Cerebral Perfusion during Cardiopulmonary Bypass

Abstract: Impaired superior vena cava (SVC) cannula outflow during cardiopulmonary bypass (CPB) is a frequent issue, often manifested by only marginal changes in routine monitoring parameters. Nevertheless, significant impact on cerebral perfusion may result. When detected, remedial actions involve cannula repositioning, raising the operating table, increasing the mean arterial pressure (MAP) and adding vacuum-assisted venous drainage to the CPB system. Increased venous outflow enables increased arterial flow and thereby also increased MAP and cerebral perfusion pressure (CPP). Although representing a common clinical problem, controlled studies on SVC obstruction are few and the phenomenon has not been satisfactorily characterized. This licentiate thesis is based on two animal studies. The first (I) study describes the effects on cerebral perfusion and oxygen saturation by stepwise SVC cannula obstruction in increments of 25% until fully occluded. The second (II) study describes the effects on CPP and cerebral perfusion of two different strategies for dealing with restricted cerebral venous outflow. In Study I, ten pigs during 34 ºC CPB were examined. The animals were divided into two groups receiving either low CPB blood flow (LQ), or normal CPB blood flow (HQ). Cerebral perfusion and oxygen saturation were monitored by blood gases, near-infrared light spectroscopy (NIRS) of tissue oxygen saturation (TOI), and cerebral micro-dialysis. SVC obstruction caused increased CVP and deteriorated cerebral oxygen saturation parameters, but no metabolic effects were detectable at the group level by the micro-dialysis. However, four of ten animals showed a combined pattern of decreased TOI and SVC oxygen saturation along with increased lactate/pyruvate ratio. The phenomenon appeared in both groups and in connection with both obstruction and release of obstruction, indicating the presence of individual sensitivity to impaired cerebral perfusion. CPB tubing flow measurements revealed that the total venous drainage was preserved even with the SVC completely clamped, indicating that the drainage, but not the CVP elevation, could be fully compensated by the inferior vena cava. In Study II, intracranial pressure monitoring, NIRS, and cerebral laser-Doppler flow measurements were used for surveillance along with blood gases and analysis of the glial cellmarker S100ß in sagittal sinus blood. A SVC obstruction of 75% was applied in order to achieve a distinct CPP reduction in fourteen pigs subjected to 34 ºC CPB. Two randomly assigned strategies for restoration of the CPP were examined; vasopressor treatment (VP)and partial release of obstruction (PR) mimicking a successful repositioning of the SVC cannula. Both strategies successfully restored the CPP to baseline levels, without immediate signs of severe ischemia, although intracranial and central pressures remained elevated in the VP group throughout the experiments. The analysis of S100ß showed no signs of brain damage. In conclusion, SVC congestion may impair cerebral perfusion during CPB. Reduced SVC cannula flow may pass undetected during bi-caval CPB due to a compensatory increase in IVC flow. Experimental SVC obstruction during CPB may reduce the CPP, resulting in impaired cerebral perfusion. Both vasopressor therapy and improved venous drainage can in the short term individually restore the CPP during these circumstances.