The severity of shock is associated with impaired rates of net alveolar fluid clearance in clinical acute lung injury

YF Zeyed, JA Bastarache… - American Journal of …, 2012 - journals.physiology.org
YF Zeyed, JA Bastarache, MA Matthay, LB Ware
American Journal of Physiology-Lung Cellular and Molecular …, 2012journals.physiology.org
The rate of alveolar fluid clearance (AFC) is associated with mortality in clinical acute lung
injury (ALI). Patients with ALI often develop circulatory shock, but how shock affects the rate
of AFC is unknown. To determine the effect of circulatory shock on the rate of AFC in patients
with ALI, the rate of net AFC was measured in 116 patients with ALI by serial sampling of
pulmonary edema fluid. The primary outcome was the rate of AFC in patients with shock
compared with those without shock. We also tested the effects of shock severity and …
The rate of alveolar fluid clearance (AFC) is associated with mortality in clinical acute lung injury (ALI). Patients with ALI often develop circulatory shock, but how shock affects the rate of AFC is unknown. To determine the effect of circulatory shock on the rate of AFC in patients with ALI, the rate of net AFC was measured in 116 patients with ALI by serial sampling of pulmonary edema fluid. The primary outcome was the rate of AFC in patients with shock compared with those without shock. We also tested the effects of shock severity and bacteremia. Patients with ALI and shock (n = 86) had significantly slower rates of net AFC compared with those without shock (n = 30, P = 0.03), and AFC decreased significantly as the number of vasopressors increased. Patients with positive blood cultures (n = 21) had slower AFC compared with patients with negative blood cultures (n = 96, P = 0.023). In addition, the edema fluid-to-plasma protein ratio, an index of alveolar-capillary barrier permeability, was highest in patients requiring the most vasopressors (P < 0.05). Patients with ALI complicated by circulatory shock and bacteremia had slower rates of AFC compared with patients without shock or bacteremia. An impaired capacity to reabsorb alveolar edema fluid may contribute to high mortality among patients with sepsis-induced ALI. These findings also suggest that vasopressor use may be a marker of alveolar-capillary barrier permeability in ALI and provide justification for new therapies that enhance alveolar epithelial and endothelial barrier integrity in ALI, particularly in patients with shock.
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