title: Cerebral consequences of hypothermic circulatory arrest in adults.
abstract: Despite widespread use of hypothermic circulatory arrest (HCA) in aneurysm surgery and for repair of congenital heart defects, there is continued concern about possible adverse cerebral sequelae. The search for ways to improve implementation of HCA has inspired retrospective clinical studies to try to identify risk factors for cerebral injury, and clinical and laboratory investigations to explore the physiology of HCA. At present, risk factors associated with less favorable cerebral outcome after HCA include: prolonged duration of HCA (usually greater than 60 min); advanced patient age; rapid cooling (less than 20 min); hyperglycemia either before HCA or during reperfusion; preoperative cyanosis or lack of adequate hemodilution; evidence of increased oxygen extraction before HCA or during reperfusion; and delayed reappearance of electroencephalogram (EEG) or marked EEG abnormality. Strategies advocated to increase safety of HCA include: pretreatment with barbiturates and steroids; use of alpha-stat pH regulation during cooling and rewarming; intraoperative monitoring of EEG; slow and adequate cooling, including packing of the head in ice; monitoring of jugular venous oxygen content; hemodilution; and avoidance of hyperglycemia. Current investigation focuses on delineating the relationship of cerebral blood flow (CBF) to cerebral oxygen consumption and glucose metabolism during cooling, HCA, rewarming, and later recovery, and identifying changes in acute intraoperative parameters, including the presence of intracerebral enzymes in cerebral spinal fluid, with cerebral outcome as assessed by neurological evaluation, quantitative EEG, and postmortem histology. Clinically, intraoperative monitoring of EEG and measurement of CBF by tracer washout or Doppler flows are contributing to better understanding of the physiology of HCA, and in the laboratory, nuclear magnetic resonance (NMR) spectroscopy has provided valuable insights into the kinetics of intracerebral energy metabolism. Promising strategies for the future include investigation of other pharmacological agents to increase cerebral protection, and use of "cerebroplegia" or intermittent perfusion between intervals of HCA to improve cerebral tolerance for longer durations of HCA.
authors.affiliation: Department of Cardiothoracic Surgery, Mount Sinai Medical Center, New York, New York 10029.
authors.forename: E B
authors.initials: EB
authors.lastname: Griepp
authors.forename: R B
authors.initials: RB
authors.lastname: Griepp
mesh_terms: D000818:Animals; D001463:Barbiturates / Q000627:therapeutic use; D001831:Body Temperature; D001921:Brain / Q000098:blood supply / Q000378:metabolism; D001930:Brain Injuries / Q000175:diagnosis / Q000453:epidemiology* / Q000517:prevention & control; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D004285:Dogs; D005947:Glucose / Q000378:metabolism; D006324:Heart Arrest, Induced / Q000009:adverse effects* / Q000379:methods / Q000592:standards; D006438:Hemodilution / Q000379:methods; D006801:Humans; D007036:Hypothermia, Induced / Q000009:adverse effects* / Q000379:methods / Q000592:standards; D007361:Intelligence Tests; D016343:Monitoring, Intraoperative; D009460:Neurologic Examination; D010100:Oxygen / Q000378:metabolism; D011433:Propranolol / Q000627:therapeutic use; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D001463:Barbiturates; D002121:Calcium Channel Blockers; D011433:Propranolol; D005947:Glucose; D010100:Oxygen