Septic shock is not only an infection problem. It is a vascular biology problem.
Patients develop vasodilation, endothelial dysfunction, capillary leak, inflammatory dysregulation, impaired catecholamine responsiveness, and sometimes relative corticosteroid insufficiency. This is why corticosteroids remain part of the septic shock conversation.
The central physiologic idea is vascular responsiveness. In septic shock, blood vessels may become less responsive to endogenous catecholamines and administered vasopressors.
Corticosteroids may improve vascular tone by increasing adrenergic receptor sensitivity, reducing nitric oxide-mediated vasodilation, stabilizing endothelial function, and modulating inflammatory signaling.
This does not mean steroids are simply "anti-inflammatory drugs" in sepsis. At the bedside, they often function as hemodynamic support.