الفهرس | Only 14 pages are availabe for public view |
Abstract Rational approaches to the prevention and treatment of pulmonary edema begin with a firm understanding of not only those factors that regulate fluid flux out of the capillary, but also the removal of fluid from the interstitium. Left atrial pressure or its estimate (PCWP) may not accurately reflect changes in the true Pc, which represents the primary force driving fluid out of the capillary. The primary effect of permeability increase is to exaggerate the effect of increase in capillary pressure on edema production. Another confounding problem in critically ill patients may be increased central venous pressure, which slows the maximal rate of lymph flow from the lungs and thereby impairs a key anti edema safety factor. Postanesthetic pulmonary edema is either cardiogenic or none cardiogenic. Acute cardiogenic pulmonary edema is the manifestation of systolic and/or diastolic cardiac dysfunction and is a common reason for acute in-patient hospitalization. The hallmark of acute pulmonary edema is an increased pulmonary capillary pressure attributed to systolic and/or diastolic left ventricular dysfunction. Normal lungs have tight junctions between alveolar epithelial cells, an extensive lymphatic system, low hydrostatic pressure in the pulmonary capillaries, and other mechanisms to avoid pulmonary edema. Thus, lung injury from any number of insults can promote pulmonary edema by damaging these mechanisms. One of the important causes of postanesthetic NCPE pulmonary edema is negative pressure pulmonary edema in which it was a long time misdiagnosed. Negative pressure pulmonary edema probably occurs much more commonly than in generally recognized. Its features can easily be mistaken for other conditions such as the pulmonary aspiration of gastric contents, but it differs in that resolution is usually rapid and complete within hours of the inciting episode. Subtle episodes may be detected by pulse oximetry when clinical manifestations are minimal or absent. Preventing the development of significant amounts of pulmonary edema in critically ill patients may be associated with improved outcome. Thus, techniques that allow precise monitoring at the bedside of preload volume and lung water content may be of benefit in the management of these critically ill patients. |