Cerebral metabolic suppression during hypothermic circulatory arrest in humans.

Abstract

Hypothermic circulatory arrest (HCA) is used in surgery for aortic and congenital cardiac diseases. Although studies of the safety of HCA in animals have been carried out, the degree to which metabolism is suppressed in patients during hypothermia has been difficult to determine because of problems with serial measurements of cerebral blood flow in the clinical setting.
To quantify the degree of metabolic suppression achieved by hypothermia, we studied 37 adults undergoing operations employing HCA. Cerebral blood flow was estimated using an ultrasonic flow probe on the left common carotid artery, and cerebral arteriovenous oxygen content differences were calculated from jugular venous bulb and arterial oxygen saturations. Cerebral metabolic rates while cooling were then ascertained. The temperature coefficient, Q10, which is the ratio of metabolic rates at temperatures 10 degrees C apart, was determined.
The human cerebral Q10 was found to be 2.3. The cerebral metabolic rate is still 17% of baseline at 15 degrees C. If one assumes that cerebral blood flow can safely be interrupted for 5 min at 37 degrees C, and that cerebral metabolic suppression accounts for the protective effects of hypothermia, the predicted safe duration of HCA at 15 degrees C is only 29 min.
The safe intervals calculated from measured cerebral oxygen consumption suggest that shorter intervals and lower temperatures than those currently used may be necessary to assure adequate cerebral protection during hypothermic circulatory arrest.