Fig. 2

Summary figure. Cardiac surgery with cardiopulmonary bypass impairs microcirculatory perfusion, which is monitored sublingually in patients in the perioperative period. Onset of cardiopulmonary bypass reduces sublingual microcirculatory perfusion reflected by functional capillary density (FCD), proportion of perfused vessels (PPV), and perfused vessel density (PVD) compared to baseline, whereas total vessel density (TVD) remained unaltered. The effect of cardiopulmonary bypass on microvascular flow index (MFI) differed between studies. Pathophysiological mechanisms include systemic inflammation, and activation of complement and coagulation, which causes shedding of the endothelial protective glycocalyx layer leading to endothelial injury. In addition, release of barrier disruptive mediators induce endothelial barrier disruptive signaling, resulting in capillary leakage and edema formation. Activation of the endothelium stimulates the release of nitric oxide (NO), affecting vascular tone and systemic blood pressure. Moreover, induction of endothelial adhesion molecule expression increases leucocyte rolling and extravasation. Also, activation of polymorphonuclear neutrophils causes the release of reactive oxygen species (ROS), contributing to tissue injury. Activation of platelets and coagulation are associated with the formation of microthrombi and microvascular occlusion. Collectively, these mechanisms impair microcirculatory perfusion and contribute to organ injury following cardiac surgery with cardiopulmonary bypass, with clinical and experimental treatment strategies presented in italic in white boxes. IL, interleukin; IFNy, interferon gamma; TNFα, tumor necrosis factor alpha