Abstract

The water flux across the capillary membrane is directly related to a gradient of hydrostatic and colloid osmotic forces. The membrane is not an absolute barrier to proteins. Any change in the capillary permeability tends to decrease the plasmatic colloid osmotic pressure. The interstitial space includes a perimicrovascular space and a compliant connective tissue space, where oedema accumulates. The lymphatics may easily drain excess filtration, but cannot clear constituted oedema. Primarily, the risk of pulmonary oedema determines the lower limit of the colloid osmotic pressure. During the perioperative period, any extrapolation of the colloid, osmotic pressure from protidaemia or albuminaemia would be approximate. Two major conclusions can be drawn from the results of Guyton and Lindsey. First, in the absence of left ventricular failure, a 50% decrease in colloid osmotic pressure does not increase extravascular lung water. Second, in the case of left ventricular failure, when the left atrial pressure exceeds 10 mmHg, a 50% decrease in colloid osmotic pressure significantly increases the risk of pulmonary oedema. In these experiments, an impairment in capillary membrane permeability is likely. As a result, the threshold at which extravascular water starts to accumulate cannot be precisely defined. However, in the perioperative period, capillary membrane permeability is frequently altered by the acute phase reaction. Finally, in most perioperative clinical situations, a 50% decrease in colloid osmotic pressure may not require any treatment.

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