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Canadian Journal of Anesthesia, Vol 21, 275-284, Copyright © 1974 by Canadian Anesthesiologists' Society
1 Departments of Anaesthesia and Pathology, St. Michael's Hospital and University of Toronto, Toronto, Ontario, Canada
Pulmonary oedema was induced in dogs by dextran overload and the amount of fluid quantitatively assessed by using a double indicator dilution technique (ETVL). Changes in ETVL and arterial oxygenation were related to light and electron microscopic alterations of lung in early oedema and in gross oedema before and after continuous positive pressure ventilation (CPPV) was applied.
In early oedema oxygenation was only minimally impaired while there was extensive fluid accumulation in the interstitium. In late oedema oxygenation was severely reduced. At the same time alveoli were filled with plasma fluid, fibrin fibres, platelets, red blood cells and polymorphonuclear leucocytes. Endothelial cells exhibited severe injury and type II pneumocytes were also abnormal. Mast cells were found to be degranulated, which may indicate that vasoactive substances released from their cytoplasm play a role in establishing the alveolar stage of oedema. Once CPPV was applied, oxygenation improved significantly. Although alveolar fluid accumulation seemed to be somewhat less, endothelial cells still exhibited abnormalities and the interstitium remained distended by accumulated fluid.
Present results indicate that CPPV improves oxygenation in gross pulmonary oedema. As CPPV can only provide a temporary symptomatic improvement without influencing underlying pathology, it can be concluded that in gross pulmonary oedema other therapeutic measures are also required to reduce the amount of accumulated fluid in the lungs.
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