Cardiac output augmentation during hypoxemia improves cerebral metabolism after hypothermic cardiopulmonary bypass

Hypothermic circulatory arrest (HCA) impairs cerebral oxygen delivery (CDO2) and cerebral oxygen consumption (CMRO2), which are further reduced by perioperative hypoxemia. This study investigates if continuous hypothermic low-flow cardiopulmonary bypass (HLF) or intermittent hypothermic low-flow cardiopulmonary bypass (IHLF) can prevent reductions in CDO2 and CMRO2 during hypoxemia.

Eighteen neonatal piglets, cooled to 16 degrees to 18 degrees C with cardiopulmonary bypass (CPB), were randomly assigned into three groups: HCA, HLF (50 cc.kg(-1).min(-1)), or IHLF (1 minute of HLF for every 15 minutes of HCA). After 60 minutes of hypothermia, normothermic CPB (100 cc.kg(-1).min(-1)) was established and cerebral perfusion data measured at hyperoxemia (PaO2 150 to 250 mm Hg), hypoxemia (PaO2 50 to 60 mm Hg), and severe hypoxemia (PaO2 30 to 40 mm Hg), and with increased CPB flow (200 cc.kg(-1).min(-1)) during severe hypoxemia.

The CMRO2 (in mL O2.100 g(-1).min(-1)) was lower after HCA (2.5 +/- 0.3), compared with HLF (4.1 +/- 0.5, p = 0.02) and IHLF (6.2 +/- 0.8, p = 0.002). Within groups, the change from hyperoxemia to severe hypoxemia resulted in decreased CMRO2: HCA (1.3 +/- 0.2, p = 0.004), HLF (3.0 +/- 0.5, p = 0.01), and IHLF (2.9 +/- 0.5, p = 0.01). During severe hypoxemia, increasing CPB flow (from 100 cc.kg(-1).min(-1) to 200 cc.kg(-1).min(-1)) improved CMRO2: HCA (1.9 +/- 0.5, p = 0.05), HLF (4.2 +/- 0.5, p = 0.05), and IHLF (7.4 +/- 0.5, p = 0.04).

Hypoxemia reduces CDO2 and CMRO2 despite the method of hypothermic CPB. Increased CPB flow during hypoxemia can restore both CDO2 and CMRO2 to values found with hyperoxemia and slower CPB flows. Augmenting cardiac output during periods of perioperative hypoxemia may prevent cerebral injury after exposure to hypothermic cardiopulmonary bypass.