Cressoni Massimo, Chiurazzi Chiara, Gotti Miriam, Amini Martina, Brioni Matteo, Algieri Ilaria, Cammaroto Antonio, Rovati Cristina, Massari Dario, di Castiglione Caterina Bacile, Nikolla Klodiana, Montaruli Claudia, Lazzerini Marco, Dondossola Daniele, Colombo Angelo, Gatti Stefano, Valerio Vincenza, Gagliano Nicoletta, Carlesso Eleonora, Gattinoni Luciano
From the Dipartimento di Fisiopatologia Medico-Chirurgica e dei Trapianti, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milan, Italy (M.C., C.C., M.G., M.A., M.B., I.A., A. Cammaroto, C.R., D.M., C.B.d.C., K.N., C.M., E.C.); Dipartimento di Radiologia, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy (M.L.); Centro di Ricerche Precliniche, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy (D.D., S.G.); Dipartimento di Anestesia, Rianimazione ed Emergenza Urgenza, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milan, Italy (A. Colombo, L.G.); and Dipartimento di Scienze Biomediche per la Salute, Università degli Studi di Milano, Milan, Italy (V.V., N.G.).
Anesthesiology. 2015 Sep;123(3):618-27. doi: 10.1097/ALN.0000000000000727.
During mechanical ventilation, stress and strain may be locally multiplied in an inhomogeneous lung. The authors investigated whether, in healthy lungs, during high pressure/volume ventilation, injury begins at the interface of naturally inhomogeneous structures as visceral pleura, bronchi, vessels, and alveoli. The authors wished also to characterize the nature of the lesions (collapse vs. consolidation).
Twelve piglets were ventilated with strain greater than 2.5 (tidal volume/end-expiratory lung volume) until whole lung edema developed. At least every 3 h, the authors acquired end-expiratory/end-inspiratory computed tomography scans to identify the site and the number of new lesions. Lung inhomogeneities and recruitability were quantified.
The first new densities developed after 8.4 ± 6.3 h (mean ± SD), and their number increased exponentially up to 15 ± 12 h. Afterward, they merged into full lung edema. A median of 61% (interquartile range, 57 to 76) of the lesions appeared in subpleural regions, 19% (interquartile range, 11 to 23) were peribronchial, and 19% (interquartile range, 6 to 25) were parenchymal (P < 0.0001). All the new densities were fully recruitable. Lung elastance and gas exchange deteriorated significantly after 18 ± 11 h, whereas lung edema developed after 20 ± 11 h.
Most of the computed tomography scan new densities developed in nonhomogeneous lung regions. The damage in this model was primarily located in the interstitial space, causing alveolar collapse and consequent high recruitability.
在机械通气期间，应力和应变可能在不均匀的肺中局部放大。作者研究了在健康肺中，在高压/高容量通气期间，损伤是否始于自然不均匀结构（如脏层胸膜、支气管、血管和肺泡）的界面。作者还希望对病变的性质（肺萎陷与实变）进行表征。
对12只仔猪进行通气，使其应变大于2.5（潮气量/呼气末肺容积），直至出现全肺水肿。作者至少每3小时进行一次呼气末/吸气末计算机断层扫描，以确定新病变的部位和数量。对肺的不均匀性和可复张性进行量化。
首次出现新的密度影是在8.4±6.3小时（平均值±标准差）之后，其数量呈指数增加，直至15±12小时。之后，它们融合成全肺水肿。病变的中位数有61%（四分位间距，57%至76%）出现在胸膜下区域，19%（四分位间距，11%至23%）位于支气管周围，19%（四分位间距，6%至25%）位于实质内（P<0.0001）。所有新的密度影均完全可复张。肺弹性和气体交换在18±11小时后显著恶化，而肺水肿在20±11小时后出现。
计算机断层扫描显示的大多数新密度影出现在不均匀的肺区域。该模型中的损伤主要位于间质空间，导致肺泡萎陷并因此具有高可复张性。
