What causes systemic vasodilation in septic shock?

In septic shock, systemic vasodilation is primarily caused by the endo/exotoxins released by bacteria. These toxins trigger a complex inflammatory response in the body, leading to the release of various pro-inflammatory cytokines and mediators. This inflammatory cascade results in the relaxation of vascular smooth muscle, increasing the diameter of blood vessels and ultimately causing vasodilation.

As the blood vessels dilate, there is a significant drop in systemic vascular resistance, which can lead to hypotension and impaired tissue perfusion. This condition is critical in septic shock, as it ensures that despite the body's response to infection, the circulation becomes more compromised due to the inability of the vessels to maintain normal blood pressure, contributing to the multi-organ dysfunction seen in this state.

The other options, while relevant to different pathophysiological scenarios, do not specifically account for the impaired vascular tone seen in septic shock as effectively as the release of endotoxins does. For instance, an allergic reaction typically involves histamine release and localized responses, loss of circulating blood volume relates more to hypovolemic shock, and increased venous return would generally lead to better cardiac output rather than vasodilation.