Relationship of pulmonary edema after hemorrhagic shock to intravascular coagulation.

We examined the relationship between hemorrhage-induced alterations in the extravascular lung water content and the degree of intravascular coagulation in nonheparinized dogs. The severity of pulmonary edema was assessed by the extravascular lung water content to bloodless dry lung weight ratio (W/D), and the degree of intravascular coagulation in the lung was assessed by prior injection of 125I-labeled fibrinogen. Pulmonary edema developed in only 4 of 12 dogs (ie, W/D ratio of 4.86 +/- 0.12 ml/gm vs 3.21 +/- 0.056 in controls), while in others the W/D ratio of 3.23 +/- 0.11 was in the normal range. The animals that developed pulmonary edema also had increased 125I-activity in the lungs, while the activity was not increased in dogs that did not develop pulmonary edema. Pulmonary vascular resistance (PVR) increased to the same extent in both groups, while arterial pO2 decreased and venous admixture increased during hemorrhage only in dogs that developed pulmonary edema. Pulmonary blood volume decreased in dogs with pulmonary edema, and the decrease was largely confined to the dependent lung regions. The results suggest the activation of intravascular coagulation and pulmonary thromboembolization in only those dogs developing pulmonary edema. The relationship of intravascular coagulation to edema in these animals suggests that the edema was due to activation of cellular (eg, granulocytes) or humoral factors (eg, fibrin degradation products) associated with intravascular coagulation. However, most dogs subjected to hemorrhage did not have intravascular coagulation in lungs and did not develop pulmonary edema. Thus, differences in activation of intravascular coagulation may explain why pulmonary edema does not commonly occur after hemorrhage.