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Ann Thorac Surg 1999;68:4-12
© 1999 The Society of Thoracic Surgeons

Hawley H. Seiler Resident Award Papers

Intermittent perfusion protects the brain during deep hypothermic circulatory arrest1

Stephen M. Langley, FRCSa, Paul J. Chai, MDa, Sara E. Miller, PhDa, James R. Mault, MDa, James J. Jaggers, MDa, Steven S. Tsui, MDa, Andrew J. Lodge, MDa, Ann Lefurgey, PhDa, Ross M. Ungerleider, MDa

a Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA

Address reprint requests to Dr Langley, Department of Cardiothoracic Surgery, Southampton General Hospital, Southampton, Hampshire, SO16 6YD, United Kingdom
e-mail: stephenlangley{at}dial.pipex.com

Presented at the Forty-fifth Annual Meeting of the Southern Thoracic Surgical Association, Orlando, FL, Nov 12–14, 1998.

Background. Deep hypothermic circulatory arrest (DHCA) has been shown to cause impairment in recovery of cerebral blood flow (CBF) and cerebral metabolism (CMRO2) proportional to the duration of the DHCA period. This effect on CMRO2 may be a marker for brain injury, because CMRO2 recovers normally after cardiopulmonary bypass (CPB) when DHCA is not used. The aim of this study was to investigate the effects of intermittent perfusion during DHCA on the recovery of CMRO2 after CPB and to correlate these findings with electron microscopy (EM) of the cerebral microcirculatory bed.

Methods. Fifteen neonatal piglets were placed on CPB and cooled to 18°C. Each animal then underwent either: (1) 60 minute continuous CPB (control), (2) 60 minute uninterrupted DHCA (UI-DHCA), or (3) 60 minute DHCA with intermittent perfusion (1 minute every 15 minutes) (I-DHCA). All animals were then rewarmed and weaned from CPB. Measurements of CBF and CMRO2 were taken before and after CPB. A further 9 animals underwent CPB without DHCA (2 animals) or with DHCA (7 animals), under various conditions of arterial blood gas management, intermittent perfusion, and reperfusion time.

Results. UI-DHCA resulted in significant impairment to recovery of CMRO2 after CPB (p < 0.05). Regardless of the blood gas strategy used, the EM after UI-DHCA revealed extensive damage characterized by perivascular intracellular and organelle edema, and vascular collapse. I-DHCA, on the other hand, produced a pattern of normal CMRO2 recovery identical to controls, and the EM was normal for both these groups.

Conclusions. Intermittent perfusion during DHCA is clinically practical and results in normal cerebral metabolic and ultrastructural recovery. Furthermore, the correlation between brain structure and CMRO2 suggests that monitoring CMRO2 during the operation may be an outstanding way to investigate new strategies for neuroprotection designed to reduce cerebral damage in children undergoing correction of congenital cardiac defects.




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