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J Thorac Cardiovasc Surg 2002;123:943-950
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Failure of retrograde cerebral perfusion to attenuate metabolic changes associated with hypothermic circulatory arrest

From the Cardiothoracic Surgical Unit^a and Department of Anaesthesia and Intensive Care,^b University Hospital Birmingham Queen Elizabeth Medical Centre, Birmingham, United Kingdom.

This work was supported by the Kate Weeks Research Fellowship of the Royal College of Surgeons of England.

These data were presented in part at the American Heart Association Scientific Sessions, Atlanta, November 1999.

Received for publication Oct 11, 2000. Revisions requested Feb 5, 2001; revisions received Aug 1, 2001. Accepted for publication Sept 18, 2001. Address for reprints: Robert S. Bonser, FRCS, MRCP, Cardiothoracic Surgical Unit, Queen Elizabeth Hospital, Edgbaston, Birmingham, B15 2TH, United Kingdom (E-mail: r.s.bonser{at}bham.ac.uk).

Objectives: 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°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°C vs 15.3°C). Retrograde perfusion did not affect post-arrest oxygen extraction, glucose extraction, or jugular bulb PO₂. 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 PO₂ suggests equivalent ischemia. These findings cast doubt on the effectiveness of retrograde cerebral perfusion as a metabolic adjunct to hypothermic circulatory arrest.

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