ALTERED MICROCIRCULATION IN SEPTIC SHOCK

Retrospective data analysis of microcirculation in septic shock was conducted. Sepsis is characterized by a severe microvascular dysfunction that persists despite fluid resuscitation and leads to multi-organ failure even after normalization of hemodynamics in response to fluid resuscitation, vasopressors and the treatment of infection. Several clinical studies suggest that microcirculatory alterations in severe sepsis are stronger predictors of outcome than global hemodynamic variables. Microvascular dysfunction under septic shock is related to: increased capillary permeability that manifests as a breakdown of the microvascular endothelial barrier (factors which may contribute to capillary leak syndrome include endogenous proinflammatory cytokines, angiopoietin 2, vascular endothelial growth factor); arteriolar hyporesponsiveness to vasoconstrictors and vasodilators, the loss of adrenergic sensitivity and tone of smooth muscle cells lining the arterioles; loss of the anti-adhesive function of endothelial surfaces; decreased density of perfused capillaries (due to several contributing factors: decreased deformability of erythrocytes and neutrophils; activation of the clotting cascade with fibrin deposition and the formation of microthrombi; dysfunction of vascular autoregulatory mechanisms by nitric oxide; enhanced functional arteriovenous shunting of the microcirculation).