Pathophysiology

It is driven by the initiation of the systemic inflammatory response syndrome (SIRS). This may be infective as in sepsis or noninfective as in pancreatitis or a result of multisystem organ failure. ARDS progresses through an inflammatory, exudative, proliferative and fibrotic phase. Neutrophil activation as well as the production of TNF, IL-1, IL-6 and IL-8 lead to cell injury and death. This results in an inflammatory infiltration of the lung with altered capillary permeability and accumulation of proteinaceous pulmonary edema manifest as increased extravascular lung water. Frequently hypoxic vasoconstriction is lost in the ventilated patient when 100% FiO2 is utilized. Ultimately pulmonary hypertension is the end result due to vasoconstrictors as well as microvascular thrombosis.

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