Cerebral blood flow during cardiopulmonary bypass: Influence of temperature and pH management strategy

Because disordered autoregulation of cerebral blood flow may underlie neurologic injury associated with cardiopulmonary bypass (CPB), we studied the effects of normothermic (37°C) and hypothermic (18°C) CPB on cerebral vascular reactivity in 6 to 8-week-old piglets. Hypothermic CPB animals were subdivided into alpha-stat and pH-stat groups (n = 6 animals each group) according to acid-base management protocol. Cerebral blood flow (CBF), cerebral oxygen consumption (CMRO₂), cerebral vascular resistance (CVR), and CBF response to hypercapnia were examined before, during, and 1 hour after CPB and used to calculate CVR per millimeter of mercury change in arterial partial pressure of CO₂: (CVR_normocapnia − CVR_hypercapnia)/(PaCO_{2 hypercapnia} − PaCO_{2 normocapnia}). Before CPB, CBF, CMRO₂, and vascular reactivity to elevated CO₂ were similar in the three groups; these parameters remained unchanged by normothermic CPB. However, during hypothermic CPB, CBF and CMRO₂ decreased in both alpha-stat and pH-stat groups; in the alpha-stat group, CBF decreased from 27 ± 5 mL · min⁻¹ · 100 g⁻¹ (normothermic CPB) to 5 ± 1 mL · min⁻¹ · 100 g⁻¹ (hypothermic CPB) (p < 0.05) and CMRO₂ decreased from 1.8 ± 0.21 to 0.24 ± 0.04 mL · min⁻¹ · 100 g⁻¹ (p < 0.05), whereas in the pH-stat group CBF decreased from 28 ± 2 to 9 ± 1 mL · min⁻¹ · 100 g⁻¹ (p < 0.05) and CMRO₂ decreased from 1.63 ± 0.07 to 0.31 ± 0.09 mL · min⁻¹ · 100 g⁻¹ (p < 0.05). Hypercapnic vascular reactivity during hypothermic CPB was abolished during alpha-stat management (0.065 ± 0.013 [normothermic CPB] to −0.010 ± 0.049 mm Hg · mL⁻¹ · min⁻¹ · 100 g⁻¹ · mm Hg CO₂⁻¹ [hypothermic CPB]; p = not significant), but was preserved by pH-stat management (0.057 ± 0.009 to 0.113 ± 0.006 mm Hg · mL⁻¹ · min⁻¹ · 100 g⁻¹ · mm Hg CO₂⁻¹) (p < 0.05). After CPB, there was full recovery of normocapnic CBF, CMRO₂, and hypercapnic reactivity in all groups. We conclude that in this model of the immature animal on CPB (1) hypothermic CPB causes a profound decrease in CBF and CMRO₂, (2) cerebrovascular reactivity to CO₂ is decreased during hypothermic CPB with alpha-stat but not pH-stat management of arterial blood gases, and (3) regardless of method of blood gas management during CPB, CBF, CMRO₂, and hypercapnic reactivity are restored to pre-CPB values after CPB.