The effects of plasmapheresis and hemofiltration on canine acid aspiration pulmonary edema

Aspiration of hydrochloric acid causes pulmonary capillary endothelial damage and edema. One approach to treatment is reduction of circulating volume and pulmonary wedge pressure (Ppw) to low values compatible with adequate cardiac output (Q̇T) and oxygen delivery (Q̇O₂) to the tissue. We investigated this approach in 18 dogs after intratracheal instillation of HCl. One hour after injury, animals were randomized into 3 equal groups and studied for another 4 h. Control dogs (Group C) were maintained at a Ppw of 12 mmHg throughout the experiment. In a second group (Group H), Ppw was reduced over 30 min to 5 mmHg by hemofiltration and maintained at this amount throughout the experiment. In a third group (Group P) Ppw was reduced and maintained at 5 mmHg by plasmapheresis. In Group C, extravascular thermal volume (ETV), measured in vivo, increased to 520 ml by 5 h, and venous admixture (Q̇VA/Q̇T) increased to 30%. In contrast, plasmapheresis stopped ETV accumulation at the 1-h value of 250 ml, whereas Q̇VA/Q̇T decreased to 8% at 5 h. Hemofiltration did not significantly reduce either ETV or Q̇VA/Q̇T, which were 420 ml and 30%, respectively, at 5 h. The wet weights of lungs excised at 5 h and normalized to body weight (WW/BW) confirmed that plasmapheresis reduced edema (WW/BW, 19 ml/kg) compared (p<0.05 ANOVA) with that in the control group (WW/BW, 27), and that hemofiltration did not significantly reduce edema (WW/BW, 24). We conclude that plasmapheresis reduces pulmonary capillary leak by reducing pulmonary vascular pressure, but hemofiltration to the same Ppw does not reduce edema accumulation because it aggravates the acute lung injury.