Therapeutic Hypothermia

Abstract

Therapeutic hypothermia, introduced more than 5 decades ago, remains an important neuroprotective factor in the surgery for the correction of congenital heart disease, in particular when intraoperative circulatory arrest is required. Hypothermia decreases cerebral metabolism and energy consumption and reduces the extent of degenerative processes such as the excitotoxic cascade, apoptotic and necrotic cell death, microglial activation, oxidative stress, and inflammation. Neurological outcome has become the focus of several studies in the recent years, and deep hypothermic circulatory arrest durations of more than 40 minutes are associated with increased mid-and long-term disability. Physiologic cerebral flowmetabolism coupling seems to be preserved with moderate and mild hypothermia, but cerebral blood flow autoregulation is probably altered after deep hypothermic circulatory arrest, suggesting disordered cerebral metabolism and oxygen use. Although evidence from animal studies suggests potential benefit from very low temperatures, postoperative development of choreoathetosis has been found to correlate with the degree of intraoperative hypothermia, recommending the use of central temperatures greater than 15°C in the clinical practice. Cooling times longer than 20 minutes are needed to obtain homogeneous brain cooling and effective neuroprotection. Finally, there is evidence that the sites of temperature monitoring used in the clinical practice may underestimate brain temperature after cardiopulmonary bypass, with the risk of postoperative hyperthermic brain damage.