All of the above-clinically the multiple-organ failure patient progresses through well-defined phases. these phases include: phase 1a generalized increased capillary permeability resulting in edema, weight gain, and intravenous volume replacement, increased protein concentration in urine and lymph. although the pulmonary microvasculature has been most thoroughly studied, it is apparent that the lung is simply the most obvious end organ in a generalized permeability defect. phase 2a hypermetabolic state, with increased oxygen consumption and a compensatory increase in oxygen delivery characterized by tachycardia and high cardiac output. this condition following systemic ischemic and reperfusion is similar to hypermetabolism following endotoxemia, localized sterile inflammation, and infusion of stress hormones, suggesting a common mechanism. phase 3organ malfunction due to localized edema and cellular injury, particularly in the kidney, liver, brain, and host defense system. hemorrhagic shock predisposes to bacterial translocation and endotoxin absorption from the intestine. phase 4in the absence of systemic sepsis, organs may recover to normalcy or may be irreversibly damaged, leading to a need for chronic support. if the organ failure phases lead to systemic infection or irreversible tissue damage in the lung or brain, the death of the entire organ is likely.