Individualizing mechanical ventilation: titration of driving pressure to pulmonary elastance through Young’s modulus in an acute respiratory distress syndrome animal model

Abstract

Background Mechanical ventilation increases the risk of lung injury (VILI). Some authors propose that the way to reduce VILI is to find the threshold of driving pressure below which VILI is minimized. In this study, we propose a method to titrate the driving pressure to pulmonary elastance in an acute respiratory distress syndrome model using Young’s modulus and its consequences on ventilatory-induced lung injury. Material and methods 20 Wistar Han male rats were used. After generating an acute respiratory distress syndrome, two groups were studied: (a) standard protective mechanical ventilation: 10 rats received 150 min of mechanical ventilation with driving pressure = 14 cm H2O, tidal volume < 6 mL/kg) and (b) individualized mechanical ventilation: 10 rats received 150 min of mechanical ventilation with an individualized driving pressure according to their Young’s modulus. In both groups, an individualized PEEP was programmed in the same manner. We analyzed the concentration of IL-6, TNF-α, and IL-1ß in BAL and the acute lung injury score in lung tissue postmortem. Results Global driving pressure was different between the groups (14 vs 11 cm H2O, p = 0.03). The individualized mechanical ventilation group had lower concentrations in bronchoalveolar lavage of IL-6 (270 pg/mL vs 155 pg/mL, p = 0.02), TNF-α (292 pg/mL vs 139 pg/mL, p < 0.01) and IL-1ß (563 pg/mL vs 131 pg/mL, p = 0.05). They presented lower proportion of lymphocytes (96% vs 79%, p = 0.05) as well as lower lung injury score (6.0 points vs 2.0 points, p = 0.02). Conclusion In our model, individualization of DP to pulmonary elastance through Young’s modulus decreases lung inflammation and structural lung injury without a significant impact on oxygenation.

Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway

“…However, MV can cause lung injury, namely ventilator-induced lung injury (VILI), which predisposes patients to inflammatory response syndrome or multiple organ failure with a mortality rate of nearly 50% [ 1 ], making it an urgent clinical problem to be solved. The primary causes of VILI are mechanical power and the duration of ventilator exposure [ 2 ]. Current studies suggest that VILI is not only a mechanical trauma but also a biotrauma, which activates a complex signaling cascade in the lung [ 3 , 4 ].…”

Predictive performance of the variation rate of the driving pressure on the outcome of invasive mechanical ventilation in patients with acute respiratory distress syndrome

“… 8 ΔP is positively correlated to the incidence of ventilator-induced lung injury. 9 , 10 High ΔP values, specifically exceeding 14 cmH 2 O (1 cmH 2 O = 0.098 kPa), can be associated with poor prognosis and increased mortality in patients with ARDS. 1 , 8 , 11 Amato et al.…”

Dynamic lung aeration and strain with positive end-expiratory pressure individualized to maximal compliance versus ARDSNet low-stretch strategy: a study in a surfactant depletion model of lung injury

“…However, a fixed protocolized PEEP, even when relatively high, failed to improve outcomes in acute respiratory distress syndrome (ARDS) [9] and surgical patients [10,11]. With this, more recently, old [12] and new [13][14][15] methods to individualize PEEP have been emphasized in the expectation that those would more appropriately optimize lung physiology and outcomes.…”