title: Failure of retrograde cerebral perfusion to attenuate metabolic changes associated with hypothermic circulatory arrest.
abstract: OBJECTIVE
  Although retrograde cerebral perfusion has become a popular adjunctive technique and may improve cerebral ischemic tolerance during hypothermic circulatory arrest, direct cerebral metabolic benefit has yet to be demonstrated in human subjects. We investigated the post-arrest metabolic phenomena with and without retrograde cerebral perfusion in patients.
  
  
  METHODS
  In a prospective randomized trial, 42 patients undergoing aortic surgery requiring hypothermic circulatory arrest were allocated to receive hypothermic circulatory arrest alone (n = 21) or hypothermic circulatory arrest with additional retrograde cerebral perfusion (n = 21). Circulatory arrest was commenced at 15 degrees C, and retrograde perfusion was instituted through the superior vena cava at a maximum jugular bulb pressure of 25 mm Hg. Transcranial, paired, repeated samples of the arterial and jugular bulb blood were analyzed for oxygen and glucose. Velocity in the right middle cerebral artery was also measured simultaneously.
  
  
  RESULTS
  There were 3 (7.1%) deaths and 3 (7.1%) episodes of neurologic deficit. Mean bypass and circulatory arrest duration (in minutes) were similar between groups (P =.4 and.14). The mean retrograde perfusion duration was 23 minutes. Post-arrest nasopharyngeal temperature was similar (15.3 degrees C vs. 15.3 degrees C). Retrograde perfusion did not affect post-arrest oxygen extraction, glucose extraction, or jugular bulb Po(2). There was no immediate lactate release immediately after hypothermic circulatory arrest.
  
  
  CONCLUSIONS
  Retrograde cerebral perfusion did not influence immediate post-arrest nasopharyngeal temperature or cerebral metabolic recovery. The low jugular bulb Po(2) suggests equivalent ischemia. These findings cast doubt on the effectiveness of retrograde cerebral perfusion as a metabolic adjunct to hypothermic circulatory arrest.
authors.affiliation: Cardiothoracic Surgical Unit and Department of Anaesthesia and Intensive Care, University Hospital Birmingham Queen Elizabeth Medical Centre, Birmingham, United Kingdom. r.s.bonser@bham.ac.uk
authors.forename: R S
authors.initials: RS
authors.lastname: Bonser
authors.forename: C H
authors.initials: CH
authors.lastname: Wong
authors.forename: D
authors.initials: D
authors.lastname: Harrington
authors.forename: D
authors.initials: D
authors.lastname: Pagano
authors.forename: M
authors.initials: M
authors.lastname: Wilkes
authors.forename: T
authors.initials: T
authors.lastname: Clutton-Brock
authors.forename: M
authors.initials: M
authors.lastname: Faroqui
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002545:Brain Ischemia / Q000378:metabolism / Q000517:prevention & control*; D001026:Coronary Artery Bypass / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D006324:Heart Arrest, Induced / Q000379:methods*; D006350:Heart Valve Prosthesis; D006801:Humans; D007036:Hypothermia, Induced; D008297:Male; D008875:Middle Aged; D016343:Monitoring, Intraoperative; D010477:Perfusion / Q000009:adverse effects* / Q000379:methods; D011336:Probability; D011446:Prospective Studies; D012016:Reference Values; D015996:Survival Rate; D017211:Treatment Failure