Cerebral blood flow decreases with time whereas cerebral oxygen consumption remains stable during hypothermic cardiopulmonary bypass in humans

Donald Prough, A. T. Rogers, D. A. Stump, R. C. Roy, A. R. Cordell, J. Phipps, C. L. Taylor

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Recent investigations demonstrate that cerebral blood flow (CBF) progressively declines during hypothermic, nonpulsatile cardiopulmonary bypass (CPB). If CBF declines because of brain cooling, The cerebral metabolic rate for oxygen (CMRO2) should decline in parallel with the reduction in CBF. Therefore we studied the response of CBF, the cerebral arteriovenous oxygen content difference (A - VD(cere)O2), and CMRO2 as a function of the duration of CPB in humans. To do this, we compared the cerebrovascular response to changes in the PaCO2. Because sequential CBF measurements using xenon 133 (133Xe) clearance must be separated by 15-25 min, we hypothesized that a time-dependent decline in CBF would accentuate the CBF reduction caused by a decrease in PaCO2, but would blunt the CBF increase associated with a rise in PaCO2. We measured CBF in 25 patients and calculated the cerebral arteriovenous oxygen content difference using radial arterial and jugular venous bulb blood samples. Patients were randomly assigned to management within either a lower (32-48 mm Hg) or higher (50-71 mm Hg) range of PaCO2 uncorrected for temperature. Each patient underwent two randomly ordered sets of measurements, one at a lower PaCO2 and the other at a higher PaCO2 within the respective ranges. Cerebrovascular responsiveness to changes in PaCO2 was calculated as specific reactivity (SR), the change in CBF divided by the change in PaCO2, expressed in mL·100 g-1·min-1·mm Hg-1. In the entire group of 25 subjects, SR was 0.69 ± 0.33 mL·100 g-1·min-1·mm Hg-1 (SD) if PaCO2 was reduced and 0.10 ± 0.30 mL·100 g-1·min-1·mm Hg-1 if PaCO2 was increased (P < 0.001). In patients managed within the lower range of PaCO2, SR was 0.63 ± 0.31 and 0.21 ± 0.17, respectively, when PaCO2 was reduced or increased (P < 0.05). In patients managed within the higher range of PaCO2, SR was 0.76 ± 0.38 and -0.01 ± 0.36, respectively, when PaCO2 was reduced or increased (P < 0.01). Estimated CMRO2 remained constant within groups from the initial to the repeat measurements. These results confirm a significant time-dependent decline of CBF during CPB. Moreover, by demonstrating that CMRO2 did not change significantly as PaCO2 was altered in either direction, they suggest that the CBF reduction cannot be attributedd to progressive brain cooling during stable, hypothermic, nonpulsatile CPB, but must result from an alteration in cerebrovascular resistance.

Original languageEnglish (US)
Pages (from-to)161-168
Number of pages8
JournalAnesthesia and Analgesia
Issue number2
StatePublished - 1991
Externally publishedYes



  • Brain, oxygen consumption-blood flow
  • Hypothermia, Induced
  • Measurement techniques, cerebral blood flow
  • Surgery, cardiac

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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