Cerebral energy failure following experimental cardiac arrest Hypothermia treatment reduces secondary...

This was an experimental study performed to investigate cerebral metabolism during hypothermia treatment and rewarming after resuscitation from cardiac arrest (CA).

Sixteen pigs underwent CA followed by cardiopulmonary resuscitation (CPR). After randomisation into one hypothermic (n=8) and one normothermic group (n=8) the animals received infusion of 4 or 38 degrees C saline, respectively. Following restoration of spontaneous circulation (ROSC) both groups were observed for 360min. The hypothermic group was cooled for 180 min and then rewarmed. Temperature was not modulated in the normothermic group. Cerebral microdialysis was conducted and lactate/pyruvate (L/P)-ratio and glutamate were analysed. Intracranial pressure probe was inserted. Oxygen saturation in venous jugular bulb blood (SjO2) was analysed.

All animals initially had increased L/P-ratio (>30). A total of nine animals developed secondary increase. In the hypothermic group this was observed in 2/7 animals and in the normothermic group in 7/8 (p=0.04). Glutamate increased initially in all animals with secondary increases in two animals in each group. No differences in L/P-ratio or glutamate were detected during the rewarming phase compared to the hypothermic phase. The hypothermic group had higher SjO(2) (p=0.04). In both groups intracranial pressure increased after ROSC.

After resuscitation from CA there was a risk of cerebral secondary energy failure (reflected as an increased L/P-ratio) but hypothermia treatment seemed to counteract this effect. Cerebral oxygen extraction, measured by SjO(2,) was increased in the hypothermic group probably due to reduced metabolism. Rewarming did not reveal any obvious harmful events.