Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome
Abstract Background We dissected total power into its primary components to resolve its relative contributions to tissue damage (VILI). We hypothesized that driving power or elastic (dynamic) power offers more precise VILI risk indicators than raw total power. The relative correlations of these thre...
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| Format: | Article |
| Language: | English |
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BMC
2020-06-01
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| Series: | Critical Care |
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| Online Access: | http://link.springer.com/article/10.1186/s13054-020-03011-4 |
| _version_ | 1818108585201106944 |
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| author | Patricia R. M. Rocco Pedro L. Silva Cynthia S. Samary Muhammad K. Hayat Syed John J. Marini |
| author_facet | Patricia R. M. Rocco Pedro L. Silva Cynthia S. Samary Muhammad K. Hayat Syed John J. Marini |
| author_sort | Patricia R. M. Rocco |
| collection | DOAJ |
| description | Abstract Background We dissected total power into its primary components to resolve its relative contributions to tissue damage (VILI). We hypothesized that driving power or elastic (dynamic) power offers more precise VILI risk indicators than raw total power. The relative correlations of these three measures of power with VILI-induced histologic changes and injury biomarkers were determined using a rodent model of acute respiratory distress syndrome (ARDS). Herein, we have significantly extended the scope of our previous research. Methods Data analyses were performed in male Wistar rats that received endotoxin intratracheally to induce ARDS. After 24 h, they were randomized to 1 h of volume-controlled ventilation with low V T = 6 ml/kg and different PEEP levels (3, 5.5, 7.5, 9.5, and 11 cmH2O). Applied levels of driving power, dynamic power inclusive of PEEP, and total power were correlated with VILI indicators [lung histology and biological markers associated with inflammation (interleukin-6), alveolar stretch (amphiregulin), and epithelial (club cell protein (CC)-16) and endothelial (intercellular adhesion molecule-1) cell damage in lung tissue]. Results Driving power was higher at PEEP-11 than other PEEP levels. Dynamic power and total power increased progressively from PEEP-5.5 and PEEP-7.5, respectively, to PEEP-11. Driving power, dynamic power, and total power each correlated with the majority of VILI indicators. However, when correlations were performed from PEEP-3 to PEEP-9.5, no relationships were observed between driving power and VILI indicators, whereas dynamic power and total power remained well correlated with CC-16 expression, alveolar collapse, and lung hyperinflation. Conclusions In this mild-moderate ARDS model, dynamic power, not driving power alone, emerged as the key promoter of VILI. Moreover, hazards from driving power were conditioned by the requirement to pass a tidal stress threshold. When estimating VILI hazard from repeated mechanical strains, PEEP must not be disregarded as a major target for modification. |
| first_indexed | 2024-12-11T02:17:42Z |
| format | Article |
| id | doaj.art-90255798a79a436fbace49c6c52bf07d |
| institution | Directory Open Access Journal |
| issn | 1364-8535 |
| language | English |
| last_indexed | 2024-12-11T02:17:42Z |
| publishDate | 2020-06-01 |
| publisher | BMC |
| record_format | Article |
| series | Critical Care |
| spelling | doaj.art-90255798a79a436fbace49c6c52bf07d2022-12-22T01:24:08ZengBMCCritical Care1364-85352020-06-012411810.1186/s13054-020-03011-4Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndromePatricia R. M. Rocco0Pedro L. Silva1Cynthia S. Samary2Muhammad K. Hayat Syed3John J. Marini4Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de JaneiroLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de JaneiroLaboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de JaneiroDepartment of Pulmonary and Critical Care, Regions Hospital, MS11203BDepartment of Pulmonary and Critical Care, Regions Hospital, MS11203BAbstract Background We dissected total power into its primary components to resolve its relative contributions to tissue damage (VILI). We hypothesized that driving power or elastic (dynamic) power offers more precise VILI risk indicators than raw total power. The relative correlations of these three measures of power with VILI-induced histologic changes and injury biomarkers were determined using a rodent model of acute respiratory distress syndrome (ARDS). Herein, we have significantly extended the scope of our previous research. Methods Data analyses were performed in male Wistar rats that received endotoxin intratracheally to induce ARDS. After 24 h, they were randomized to 1 h of volume-controlled ventilation with low V T = 6 ml/kg and different PEEP levels (3, 5.5, 7.5, 9.5, and 11 cmH2O). Applied levels of driving power, dynamic power inclusive of PEEP, and total power were correlated with VILI indicators [lung histology and biological markers associated with inflammation (interleukin-6), alveolar stretch (amphiregulin), and epithelial (club cell protein (CC)-16) and endothelial (intercellular adhesion molecule-1) cell damage in lung tissue]. Results Driving power was higher at PEEP-11 than other PEEP levels. Dynamic power and total power increased progressively from PEEP-5.5 and PEEP-7.5, respectively, to PEEP-11. Driving power, dynamic power, and total power each correlated with the majority of VILI indicators. However, when correlations were performed from PEEP-3 to PEEP-9.5, no relationships were observed between driving power and VILI indicators, whereas dynamic power and total power remained well correlated with CC-16 expression, alveolar collapse, and lung hyperinflation. Conclusions In this mild-moderate ARDS model, dynamic power, not driving power alone, emerged as the key promoter of VILI. Moreover, hazards from driving power were conditioned by the requirement to pass a tidal stress threshold. When estimating VILI hazard from repeated mechanical strains, PEEP must not be disregarded as a major target for modification.http://link.springer.com/article/10.1186/s13054-020-03011-4Ventilatory powerVentilator-induced lung injuryAcute respiratory distress syndromeInflammationAlveolar collapse |
| spellingShingle | Patricia R. M. Rocco Pedro L. Silva Cynthia S. Samary Muhammad K. Hayat Syed John J. Marini Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome Critical Care Ventilatory power Ventilator-induced lung injury Acute respiratory distress syndrome Inflammation Alveolar collapse |
| title | Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome |
| title_full | Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome |
| title_fullStr | Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome |
| title_full_unstemmed | Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome |
| title_short | Elastic power but not driving power is the key promoter of ventilator-induced lung injury in experimental acute respiratory distress syndrome |
| title_sort | elastic power but not driving power is the key promoter of ventilator induced lung injury in experimental acute respiratory distress syndrome |
| topic | Ventilatory power Ventilator-induced lung injury Acute respiratory distress syndrome Inflammation Alveolar collapse |
| url | http://link.springer.com/article/10.1186/s13054-020-03011-4 |
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