Cerebral metabolism and circulatory arrest: Effects of duration and strategies for protection

Abstract

Hypothermic total circulatory arrest (CA) is commonly used to facilitate repair of complex congenital heart defects. However, the “safe” period of CA remains to be defined. Extended periods of hypothermic total circulatory arrest may impair cerebral metabolism and cause ischemic brain injury. This study defines the relationship between increasing durations of CA at 18 °C and cerebral metabolism, and examines the protective value of topical cooling of the head or continuous “trickle” flow (5 to 10 mL · kg −1 · min −1). Thirty-three 1-week-old piglets were randomized to six experimental groups: control; 15, 30, or 60 minutes of CA; 60 minutes of CA with topical cooling of the head; and 60 minutes of trickle flow. Animals were placed on cardiopulmonary bypass (CPB) at 100 mL · kg −1 · min −1 and cooled to 18 °C. After the experimental period of CA or trickle flow (or 60 minutes of CPB at normal flow for the control group), animals were rewarmed to 37 °C and weaned from CPB. Data were obtained before and immediately after CPB at 37 °C, and before and immediately after the experimental period at 18 °C. Parameters measured included cerebral blood flow by xenon 133 clearance, arterial and sagittal sinus blood gases, and cerebral metabolism. Hypothermic total circulatory arrest caused an impairment of cerebral metabolism that was directly proportional to CA duration ( r 2 = 0.73; p = 0.0001), and recovery of metabolic function after 60 minutes of CA improved more than 50% if the head was packed in ice. If technically feasible, CPB flow of only 5 to 10 mL · kg −1 · min −1 during hypothermia is superior to CA with respect to cerebral protection. Future studies with this model can be used to develop optimal modes of cerebral protection during neonatal heart operations.