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Eur J Cardiothorac Surg · Oct 2004
Effect of cardiopulmonary bypass on cortical cerebral oxygenation during coronary artery bypass grafting.
- Sudath P Talpahewa, A Timothy Lovell, Gianni D Angelini, and Raimondo Ascione.
- Cardiothoracic Surgery, Bristol Heart Institute, Bristol Royal Infirmary, University of Bristol, Bristol BS2 8HW, UK.
- Eur J Cardiothorac Surg. 2004 Oct 1;26(4):676-81.
ObjectiveTo investigate the changes in cerebral oxygenation during coronary artery bypass grafting (CABG) with normothermic cardiopulmonary bypass (CPB) using near infrared spectroscopy.MethodsMeasurement of cerebral cortical oxygenation changes included concentration of deoxygenated haemoglobin [HHb], oxygenated haemoglobin [O(2)Hb], changes in the redox status of the cytochrome c oxidase [Cyt-Ox], cerebral saturation as expressed by the tissue oxygenation index (TOI), and cerebral blood volume (CBV) as expressed by tissue haemoglobin index (THI). Measurements were performed in 19 consecutive patients undergoing normothermic (34-36 degrees C) CPB. Data were recorded at 0.5s intervals and averaged into 30 s epochs. Data analysis was carried at baseline, 1, 20, and 40 min after start of CPB, at rewarming, on weaning from CPB, and at closing of chest.ResultsThere were no in-hospital death, neurological deficits, or myocardial infarcts. Compared to baseline, during the entire CPB duration, there was a marked reduction in [O(2)Hb] and CBV which reached their worst level 40 min after initiation of CPB (from -3.03+/-5.1 to -9.25+/-7.20 micromol/l for [O(2)Hb], and a 24% reduction for CBV (both P<0.0001). The deterioration in [O(2)Hb] was recovered by the end of surgery, while the changes in CBV persisted. No significant changes occurred with respect to [HHb], [Cyt-Ox], and TOI.ConclusionsConventional CABG is responsible for deterioration in [O(2)Hb], and CBV, which peak at 40-60 min following initiation of CPB. The changes in [O(2)Hb] are reversible whereas the reduction of CBV persists to the end of the surgery. This suggests a transient impairment in the autoregulatory mechanisms controlling cerebral blood flow following discontinuation of cardiopulmonary bypass.
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