CEREBRAL BLOOD-FLOW DURING CARDIOPULMONARY BYPASS - INFLUENCE OF TEMPERATURE AND PH MANAGEMENT STRATEGY

Because disordered autoregulation of cerebral blood now may underlie neurologic injury associated with cardiopulmonary bypass (CPB), we studied the effects of normothermic (37 degrees C) and hypothermic (18 degrees 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 now (CBF), cerebral oxygen consumption (CMRO(2)), 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))/(PaCO2 hypercapnia - PaCO2 normocapnia). Before CPB, CBF, CMRO(2), 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 CMRO(2) 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 CFB) to 5 +/- 1 mL . min(-1). 100 g(-1) (hypothermic CPB) (p < 0.05) and CMRO(2) 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 CMRO(2) 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, CMRO(2), 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 CMRO(2), (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, CMRO(2), and hypercapnic reactivity are restored to pre-CPB values after CPB.