Mechanical ventilation resulted in increased pulmonary concentrations of IL-1β and KC and increased pulmonary neutrophil influx compared with non-ventilated mice.
Sepsis-induced increased pulmonary permeability also plays an important role in increased EVLWI in patients with sepsis-induced MODS.
Chronic hypoxia causes remodeling of the pulmonary vasculature with increased proliferation and migration of vascular smooth muscle cells (VSMC), increased pulmonary vascular resistance, increased pulmonary artery pressure, and right ventricular hypertrophy.
Atrial pressure must be increased in order to fill the ventricle, resulting in increased pulmonary venous pressure.
The likely explanation for these findings can be increased pulmonary transit time.
OD + HDS significantly increased pulmonary edema in ALIT as compared with OD + LDS (Fig. 4).
Moreover, underestimation of residual gastric volume due to gastric emptying disorders provides increased pulmonary aspiration risk.
Patients with acute severe thoracic trauma often have increased pulmonary EVLW.
Excessive volume administration could lead to increased pulmonary edema and subsequent ARDS.
When PEEP was increased, pulmonary edema, as evaluated by extravascular lung water (Qwl), occurred.
This maladaptive response results in increased pulmonary vascular resistance and consequently, sustained pulmonary hypertension.
