Positive end-expiratory pressure accelerates lung water accumulation in high surface tension edema.
The effect of positive end expiratory pressure (PEEP) on the rate of lung water accumulation with high surface tension pulmonary edema was examined. Alveolar surface tension was elevated by inhalation of 15 mg/kg of the aerosolized detergent dioctyl sodium sulfosuccinate (OT). Hemodynamic measurements, blood gases, and colloid oncotic pressures were recorded in anesthesized dogs for 2 hours after surfactant displacement and elevation of PEEP to 10 cm H2O pressure (group II; n = 10). These data were compared with those of an identical protocol that used only 5 cm H2O PEEP (group I; n = 10). Pulmonary extravascular water volume (PEWV) was measured gravimetrically at the end of the experiment. OT inhalation resulted in an immediate fall in Pao2 and rise in venous admixture (QVa/QT), with little change in colloid oncotic pressure or left atrial pressure. In group I, Pao2 and QVa/QT did not improve significantly over 2 hours, whereas both returned to near baseline in group II. PEWV was elevated in group I compared with normal PEWV (historic controls; n = 11) (6.1 +/- 0.07 - 3.6 +/- 0.01 ml/gm dry lung; p less than 0.01); however, PEWV in group II (9.1 +/- 1.0 ml/gm dry lung; p less than 0.01) was greater than in both group I and historic controls. These data indicate that high alveolar surface tension induces pulmonary edema and PEEP accelerates this edema formation.[1]References
- Positive end-expiratory pressure accelerates lung water accumulation in high surface tension edema. Nieman, G.F., Bredenberg, C.E., Paskanik, A.M. Surgery (1990) [Pubmed]
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