STUDIES OF THERMAL INJURY. VII. PHYSIOLOGICAL MECHANISMS RESPONSIBLE FOR DEATH DURING CUTANEOUS EXPOSURE TO EXCESSIVE HEAT1

Abstract

The physiological mechanisms involved in cutaneous hyperthermia which results in acute circulatory failure and death were explored by means of kymographic recordings of respiration and carotid and right auricular pressure, electrocardiograms, rectal and sometimes heart temps., and plasma K analyses. In 27 young pigs and 5 adult dogs under nembutal anesthesia 60-75% of body was immersed in constant water bath of 47-75 [degree]C. With plasma K levels of 10 meq/L or less in unburned pigs infused with 1.12% KC1 changes in P wave or widening of QRS complex were not produced. K levels and ECG findings were similar in pigs immersed at 47-50[degree] and in dogs at 55-75 [degree]C. In pigs at 75[degree] plasma K rose rapidly above 11 meq. and was associated with or followed by serious changes in ECG. For the development of hyperthermic K poisoning, erythrocytes must have a high original conc, of this element. Thus, fatal hyperpotassemia, due to hyperthermia may occur in the pig but not in the dog. Since man and pig have similar K concs, in their erythrocytes, they are probably similarly susceptible to the development of fatal hyperpotassemia following cutaneous exposures to excessive heat. Although thermally induced disturbances of the respiratory centers may contribute to either type of hyperthermic circulatory failure, maintenance of pulmonary ven-tilation by artificial respiration does not prevent death or cause significant prolongation of the survival period.