Mild hypothermia reduces ventilator–induced lung injury, irrespective of reducing respiratory rate

2012 ◽  
Vol 159 (2) ◽  
pp. 110-117 ◽  
Author(s):  
Hamid Aslami ◽  
Maria T. Kuipers ◽  
Charlotte J.P. Beurskens ◽  
Joris J.T.H. Roelofs ◽  
Marcus J. Schultz ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Mild Hypothermia ◽  
Ventilator Induced Lung Injury

Mechanical Power and Development of Ventilator-induced Lung Injury

2016 ◽  
Vol 124 (5) ◽  
pp. 1100-1108 ◽  
Author(s):  
Massimo Cressoni ◽  
Miriam Gotti ◽  
Chiara Chiurazzi ◽  
Dario Massari ◽  
Ilaria Algieri ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Transpulmonary Pressure ◽  
Lung Parenchyma ◽  
Plateau Pressure ◽  
Mechanical Power ◽  
Lung Edema ◽  
Lung Weight ◽  
Ventilator Induced Lung Injury ◽  
Power Threshold

Abstract Background The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung. Methods Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold. Results In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r2 = 0.41, P = 0.001) and lung elastance (r2 = 0.33, P < 0.01) and decrease in Pao2/Fio2 (r2 = 0.40, P < 0.001) at the end of the study. Conclusion In piglets, VILI develops if a mechanical power threshold is exceeded.

Effects of respiratory rate on ventilator-induced lung injury at a constant Paco2 in a mouse model of normal lung

2008 ◽  
Vol 36 (4) ◽  
pp. 1277-1283 ◽  
Author(s):  
Katerina Vaporidi ◽  
Giorgos Voloudakis ◽  
George Priniannakis ◽  
Eumorfia Kondili ◽  
Anastasis Koutsopoulos ◽  
...  
Keyword(s):  
Lung Injury ◽  
Mouse Model ◽  
Respiratory Rate ◽  
Normal Lung ◽  
Ventilator Induced Lung Injury

scholarly journals Does Iso-mechanical Power Lead to Iso-lung Damage?

2020 ◽  
Vol 132 (5) ◽  
pp. 1126-1137 ◽  
Author(s):  
Francesco Vassalli ◽  
Iacopo Pasticci ◽  
Federica Romitti ◽  
Eleonora Duscio ◽  
David Jerome Aßmann ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tidal Volume ◽  
Respiratory Rate ◽  
Functional Residual Capacity ◽  
Mechanical Power ◽  
High Tidal Volume ◽  
High Peep ◽  
High Respiratory Rate ◽  
Ventilator Induced Lung Injury ◽  
Residual Capacity

Abstract Background Excessive tidal volume, respiratory rate, and positive end-expiratory pressure (PEEP) are all potential causes of ventilator-induced lung injury, and all contribute to a single variable: the mechanical power. The authors aimed to determine whether high tidal volume or high respiratory rate or high PEEP at iso-mechanical power produce similar or different ventilator-induced lung injury. Methods Three ventilatory strategies—high tidal volume (twice baseline functional residual capacity), high respiratory rate (40 bpm), and high PEEP (25 cm H2O)—were each applied at two levels of mechanical power (15 and 30 J/min) for 48 h in six groups of seven healthy female piglets (weight: 24.2 ± 2.0 kg, mean ± SD). Results At iso-mechanical power, the high tidal volume groups immediately and sharply increased plateau, driving pressure, stress, and strain, which all further deteriorated with time. In high respiratory rate groups, they changed minimally at the beginning, but steadily increased during the 48 h. In contrast, after a sudden huge increase, they decreased with time in the high PEEP groups. End-experiment specific lung elastance was 6.5 ± 1.7 cm H2O in high tidal volume groups, 10.1 ± 3.9 cm H2O in high respiratory rate groups, and 4.5 ± 0.9 cm H2O in high PEEP groups. Functional residual capacity decreased and extravascular lung water increased similarly in these three categories. Lung weight, wet-to-dry ratio, and histologic scores were similar, regardless of ventilatory strategies and power levels. However, the alveolar edema score was higher in the low power groups. High PEEP had the greatest impact on hemodynamics, leading to increased need for fluids. Adverse events (early mortality and pneumothorax) also occurred more frequently in the high PEEP groups. Conclusions Different ventilatory strategies, delivered at iso-power, led to similar anatomical lung injury. The different systemic consequences of high PEEP underline that ventilator-induced lung injury must be evaluated in the context of the whole body. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

scholarly journals Inhaled Hydrogen Sulfide Protects against Ventilator-induced Lung Injury

2010 ◽  
Vol 113 (1) ◽  
pp. 104-115 ◽  
Author(s):  
Simone Faller ◽  
Stefan W. Ryter ◽  
Augustine M. K. Choi ◽  
Torsten Loop ◽  
René Schmidt ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Hydrogen Sulfide ◽  
Heat Shock ◽  
Lung Injury ◽  
Heme Oxygenase ◽  
Heat Shock Protein 70 ◽  
Mild Hypothermia ◽  
Heme Oxygenase 1 ◽  
Neutrophil Accumulation ◽  
Ventilator Induced Lung Injury

Background Mechanical ventilation still causes an unacceptably high rate of morbidity and mortality because of ventilator-induced lung injury (VILI). Therefore, new therapeutic strategies are needed to treat VILI. Hydrogen sulfide can induce hypothermia and suspended animation-like states in mice. Hydrogen sulfide can also confer antiinflammatory and antiapoptotic effects. This study investigates the organ-protective effects of inhaled hydrogen sulfide during mechanical ventilation. Methods Mice were ventilated with a tidal volume of 12 ml/kg body weight for 6 h with synthetic air in the absence or presence of hydrogen sulfide (80 parts per million) and, in a second series, at either mild hypothermia or normothermia. Staining of lung sections determined the degree of lung damage by VILI score and apoptotic cells. Bronchoalveolar lavage fluid was analyzed for the cytokines interleukin-1beta and macrophage inflammatory protein-1beta and for neutrophil accumulation. Heme oxygenase-1 and heat shock protein 70 expression were assessed in the lung tissue by Western immunoblot analysis. Results Mechanical ventilation at both hypothermia and normothermia led to a profound development of VILI, characterized by pulmonary edema, increased apoptosis, cytokine release, neutrophil recruitment, and up-regulation of the stress proteins such as heme oxygenase-1 and heat shock protein 70. In contrast, the application of hydrogen sulfide during ventilation at either mild hypothermia or normothermia prevented edema formation, apoptosis, proinflammatory cytokine production, neutrophil accumulation, and inhibited heme oxygenase-1 expression. Conclusions Inhalation of hydrogen sulfide during mechanical ventilation protects against VILI by the inhibition of inflammatory and apoptotic responses. Hydrogen sulfide confers lung protection independently of its ability to induce mild hypothermia during ventilation.

Ventilator-induced lung injury

2003 ◽  
Vol 9 (3) ◽  
pp. 343-362 ◽  
Author(s):  
A ADAMS ◽  
D SIMONSON ◽  
D DRIES
Keyword(s):  
Lung Injury ◽  
Ventilator Induced Lung Injury

The circadian clock modulates susceptibility of mice to ventilator-induced lung injury

Pneumologie ◽  
2018 ◽  
Vol 72 (S 01) ◽  
pp. S10-S11
Author(s):  
M Felten ◽  
LG Teixeira Alves ◽  
C Chaput ◽  
E Letsiou ◽  
N Suttorp ◽  
...  
Keyword(s):  
Lung Injury ◽  
Circadian Clock ◽  
Ventilator Induced Lung Injury
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