It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2supply and/or malfunctioning O2extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats ( n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15°C, kept at 15°C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by >50% in response to cooling. O2consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h ( group 2) but recovered to only 60% in those rewarmed after 5 h ( group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2extraction function well during deep/profound hypothermia, and, despite low CO, O2supply was not a limiting factor for survival in the present experiments.
Temporary severe bradycardia due to pacemaker programming