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  • Title: Postoperative hypoxemia exacerbates potential brain injury after deep hypothermic circulatory arrest.
    Author: Tsui SS, Schultz JM, Shen I, Ungerleider RM.
    Journal: Ann Thorac Surg; 2004 Jul; 78(1):188-96; discussion 188-96. PubMed ID: 15223426.
    Abstract:
    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 degrees to 18 degrees 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 x 100 g(-1) x 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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