experiment 24 dogs underwent control cooling. These animals were 

 forcibly hyperventilated with pure oxygen throughout the procedure. Technical 

 errors early in the experiment caused the death of two animals. Myocardial infarcts 

 were produced in the remaining 22 animals and caused the death of 13. None of the 

 nine animals surviving both procedures died from their experimental cooling. 



We were surprised by these results and wondered if prevention of fibrillation 

 was accomplished merely by forced hyperventilation with oxygen. Accordingly, a 

 second experiment was performed which was identical with the first except that the 

 animals were hypoventilated to the point of hypoxia. Seven of twenty dogs died 

 from control cooling alone. Five of these animals fibrillated and two died with 

 nervous system damage. Seven of the 13 animals which survived cooling were 

 quadriparetic up to 48 hours. Myocardial infarcts were produced in the 13 dogs 

 which survived control cooling and five lived to undergo later experimental cooling. 

 Four of these five dogs cooled uneventfully although two exhibited transient 

 quadriparesis afterward. Death in the fifth animal was probably related to a techni- 

 cal error, but must be evaluated as a fibrillation mortality. 



All dogs which fibrillated show the same changes in the ST segment of the 

 electrocardiogram that Dr. Hegnauer has demonstrated. 



Our conclusion from this study is that in the dog the mere presence of a recent 

 myocardial infarction, even though of large size, is not a major stimulus to ventric- 

 ular fibrillation. Clinical ai)plication of this datum must be qualified by the realization 

 that the human patient with a myocardial infarction has generalized coronary artery 



* The opinions or assertions contained herein are the private ones of the writer and are not 

 to be construed as official or reflecting the views of tlie Navy Department or the naval service 

 at large. 



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