Influence of prolonged hypothermia and hyperthermia on myocardial sodium, potassium and chloride.

THE OBSERVATION", that experimental hypothermia is associated with increased myocardial excitability as evidenced by cardiac arrhythmias and an increased incidence of ventricular fibrillation, is well documented.Gollan, Eudolph, and Olsen found that in dogs induction of hypothermia to a rectal temperature of approximately 23 C. resulted in a significant decrease in potassium, increase in bromide and no change in sodium content of the atrium. These authors suggested that the increased myocardial excitability during hypothermia is caused or accompanied by a loss of potassium and an inability to extrude sodium. Covino and Hegnauer, on the basis of coronary arteriovenous differences, reported that hypothermic-hypercapneic dogs, that subsequently developed ventricular fibrillation, exhibited a loss of myocardial K and H ions and an apparent gain of Ca ion. Xormocapneic and hypercapneic dogs that did not develop fibrillation failed to exhibit these changes. On the other hand, Swan found that at a rectal temperature of 30 C. the mildly acidotic dog shows a positive balance of potassium in the myocardium, as determined by coronary arteriovenous differ-