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Eur J Cardiothorac Surg 2007;31:906-914. doi:10.1016/j.ejcts.2007.01.006
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Hypoxemic reperfusion exacerbates the neurological injury sustained during neonatal deep hypothermic circulatory arrest: a model of cyanotic surgical repair

^a Oregon Health Science University, Portland, Oregon, USA
^b The Hospital for Sick Children, Toronto, Ontario, Canada

Received 4 September 2006; received in revised form 16 November 2006; accepted 5 January 2007.

^_* Corresponding author. Address: Congenital Heart Surgeons Society, Room 4431, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada. Tel.: +1 416 813 5184; fax: +1 416 813 8776. (Email: edward.hickey{at}sickkids.ca).

Objective: Deep hypothermic circulatory arrest (DHCA) is frequently used in infants undergoing the Norwood procedure. These infants are necessarily hypoxemic after separation from CPB. Considerable energy has been spent characterizing the physiological and histological consequences of DHCA, but these have largely focused on a normoxemic period of reperfusion. Furthermore, evidence has accumulated to suggest that the cerebral vascular autoregulatory mechanisms are dysfunctional following DHCA. In particular, the vasodilatation that elevates cerebral blood flow (CBF) in response to hypoxemia is absent. This study therefore aimed to investigate whether post-CPB hypoxemia exacerbates brain injury resulting from DHCA. Methods: Twelve neonatal piglets were subjected to 2 h DHCA and then separated from CPB. They were then randomized to either: Group 1, normoxic ventilation (n = 5); or Group 2, hypoxemia (n = 7), in which the arterial PaO₂ was reduced to 40–50 mmHg for the duration of reperfusion. Following a 20 h period of warm reperfusion, the animals were perfusion fixed and the brain analyzed for histological evidence of injury. Nine additional animals were studied in one of three control groups. Results: All animals survived the protocol. Post-operative parameters – including mean arterial pressure, acid–base status, inotrope requirements and arterial PaCO₂ – were similar. None of the control animals had any evidence of ischemia. Group 1 animals had moderate injury (total score 7.4 ± 1.6). In Group 2, three animals sustained irretrievable brain injury evidenced by gross edema and early liquefactive necrosis. The remaining four had severe ischemic histological changes (score 14.5 ± 1.6, p < 0.03). Conclusions: Hypoxemic reperfusion after prolonged DHCA results in increased neuronal loss. The use of DHCA for staged palliation may confer disproportionately greater cerebral risk than other patient groups. Alternatively, methods to augment oxygen delivery – such as by ECMO – may be of particular benefit in the early re-perfusion window.

Key Words: Cardiopulmonary bypass • Cerebral protection • Cyanotic • Congenital