No abstract

To investigate the effects on cerebral perfusion by experimental venous congestion of the superior vena cava (SVC) during bicaval cardiopulmonary bypass (CPB) at 34 °C, pigs were subjected to SVC obstruction at levels of 75%, 50%, 25% and 0% of baseline SVC flow at two arterial flow levels (low, LQ, high, HQ). The cerebral perfusion was examined with near-infrared spectroscopy (NIRS), cerebral microdialysis and blood gas analysis. SVC obstruction caused significant decreases in the NIRS tissue oxygenation index (TOI) and in SVC oxygen saturations (P<0.05, both groups), while the mixed venous saturation was decreased only in the LQ group. Sagittal sinus venous saturations were measured in the HQ group and found significantly reduced in response to venous congestion (P<0.05). No microdialysis changes were seen at the group level, however, individual ischemic patterns in terms of concomitant venous desaturation, decreased TOI and increased lactate/pyruvate occurred in both groups. The total venous drainage remained stabile throughout the experiment, indicating increased flow in the inferior vena cava cannula. The results indicate that SVC congestion may impair cerebral perfusion especially in the case of compromised arterial flow during CPB. Reduced SVC cannula flow may pass undetected during bicaval CPB, if SVC flow is not specifically monitored.

Pulsatile and non-pulsatile cardiopulmonary bypass (CPB) flows may have different impact on cerebral oxygen saturation in patients with restricted cerebral arterial blood supply. Twenty patients, ten diagnosed with carotid stenosis (CS, n = 10) and ten without known carotid disease (Controls, n = 10), were subjected to one period of pulsatile and one period of non-pulsatile flow (6-8 min each) during CPB at 32°C. Cerebral oxygen saturation was registered by near-infrared light spectroscopy (NIRS).The mean arterial pressure (MAP) was significantly lowered by pulsatile CPB flow. The NIRS tissue oxygenation index (TOI) tended to decrease in the CS group and increase in the Controls during pulsatile flow compared with non-pulsatile; however, the changes were not statistically significant.No significant correlations were seen between the changes in MAP and TOI across the observation periods.In conclusion, pulsatile CPB flow caused slightly decreased mean arterial pressure while the effect on cerebral oxygenation was unclear. Pulsatile flow was not found superior to non-pulsatile flow in patients with or without carotid stenosis.