Postoperative hypoxemia exacerbates potential brain injury after deep hypothermic circulatory arrest

S. S L Tsui, Jess M. Schultz, Irving Shen, Ross M. Ungerleider

Research output: Contribution to journalArticle

31 Citations (Scopus)

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°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.

Original languageEnglish (US)
Pages (from-to)188-196
Number of pages9
JournalAnnals of Thoracic Surgery
Volume78
Issue number1
DOIs
StatePublished - Jul 2004
Externally publishedYes

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Deep Hypothermia Induced Circulatory Arrest
Brain Injuries
Cardiopulmonary Bypass
Oxygen
Oxygen Consumption
Norwood Procedures
Hypoxia
Rewarming
Partial Pressure
Arterial Pressure
Perfusion
Hemodynamics

Keywords

  • 19

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Postoperative hypoxemia exacerbates potential brain injury after deep hypothermic circulatory arrest. / Tsui, S. S L; Schultz, Jess M.; Shen, Irving; Ungerleider, Ross M.

In: Annals of Thoracic Surgery, Vol. 78, No. 1, 07.2004, p. 188-196.

Research output: Contribution to journalArticle

Tsui, S. S L ; Schultz, Jess M. ; Shen, Irving ; Ungerleider, Ross M. / Postoperative hypoxemia exacerbates potential brain injury after deep hypothermic circulatory arrest. In: Annals of Thoracic Surgery. 2004 ; Vol. 78, No. 1. pp. 188-196.
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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°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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N2 - 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.

AB - 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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