Pulmonary transvascular fluid filtration response to hypoproteinemia and hespan infusion

Abstract

Management of major blood loss utilizing protein-free fluids for volume replacement frequently results in plasma protein depletion and plasma volume expansion. These factors can increase pulmonary transvascular fluid filtration which may lead to life-threatening pulmonary edema. We studied the combined effects of plasma protein depletion and plasma volume expansion on lung lymph flow ( Q L) in awake sheep prepared with chronic lung lymph fistulae. Animals were first chronically protein depleted by batch plasmapheresis and then infused for 2 hr with either lactated Ringer's (Hypo/LR; n = 7) or 6% hydroxyethyl starch (Hespan) (Hypo/HES; n = 6). Control normoproteinemic animals (Norm/LR; n = 13) only received lactated Ringer's. Hypoproteinemia alone resulted in an average 2-fold increase in Q L over normoproteinemic baseline levels ( P ⩽-0.05). Infusion of LR into hypoproteinemic animals caused a 7.9-fold increase in Q L ( P ⩾ 0.05). By comparison, HES infusion under similar hypoproteinemic conditions limited the increase in Q L to 3.2-fold over baseline. We attributed this reduced rise in Q L to Hespan's high oncotic pressure, which dramatically widened (by 4–5 mm Hg) the pulmonary-to-lymph oncotic pressure gradient. We did not observe this with LR infusion, or in previous studies employing intravenous infusion of plasma protein. Thus, the oncotic pressure of Hespan appears to significantly limit pulmonary fluid filtration during hypoproteinemia compared to LR. We do not believe that these effects are the result of any changes in microvascular porosity.