Abstract
Mechanical ventilation is very useful in the treatment of pulmonary edema, whether of the hydrostatic or of the permeability type. Moreover, the use of positive end-expiratory pressure (PEEP) during mechanical ventilation consistently leads to better oxygenation.1 Although it was initially hoped that PEEP might “push out” water from the lungs, such promise has not been fulfilled. Moreover, the use of PEEP has resulted in an increase in extravascular lung water content during experimental permeability edema.2–3 This increase might have been the consequence of augmentation of fluid filtration through extraalveolar vessels, because of the resulting lung volume increase.4–5 Whether such a change in lung water content may occur during PEEP ventilation of pulmonary edema in patients is difficult to prove; nevertheless, this possibility has been seriously considered.6 Another cause of concern is the production of pulmonary edema as a consequence of lung acute hyperinflation. We will first present evidence that intermittent positive pressure ventilation (IPPV) with high inflation pressure (HIPPV) results in pulmonary edema; secondly we will discuss the mechanisms of HIPPV edema; and thirdly we propose to anbalyse the respective roles of airway pressure and lung volume in the production of edema, and how PEEP influences it.
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© 1991 Springer-Verlag Italia
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Dreyfuss, D., Saumon, G. (1991). Acute Pulmonary Hyperinflation and Pulmonary Edema. In: Grassino, A., Rampulla, C., Ambrosino, N., Fracchia, C. (eds) Chronic Pulmonary Hyperinflation. Current Topics in Rehabilitation. Springer, London. https://doi.org/10.1007/978-1-4471-3782-5_6
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DOI: https://doi.org/10.1007/978-1-4471-3782-5_6
Publisher Name: Springer, London
Print ISBN: 978-1-4471-3784-9
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