The Shock Cascade (def)

As a result of the excessive inflammatory response from cytokines such as TNF-alpha, Il-1, Il-6, Il-8, and PAF, the following sequence of events may occur:

• Blood vessels dilate (def) and phagocytic WBCs called neutrophils adhere to capillary walls in massive amounts (see Fig. 3). As seen above, chemokines cause neutrophils to release proteases and toxic oxygen radicals, the same chemicals they use to kill microbes, but these toxic chemicals are now being dumped onto the vascular endothelial cells to which the neutrophils have adhered during diapedesis. This results in damage to the capillary walls.
• Prolonged vasodilation and increased capillary permeability causes plasma (def) to leave the bloodstream and enter the tissue . Prolonged vasodilation also leads to decreased vascular resistance and a resultant drop in blood pressure or hypotension (def) . Damage to the capillaries causes blood to leave the bloodstream and enter the tissue resulting in a decreased volume of circulating blood or hypovolemia (def). The increased capillary permeability also results in acute inflammation in the lungs, injury to capillaries in the alveoli of the lungs, and pulmonary edema (acute respiratory distress syndrome or ARDS) (def) . Activation of the blood clotting pathway causes clots to form within the blood vessels throughout the body (disseminated intravascular coagulation or DIC) (def).
• The combination of hypotension, hypovolemia, DIC, and ARDS, leads to acidosis (def) and decreased cardiac output that, in turn, can result in irreversible septic shock (def), multiple system organ failure or MSOF (def), and death (see Fig. 2).