Abstract

The formation of the pulmonary edema is dependent upon the intra- versus extravascular hydrostatic pressure gradient and on permeability alterations of the alveolocapillary membrane. The colloid-oncotic pressure gradient could be protective. It has been known for a long time that intravascular fluid loading does considerably worsen any pulmonary lesion. Whether colloids could be protective against pulmonary edema compared to crystalloids has long been discussed. The increase in hydrostatic pressure generated by colloids, however, may not always be compensated by the increase in oncotic pressure. In addition, in the case of a lesion of the membrane, leakage of colloids into the interstitium may be deleterious. It is difficult to recommend one type of solutes, since the main determinant of edema seems to be the capillary hydrostatic pressure level.

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