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Ann Thorac Surg 2004;78:188-196
© 2004 The Society of Thoracic Surgeons

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Original article: cardiovascular

Postoperative hypoxemia exacerbates potential brain injury after deep hypothermic circulatory arrest

^a Duke University Medical Center, Division of Thoracic Surgery, Durham, North Carolina, USA, Papworth Hospital, Cambridge, United Kingdom
^b Division of Pediatric Cardiac Surgery, Doernbecher Children's Hospital, Oregon Health and Science University, Portland, Oregon, USA

Accepted for publication November 7, 2003.

^* Address reprint requests to Dr Ungerleider, Pediatric Cardiac Surgery, Doernbecher Children's Hospital, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, DC8S, Portland, OR, USA 97201-3098
e-mail: ungerlei{at}ohsu.edu

Presented at the Thirty-ninth Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 31–Feb 2, 2003.

BACKGROUND: Deep hypothermic circulatory arrest (DHCA) is often used in infants undergoing the Norwood procedure. These infants are hypoxic after surgery. Previous investigations into the cerebral metabolic response and oxygen utilization after DHCA examined animals with normal arterial oxygenation. This study reports the cerebral metabolic consequences if hypoxemic conditions are present after DHCA.

METHODS: Eighteen neonatal piglets were randomly assigned to three groups. The control group was ventilated; the cardiopulmonary bypass group underwent 60 minutes of normothermic cardiopulmonary bypass, and the DHCA group underwent cardiopulmonary bypass and 60 minutes of DHCA (16° to 18°C) followed by rewarming. Hemodynamic and cerebral perfusion data were measured at an arterial partial pressure of oxygen (PaO₂) of 150 to 250 mm Hg, and then at moderate hypoxemia (PaO₂, 50 to 60 mm Hg) and severe hypoxemia (PaO₂, 25 to 35 mm Hg).

RESULTS: Cerebral oxygen delivery decreased by 44% from PaO₂ 150 to 250 mm Hg to severe hypoxemia (p < 0.001). Cerebral oxygen extraction increased from moderate hypoxemia to severe hypoxemia in the control (57.9% ± 3.7% to 71.8% ± 3.8%; p = 0.002) and cardiopulmonary bypass groups (61.2% ± 2.6% to 70.6% ± 1.2%; p = 0.035); however, the cerebral oxygen extraction of the DHCA group did not increase under these conditions (82.8% ± 1.8% to 77.9% ± 4.3%; p = 0.32). The cerebral metabolic rate of oxygen consumption of the DHCA group decreased from PaO₂ 150 to 250 mm Hg to severe hypoxemia (1.86 ± 0.20 to 0.99 ± 0.24 mL O₂ · 100 g^–1 · min^–1; p = 0.02), whereas the cerebral metabolic rate of oxygen consumption did not change under these conditions in the control and cardiopulmonary bypass groups.

CONCLUSIONS: Under hypoxemic conditions cerebral metabolic rate of oxygen consumption deteriorates after DHCA. Infants exposed to DHCA may be at greater risk of brain injury when postoperative hypoxemia is present. Because maximal cerebral oxygen extraction after DHCA occurs at moderate hypoxemia, techniques that increase cerebral oxygen delivery may reduce the risk of hypoxic brain injury.

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