Increased Alveolar Damage After Mechanical Ventilation in a Porcine Model of Thoracic Surgery

Protective Ventilatory Approaches to One-Lung Ventilation: More than Reduction of Tidal Volume

“…Accordingly, histological analysis of diffuse alveolar damage in a porcine model of thoracic surgery [25] established considerable alveolar and interstitial edema, neutrophil infiltration, alveolar overdistension, microhemorrhage and microatelectasis in the temporarily collapsed, surgically manipulated lung, but much more in the ventilated lung [26]. The detection of a diffusely distributed alveolar damage in both lungs indicates that mechanical ventilation may be as harmful as a period of complete lung collapse and manipulation during thoracic surgery.…”

“…Mechanical two-lung ventilation itself produces homogeneously distributed alveolar damage [26] and generates an inflammatory response in the alveoli, even in healthy lungs [27]. The resulting ventilation-induced lung injury (VILI) [28] is characterized by dysfunction of the surfactant system [29], alveolar and interstitial edema [30], leukocyte recruitment [31], cytokine production [32] and neutrophildependent tissue destruction [33].…”

Nonintubated Videothoracoscopic Operations in Thoracic Oncology

“…It is well known that OLV in itself, regardless of surgical manipulations, may induce inflammatory changes at the level of small airways and lung parenchyma, through diverse mechanisms [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22]. The latter include elevated positive pressure (barotrauma), alveolar overdistension (volutrauma) [8,10], repetitive collapse-reopening cycles (atelettrauma) [10], low oxygen tension, and the so-called reventilation injury [13,14,22].…”

“…The latter include elevated positive pressure (barotrauma), alveolar overdistension (volutrauma) [8,10], repetitive collapse-reopening cycles (atelettrauma) [10], low oxygen tension, and the so-called reventilation injury [13,14,22]. All these factors are responsible for oxidative stress [16,19,20,21] and excess recruitment of inflammatory cells, with subsequent activation of cytokine network and establishment of an inflamed microenvironment [8,[11][12][13]15].…”

“…These compartmental changes, which can involve both the dependent and non-dependent (operated) lung, configure a condition known as "Ventilator-Associated Lung Injury" (VALI). The latter leads, in turn, to interstitial edema [12,14,16], loss of surfactant [11,12], ventilationto-perfusion mismatch, and decreased lung compliance [11,12]. These effects occur in a time-dependent manner, as they increase remarkably after 1-hour of OLV [20].…”