Pulmonary edema pathophysiology

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

These processes can be complemented and enhanced by the liberation of biologically active cellular mediators from intracellular compartments or from the cell membrane. Thus, it is understandable that PFTs provoke inflammatory lesions and acute organ dysfunction in vitro and in vivo, and are lethal in experimental animals. When perfused through an isolated lung, PFTs provoke profound pathophysiological alterations in the pulmonary microvasculature and cause irreversible pulmonary edema. The underlying mechanisms are complex, but include a direct toxic action on endothelial cells, and the pro-... 

In order to better understand the pathophysiology associated with these various forms of pulmonary edema, a review of the morphology associated with the capillary-alveolar—intestinal interlace is useful (Fig. 6). From this review it can be seen that fluid in pulmonary capillaries is separated from the alveolar interstitial tissue by the capillary endothelial cells and the capillary basement membrane (commonly called the endothelial barrier). The alveolar surface is separated from the interstitial space by the alveolar-airway barrier, which consists of the alveolar basement membrane, alveolar epithelium, and a layer of pulmonary surfactant within the alveolus. As described previously, the alveolar interstitial tissue is made up of connective tissue (elastin and collagen), fibronectin, and mucopolysaccharides. The interstitial space also contains the pulmonary lympatic system, which functions to drain proteins, large particulate matter, and excess fluid away from the tissue space and to return them to the blood. 

The pathophysiological processes that develop in the upper and lower respiratory tract can greatly incapacitate a casualty or result in death within minutes of exposure. It is therefore imperative that adequate control of the casualty s airways be maintained. Medical personnel should look for hypoxia, hypercarbia, and pulmonary edema, all of which are signs of possible toxic inhalant exposure. Infectious bronchitis or pneumonitis (particularly in in-... 

Borak J, Dlller WE Phosgene exposure mechanisms of injury and treatment strategies. J Occup Environ Med 2001 43(2) 110-119. [PMID 11227628] (Review Of pathophysiology ahd treatment ot phosgene-induced pulmonary edema.)... 

Staub N.C. 1988. New concepts about the pathophysiology of pulmonary edema. /. Thorac. Imaging 3 8. 

Loss of alveolar surfactant activity is likely to have pathophysiological consequences. These might include an increase in the work of breathing, owing to focal or widespread atelectasis (222) augmentation of pulmonary edema, consequent to a reduction in interstitial hydrostatic pressure (223) and increased susceptibility to infection, owing to loss of the antibacterial properties of surfactant (97). Because many of the adverse effects of surfactant deficiency can be reversed... 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

The pathophysiology of IR injury in the lung involves increased leakage from the pulmonary microvasculature leading to interstitial and alveolar edema, excessive infiltration of polymorphonuclear cells into the lung, tissue inflammation, and apoptosis (de Perrot et al. 2003). 

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