The effect of sepsis and reduced colloid osmotic pressure on pulmonary edema.

The interrelationship of hydrostatic pressure and osmotic forces across the capillary membrane are described by the Starling equation [lo]. Increasing pulmonary capillary hydrostatic pressure is a cause of pulmonary edema 131. Pulmonary edema develops at a lower hydrostatic pressure when plasma colloid oncotic pressure is lowered suggesting that the gradient between colloid oncotic pressure (COP) and pulmonary artery wedge pressure (PAW) is an important factor in the development of pulmonary edema [3]. Decrease in plasma oncotic pressure (COP) can also result in a reduction in the COP-PAW gradient. Pulmonary edema has been attributed to the reduction of the COP alone [7,8]. We have previously shown that reduction of the COP without elevation of the pulmonary artery wedge pressure does not result in pulmonary edema [14, 163. Sepsis is a common denominator in patients with respiratory failure [2] and it has been suggested that altered pulmonary capillary permeability is a possible cause for the development of pulmonary edema [ 11. The purpose of this investigation is to determine the effect of both reduced COP and sepsis on the development of pulmonary edema and pulmonary dysfunction in baboons.