Brain Luxury Perfusion during Cardiopulmonary Bypass in Humans. A Study of the Cerebral Blood Flow Response to Changes in CO2, O2, and Blood Pressure

Abstract

CBF and related parameters were studied in 68 patients before, during, and following cardiopulmonary bypass. CBF was measured using the intraarterial ¹³³Xe injection method. The extracorporeal circuit was nonpulsatile with a bubble oxygenator administering 3–5% CO₂ in the main group of hypercapnic patients (n = 59) and no CO₂ in a second group of hypocapnic patients. In the hypercapnic patients, marked changes in CBF occurred during bypass. Evidence was found of a brain luxury perfusion that could not be related to the effect of CO₂ per se. Mean CBF was 29 ml/100 g/min just before bypass, 49 ml/100 g/min at steady-state hypothermia (27°C), reached a maximum of 73 ml/100 g/min during the rewarming phase (32°C), fell to 56 ml/100 g/min at steady-state nor-mothermic bypass (37°C), and was 48 ml/100 g/min shortly after bypass was stopped. Addition of CO₂ evoked systemic vasodilation with low blood pressure and a rebound hyperemia. The hypocapnic group responded more physiologically to the induced changes in hematocrit (Htc) and temperature, CBF being 25, 23, 25, 34, and 35 ml/100 g/min, respectively, during the five corresponding periods. Carbon dioxide was an important regulator of CBF during all phases of cardiac surgery, the responsiveness of CBF being ∼4% for each 1-mm Hg change of P_aco₂. The level of MABP was important for the CO₂ response. At low blood pressure states, the CBF responsiveness to changes in P_aco₂ was almost abolished. An optimal level of P_aco₂ during hypothermic bypass of ∼25 mm Hg (at actual temperature) is recommended. A normal autoregulatory response of CBF to changes in blood pressure was found during and following bypass. The lower limit of autoregulation was at pressure levels of ∼50–60 mm Hg. CBF autoregulation was almost abolished at P_aco₂ levels of >50 mm Hg. The degree of hemodilution neither affected the CO₂ response nor impaired CBF autoregulation, although, as would be expected, it influenced CBF: In 33 women CBF was 55 ml/100 g/min at an Htc of 24%, as compared with 42 ml/100 g/min in 35 men (Htc = 28%). High P_ao₂ was a vasoconstrictor, the autoregulatory plateau being narrowed. The lower limit of autoregulation was shifted to a higher pressure when P_ao₂ was low.