Mechanism of alveolar flooding in acute pulmonary oedema

Abstract

In severe pulmonary oedema, the alveoli fill rapidly with fluid of essentially the same protein composition as free interstitial fluid. The usual explanation is that the normally 'tight' alveolar epithelial intercellular junctions suddenly become freely permeable to proteins. But the pathophysiological basis for such a change is unknown. In seven anaesthetized dogs one lower lobe was filled with iso-osmotic fluid containing 125I-labelled albumin. The calculated alveolus-blood albumin permeability over three hours averaged 0.06 X 10(-7) cm/s. It decreased nearly 50% when the alveolar tracer concentration was tripled for three more hours. At autopsy, large interstitial free fluid cuffs around blood vessels and airways were found. Isolated lung lobes were filled with isosmotic fluid containing tracer albumin at 10 and 20 cmH2O (0.98-1.96 kPa) airway pressure. Free interstitial fluid cuffs developed within 30 and 10 minutes, respectively. The tracer protein concentration in the cuff fluid averaged 0.9 that of the alveolar fluid. It is postulated that the terminal airway epithelium is normally permeable to protein and water. In acute pulmonary oedema alveolar flooding may occur along the same pathway after the loose interstitial tissue space is fluid-filled and its pressure exceeds that in the airway. The anatomical site of the bulk fluid and protein leak has not been identified.