Distributive shock is characterized by massive systemic vasodilation leading to maldistribution of blood flow, decreased systemic vascular resistance (SVR), and relative hypovolemia despite normal or elevated circulating blood volume. The three major subtypes are septic shock (most common: inflammatory mediators cause vasodilation and capillary leak), anaphylactic shock (IgE-mediated mast cell degranulation releases histamine, causing vasodilation and bronchospasm), and neurogenic shock (loss of sympathetic tone from spinal cord injury above T6 causes vasodilation with bradycardia). In distributive shock, the pathological mechanism is fundamentally different from hypovolemic or cardiogenic shock: the blood vessels lose their tone and dilate massively, causing blood to pool in the periphery. This reduces venous return (preload), drops SVR and MAP, and impairs tissue perfusion despite adequate or even elevated cardiac output (in early septic shock). Capillary leak syndrome accompanies septic and anaphylactic shock, with fluid shifting from intravascular to interstitial space, worsening effective circulating volume. The hemodynamic profile shows low SVR, low-to-normal CVP/PAWP, and high cardiac output (warm shock phase) or low cardiac output (cold shock phase in late sepsis). Vasopressors targeting alpha-1 receptors are the cornerstone...