Activated protein C tries to achieve homeostasis during sepsis by decreasing inflammation and coagulation and increasing fibrinolysis, but during sepsis, there will be a decrease in circulating protein C. When sepsis is occurring, the body’s normal regulatory mechanisms are failing and there will be uncontrolled inflammation, which will overwhelm the body’s normal protective response. Excessive coagulation, exaggerated inflammation, and abnormal fibrinolysis will not only occur in localized areas, but due to lack of regulatory mechanisms, spread throughout the body. Due to lack of regulation, systemic vasodilation, hypotension, increasing vascular permeability, increased cellular aggregation, obstruction, and accelerated coagulation may all occur. Intravascular fluid deficit will occur due to venous pooling, capillary leakage, and vasodilation. Capillary leakage, caused by increased vascular permeability, is enhanced due to chemically mediated endothelial damage, which would lead to fluid shifts from intravascular to interstitial spaces, causing generalized edema. Systemic vascular resistance will also decrease, making the patient more refractory to normal fluid replacement therapies. The accelerated coagulation along with decreased fibrinolysis due to lack of protein C will increase clotting in the blood vessels. That, along with the combination of decreased SVR, fluid shifts into interstitial spaces, and deposition of fibrin into the microvasculature space due to increased coagulation will cause microvascular hypoperfusion, which results in decreased blood flow to organs, which damages the organ and disrupts its functioning. Due to the increasing amount of clotting throughout the body not being controlled, it could also lead to a condition called