Affiliations: [a] Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 69978, Israel | [b] Department of Emergency Medicine, Tel Aviv Sourasky Medical Center, Tel Aviv 64239 and the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel | [c] Department of Clinical Respiratory Physiology, the H. Sheba Medical Center, Tel Hashomer 52621 and the Sackler Faculty of Medicine, Tel Aviv University, Israel | [d] Department of Biological and Medical Systems, Imperial College of Science, Technology and Medicine, London SW7 2BX, UK
Correspondence:
[*]
Corresponding author: Prof. David Elad, Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 69978, Israel. Tel.: 972 3 640 8476; Fax: 972 3 640 7939; E-mail: [email protected].
Abstract: Mechanical ventilation has been associated with pulmonary edema in the clinical setting, but the pathophysiological mechanisms of this process have not been clearly defined. Experimental studies have shown that high transpulmonary pressures resulting from ventilation may damage the capillary walls, thereby leading to edema. Knowledge of the stress distribution within the alveolar septa would be an important step in understanding this phenomenon. A newly developed saline-filled alveolar sac model was utilized for analysis of septal stresses in young and aging healthy lungs, in order to examine their vulnerability to pulmonary edema during ventilation. Significant stress concentrations were shown to develop near highly curved regions (small local radii of less than 4 μm) in a lung inflated to 80% could be as high as 25 times that of average septal stresses. The combination of elevated stress sites that are formed in the stiffer parenchyma of the aging lung, together with the cyclic loading of ventilation, may explain the gaps and breaks previously observed in pulmonary edema.
