Sepsis pathogenesis involves a dual-phase immune response. The initial hyperinflammatory phase features activation of pattern recognition receptors (TLRs, NOD-like receptors) by PAMPs, triggering NF-κB-mediated cytokine release (TNF-alpha, IL-1β, IL-6). This cascade activates the complement system, coagulation cascade (tissue factor pathway), and endothelial dysfunction. Nitric oxide overproduction causes refractory vasodilation. Glycocalyx degradation increases capillary permeability. Subsequently, an immunosuppressive phase (immune paralysis) develops with lymphocyte apoptosis, monocyte deactivation, and increased susceptibility to secondary infections. Organ dysfunction is quantified by the SOFA score: a ≥2-point increase identifies sepsis. Septic shock is sepsis with vasopressor requirement to maintain MAP ≥65 and lactate >2 despite adequate fluid resuscitation. The clinician orders the initial resuscitation protocol, prescribes empiric antimicrobials, initiates vasopressor therapy, identifies and controls the infectious source, and manages multi-organ support.