Abstract

Five patients undergoing extensive cerebral monitoring during cardiopulmonary bypass (CPB) procedures were subjected to studies on cerebral CO 2 reactivity during nonpulsatile CPB. The cerebral monitoring included recording of arterial blood pressure (BP), central venous pressure (CVP), epidural intracranial pressure (EDP), cerebral electrical activity by a cerebral function monitor (CFM), and middle cerebral artery (MCA) flow velocity by transcranial Doppler technique. The cerebral perfusion pressure (CPP) was thus continuously recorded (CPP = BP - EDP). During steady-state CPB with constant hematocrit, temperature, and arterial carbon dioxide tension (PaCO 2), MCA flow velocity varied with changing CPP in a pressure-passive manner, indicating that the cerebral autoregulation was not operative. During moderately hypothermic (28 to 32°C), nonpulsatile CPB, with steady-state hematocrit, temperature, and pump flow, we deliberately and rapidly changed PaCO 2 for periods of 1 or 2 minutes by increasing gas flow to the membrane oxygenator, thereby testing the cerebral CO 2 reactivity. Nineteen CO 2 reactivity tests, performed at CPP levels ranging from 17 to 75 mm Hg, disclosed that the cerebral CO 2 reactivity decreased with CPP, especially with CPP levels below 35 mm Hg. In these patients, concomitant changes in CPP during the CO 2 reactivity test could be compensated for by adjusting the observed change in MCA flow velocity. The corrected CO 2 reactivity values obtained in this way ranged from below 1.0 (observed at CPP levels below 20 mm Hg) to a 3.0 to 4.5% · mm Hg −1 change in PaCO 2 (observed at CPP levels above 35 mm Hg). Four CO 2 reactivity tests performed after rewarming was completed revealed corrected CO 2 reactivity values in the range from 1.3 to 1.9% · mm Hg −1 change in PaCO 2, observed at CPP in the range of 41 to 50 mm Hg. Cerebral CO 2 reactivity seems to be partially retained down to CPP levels of 20 mm Hg during moderately hypothermic, nonpulsatile CPB.

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