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Rationale: Mechanical power (MP) is a summary variable incorporating all causes of ventilator-induced-lung-injury (VILI). We expressed MP as the ratio between observed and normal expected values (MPratio). Objective: To define a threshold value of MPratio leading to the development of VILI. Methods: In a population of 82 healthy pigs, a threshold of MPratio for VILI, as assessed by histological variables and confirmed by using unsupervised cluster analysis was 4.5. The population was divided into two groups with MPratio above or below the threshold. Measurements and main results: We measured physiological variables every six hours. At the end of the experiment, we measured lung weight and wet-to-dry ratio to quantify edema. Histological samples were analyzed for alveolar ruptures, inflammation, alveolar edema, atelectasis. An MPratio threshold of 4.5 was associated with worse injury, lung weight, wet-to-dry ratio and fluid balance (all p < 0.001). After 48 h, in the two MPratio clusters (above or below 4.5), respiratory system elastance, mean pulmonary artery pressure and physiological dead space differed by 32%, 36% and 22%, respectively (all p < 0.001), being worse in the high MPratio group. Also, the changes in driving pressure, lung elastance, pulmonary artery occlusion pressure, central venous pressure differed by 17%, 64%, 8%, 25%, respectively (all p < 0.001). Limitations: The main limitation of this study is its retrospective design. In addition, the computation for the expected MP in pigs is based on arbitrary criteria. Different values of expected MP may change the absolute value of MP ratio but will not change the concept of the existence of an injury threshold. Conclusions: The concept of MPratio is a physiological and intuitive way to quantify the risk of ventilator-induced lung injury. Our results suggest that a mechanical power ratio > 4.5 MPratio in healthy lungs subjected to 48 h of mechanical ventilation appears to be a threshold for the development of ventilator-induced lung injury, as indicated by the convergence of histological, physiological, and anatomical alterations. In humans and in lungs that are already injured, this threshold is likely to be different. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Mechanical power ratio threshold for ventilator-induced lung injury" published in the journal Intensive Care Medicine Experimental. The correction addresses two concerns that were brought to the attention of the journal: incorrect author affiliations in the PDF version of the article and a missing paragraph in Additional file 1 regarding the expected mechanical power formula. The published article has been corrected to address these issues. The publisher, Springer Nature, remains neutral with regard to jurisdictional claims and institutional affiliations. The authors of the article are listed at the end of the document. [Extracted from the article]

Rationale: The pathophysiological relationship between fluid administration, fluid balance, and mechanical ventilation in the development of lung injury is unclear., Objectives: To quantify the relative contribution of mechanical power and fluid balance in the development of lung injury., Methods: Thirty-nine healthy female pigs, divided into four groups, were ventilated for 48 hours with high (~18J/min) or low (~6J/min) mechanical power; and high (~4L) or low (~1L) targeted fluid balance., Measurements and Main Results: We measured physiological variables e.g., end-expiratory lung gas volume, respiratory-system mechanics, gas-exchange and hemodynamics, and pathological variables, i.e., lung weight, wet-to-dry ratio, and histology score of lung injury. End-expiratory lung gas volume, respiratory system elastance, strain and oxygenation significantly worsened in the two groups assigned to receive high fluid balance, irrespective of the mechanical power received. All four groups had similar lung weight (i.e., lung edema), lung wet-to-dry ratio and pathological variables. Animals with higher fluid balance developed more ascites, which was associated with a decrease in end-expiratory lung gas volume., Conclusions: In conclusion, our study did not detect a significant difference in lung injury between high and low mechanical power. Some damage is directly attributable to mechanical power, while additional injury appears to result indirectly from high fluid balance, which reduces end-expiratory lung gas volume, with ascites playing an important role in this process.