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

Because disordered autoregulation of cerebral blood now may underlie n eurologic injury associated with cardiopulmonary bypass (CPB), we stud ied the effects of normothermic (37 degrees C) and hypothermic (18 deg rees 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 pr otocol. 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 calcul ate CVR per millimeter of mercury change in arterial partial pressure of CO2: (CVR(normocapnia) - CVR(hypercapnia))/(PaCO2 hypercapnia - PaC O2 normocapnia). Before CPB, CBF, CMRO(2), and vascular reactivity to elevated CO2 were similar in the three groups; these parameters remain ed unchanged by normothermic CPB. However, during hypothermic CPB, CBF and CMRO(2) decreased in both alpha-stat and pH-stat groups; in the a lpha-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 m L . min(-1). 100 g(-1) (p < 0.05), whereas in the pH-stat group CBF de creased 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). 10 0 g(-1) (p < 0.05). Hypercapnic vascular reactivity during hypothermic CPB was abolished during alpha-stat management (0.065 +/- 0.013 [norm othermic 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 o n CPB (1) hypothermic CPB causes a profound decrease in CBF and CMRO(2 ), (2) cerebrovascular reactivity to CO2 is decreased during hypotherm ic CPB with alpha-stat but not pH-stat management of arterial blood ga ses, and (3) regardless of method of blood gas management during CPB, CBF, CMRO(2), and hypercapnic reactivity are restored to pre-CPB value s after CPB.