BACKGROUND: Previous studies in patients undergoing cardiopulmonary bypass (CPB) have documented gastric mucosal hypoperfusion and hypoxia. This study examines the influence of the CPB protocol on the adequacy of gut blood flow and oxygenation. METHODS:Twenty-four patients were prospectively randomized into one of four CPB groups: nonpulsatile hypothermic (NP 28); pulsatile hypothermic (P 28); non-pulsatile normothermic (NP 37); and pulsatile normothermic (P 37). Gastric wall blood flow was assessed using laser Doppler flow measurement and gastric mucosal oxygenation (intramucosal pH), using tonometry. RESULTS: After 10 minutes of CPB, the NP 28 group had the greatest reduction in gastric wall blood flow (-60.6% +/- 3.8%) compared with baseline (p < 0.05). Thirty minutes into CPB, the P 37 group had less gastric mucosal hypoperfusion (-9.7% +/- 10.3%) than the NP 28 patients (-53.0% +/- 8.6%; p < 0.05). All groups showed a hyperemic response immediately after CPB. No significant differences between the four groups were found for gastric mucosal oxygenation during or after CPB. A progressive decline occurred in this variable during the period 3 to 4 hours after CPB. At this time, total-body oxygen consumption and extraction were at their maximum. CONCLUSIONS: This study found that perfusion protocol can influence mucosal blood flow, but other overriding factors that operate during and after CPB act to cause mucosal hypoxia. These findings, particularly the timing of mucosal hypoxia, may have implications for centers contemplating early extubation or "fast tracking" of patients after CPB.
RCT Entities:
BACKGROUND: Previous studies in patients undergoing cardiopulmonary bypass (CPB) have documented gastric mucosal hypoperfusion and hypoxia. This study examines the influence of the CPB protocol on the adequacy of gut blood flow and oxygenation. METHODS: Twenty-four patients were prospectively randomized into one of four CPB groups: nonpulsatile hypothermic (NP 28); pulsatile hypothermic (P 28); non-pulsatile normothermic (NP 37); and pulsatile normothermic (P 37). Gastric wall blood flow was assessed using laser Doppler flow measurement and gastric mucosal oxygenation (intramucosal pH), using tonometry. RESULTS: After 10 minutes of CPB, the NP 28 group had the greatest reduction in gastric wall blood flow (-60.6% +/- 3.8%) compared with baseline (p < 0.05). Thirty minutes into CPB, the P 37 group had less gastric mucosal hypoperfusion (-9.7% +/- 10.3%) than the NP 28 patients (-53.0% +/- 8.6%; p < 0.05). All groups showed a hyperemic response immediately after CPB. No significant differences between the four groups were found for gastric mucosal oxygenation during or after CPB. A progressive decline occurred in this variable during the period 3 to 4 hours after CPB. At this time, total-body oxygen consumption and extraction were at their maximum. CONCLUSIONS: This study found that perfusion protocol can influence mucosal blood flow, but other overriding factors that operate during and after CPB act to cause mucosal hypoxia. These findings, particularly the timing of mucosal hypoxia, may have implications for centers contemplating early extubation or "fast tracking" of patients after CPB.