W. Cheng et al., CEREBRAL BLOOD-FLOW DURING CARDIOPULMONARY BYPASS - INFLUENCE OF TEMPERATURE AND PH MANAGEMENT STRATEGY, The Annals of thoracic surgery, 59(4), 1995, pp. 880-886
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.