The short-term effects of increasing plasma colloid osmotic pressure in patients with noncardiac pulmonary edema

We infused hyperoncotic albumin (25 or 50 gm of a 50% solution) into patients with noncardiac pulmonary edema (adult respiratory distress syndrome [ARDS]) to evaluate its effect on the transmicrovascular flux from blood to pulmonary edema fluid of two radiotracers--111In-DTPA (mol wt 504) and 125I-human serum albumin (HSA) (mol wt 69,000). Two groups of patients were studied--one with a modest increase in permeability of the pulmonary alveolocapillary membrane to 125I-HSA (group 1) and another with a large increase in permeability to 125I-HSA (group 2). We used furosemide, when necessary, to minimize the effect of albumin infusion to increase the pulmonary microvascular hydrostatic pressure (Pmv), measured clinically as the pulmonary capillary wedge pressure (PCWP). Therapy significantly increased the mean colloid osmotic pressure (COP) in both groups, but not the mean PCWP or calculated Pmv. Albumin had no significant effect on the mean pulmonary transmicrovascular flux of the radiotracers in either group, despite the increase in COP. In individual patients, a change in the Pmv in response to albumin infusion was directly correlated with the change in flux of 111In-DTPA [group 1: delta In-DTPA (%) . 8.66 + 1.4 delta Pmv (%) r . 0.51, P less than 0.02; group 2: delta In-DTPA (%) . -3.43 + 1.6 delta Pmv (%) r . 0.67, P less than 0.01]. A change in the transmicrovascular flux of I-HSA also correlated with a change in the intravascular Starling forces in both groups. We conclude that albumin infusion in patients with ARDS will not augment the pulmonary transmicrovascular flux of low or high molecular-weight solutes when the effect of albumin to increase the Pmv is minimized; nor, however, does an increase in plasma COP significantly reduce the flux of such solutes