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Driving pressure and mechanical power: new targets for VILI prevention.

ABSTRACT: Several factors have been recognized as possible triggers of ventilator-induced lung injury (VILI). The first is pressure (thus the 'barotrauma'), then the volume (hence the 'volutrauma'), finally the cyclic opening-closing of the lung units ('atelectrauma'). Less attention has been paid to the respiratory rate and the flow, although both theoretical considerations and experimental evidence attribute them a significant role in the generation of VILI. The initial injury to the lung parenchyma is necessarily mechanical and it could manifest as an unphysiological distortion of the extracellular matrix and/or as micro-fractures in the hyaluronan, likely the most fragile polymer embedded in the matrix. The order of magnitude of the energy required to break a molecular bond between the hyaluronan and the associated protein is 1.12×10-16 Joules (J), 70-90% higher than the average energy delivered by a single breath of 1L assuming a lung elastance of 10 cmH2O/L (0.5 J). With a normal statistical distribution of the bond strength some polymers will be exposed each cycle to an energy large enough to rupture. Both the extracellular matrix distortion and the polymer fractures lead to inflammatory increase of capillary permeability with edema if a pulmonary blood flow is sufficient. The mediation analysis of higher vs. lower tidal volume and PEEP studies suggests that the driving pressure, more than tidal volume, is the best predictor of VILI, as inferred by increased mortality. This is not surprising, as both tidal volume and respiratory system elastance (resulting in driving pressure) may independently contribute to the mortality. For the same elastance driving pressure is a predictor similar to plateau pressure or tidal volume. Driving pressure is one of the components of the mechanical power, which also includes respiratory rate, flow and PEEP. Finding the threshold for mechanical power would greatly simplify assessment and prevention of VILI.

SUBMITTER: Tonetti T

PROVIDER: S-EPMC5537108 | biostudies-other | 2017 Jul

REPOSITORIES: biostudies-other

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Project description:BackgroundOutcome prediction in critically ill patients under invasive ventilation remains extremely challenging. The driving pressure (ΔP) and the mechanical power of ventilation (MP) are associated with patient-centered outcomes like mortality and duration of ventilation. The objective of this study was to assess the predictive validity for mortality of the ΔP and the MP at 24 h after start of invasive ventilation.MethodsThis is a post hoc analysis of an observational study in intensive care unit patients, restricted to critically ill patients receiving invasive ventilation for at least 24 h. The two exposures of interest were the modified ΔP and the MP at 24 h after start of invasive ventilation. The primary outcome was 90-day mortality; secondary outcomes were ICU and hospital mortality. The predictive validity was measured as incremental 90-day mortality beyond that predicted by the Acute Physiology, Age and Chronic Health Evaluation (APACHE) IV score and the Simplified Acute Physiology Score (SAPS) II.ResultsThe analysis included 839 patients with a 90-day mortality of 42%. The median modified ΔP at 24 h was 15 [interquartile range 12 to 19] cm H2O; the median MP at 24 h was 206 [interquartile range 145 to 298] 10-3 J/min/kg predicted body weight (PBW). Both parameters were associated with 90-day mortality (odds ratio (OR) for 1 cm H2O increase in the modified ΔP, 1.05 [95% confidence interval (CI) 1.03 to 1.08]; P < 0.001; OR for 100 10-3 J/min/kg PBW increase in the MP, 1.20 [95% CI 1.09 to 1.33]; P < 0.001). Area under the ROC for 90-day mortality of the modified ΔP and the MP were 0.70 [95% CI 0.66 to 0.74] and 0.69 [95% CI 0.65 to 0.73], which was neither different from that of the APACHE IV score nor that of the SAPS II.ConclusionsIn adult patients under invasive ventilation, the modified ΔP and the MP at 24 h are associated with 90 day mortality. Neither the modified ΔP nor the MP at 24 h has predictive validity beyond the APACHE IV score and the SAPS II.

Project description:ImportanceMechanical power and driving pressure have known associations with survival for patients with acute respiratory distress syndrome.ObjectivesTo further understand the relative importance of mechanical power and driving pressure as clinical targets for ventilator management.DesignSecondary observational analysis of randomized clinical trial data.Setting and participantsPatients with the acute respiratory distress syndrome from three Acute Respiratory Distress Syndrome Network trials.Main outcomes and measuresAfter adjusting for patient severity in a multivariate Cox proportional hazards model, we examined the relative association of driving pressure and mechanical power with hospital mortality. Among 2,410 patients, the relationship between driving pressure and mechanical power with mortality was modified by respiratory rate, positive end-expiratory pressure, and flow.ResultsAmong patients with low respiratory rate (< 26), only power was significantly associated with mortality (power [hazard ratio, 1.82; 95% CI, 1.41-2.35; p < 0.001] vs driving pressure [hazard ratio, 1.01; 95% CI, 0.84-1.21; p = 0.95]), while among patients with high respiratory rate, neither was associated with mortality. Both power and driving pressure were associated with mortality at high airway flow (power [hazard ratio, 1.28; 95% CI, 1.15-1.43; p < 0.001] vs driving pressure [hazard ratio, 1.15; 95% CI, 1.01-1.30; p = 0.041]) and neither at low flow. At low positive end-expiratory pressure, neither was associated with mortality, whereas at high positive end-expiratory pressure (≥ 10 cm H2O), only power was significantly associated with mortality (power [hazard ratio, 1.22; 95% CI, 1.09-1.37; p < 0.001] vs driving pressure [hazard ratio, 1.16; 95% CI, 0.99-1.35; p = 0.059]).Conclusions and relevanceThe relationship between mechanical power and driving pressure with mortality differed within severity subgroups defined by positive end-expiratory pressure, respiratory rate, and airway flow.

Project description:BackgroundMechanical power (MP) is the energy delivered to the respiratory system over time during mechanical ventilation. Our aim was to compare the currently available methods to calculate MP during volume- and pressure-controlled ventilation, comparing different equations with the geometric reference method, to understand whether the easier to use surrogate formulas were suitable for the everyday clinical practice. This would warrant a more widespread use of mechanical power to promote lung protection.MethodsForty respiratory failure patients, sedated and paralyzed for clinical reasons, were ventilated in volume-controlled ventilation, at two inspiratory flows (30 and 60 L/min), and pressure-controlled ventilation with a similar tidal volume. Mechanical power was computed both with the geometric method, as the area between the inspiratory limb of the airway pressure and the volume, and with two algebraic methods, a comprehensive and a surrogate formula.ResultsThe bias between the MP computed by the geometric method and by the comprehensive algebraic method during volume-controlled ventilation was respectively 0.053 (0.77, - 0.81) J/min and - 0.4 (0.70, - 1.50) J/min at low and high flows (r2 = 0.96 and 0.97, p < 0.01). The MP measured and computed by the two methods were highly correlated (r2 = 0.95 and 0.94, p < 0.01) with a bias of - 0.0074 (0.91, - 0.93) and - 1.0 (0.45, - 2.52) J/min at high-low flows. During pressure-controlled ventilation, the bias between the MP measured and the one calculated with the comprehensive and simplified methods was correlated (r2 = 0.81, 0.94, p < 0.01) with mean differences of - 0.001 (2.05, - 2.05) and - 0.81 (2.11, - 0.48) J/min.ConclusionsBoth for volume-controlled and pressure-controlled ventilation, the surrogate formulas approximate the reference method well enough to warrant their use in the everyday clinical practice. Given that these formulas require nothing more than the variables already displayed by the intensive care ventilator, a more widespread use of mechanical power should be encouraged to promote lung protection against ventilator-induced lung injury.

Project description:BackgroundMechanical power may serve as a valuable parameter for predicting ventilation-induced injury in mechanically ventilated patients. Over time, several equations have been developed to calculate power in both volume control ventilation (VCV) and pressure control ventilation (PCV). Among these equations, the linear model mechanical power equation (MPLM) closely approximates the reference method when applied in PCV. The dynamic mechanical power equation (MPdyn) computes power by utilizing the ventilatory work of breathing parameter (WOBv), which is automatically measured by the mechanical ventilator. In our study, conducted in patients with Covid-19 Acute Respiratory Distress Syndrome (C-ARDS), we calculated mechanical power using both the MPLM and MPdyn equations, employing different inspiratory rise times (Tslope) at intervals of 5%, ranging from 5 to 20% and compared the obtained results.ResultsIn our analysis, we used univariate linear regression at both I:E ratios of 1:2 and 1:1, considering all Tslope values. These analyses revealed that the MPdyn and MPLM equations exhibited strong correlations, with R2 values exceeding 0.96. Furthermore, our Bland-Altman analysis, which compared the power values derived from the MPdyn and MPLM equations for patient averages and all measurements, revealed a mean difference of -0.42 ± 0.41 J/min (equivalent to 2.6% ± 2.3%, p < 0.0001) and -0.39 ± 0.57 J/min (equivalent to 3.6% ± 3.5%, p < 0.0001), respectively. While there was a statistically significant difference between the equations in both absolute value and relative proportion, this difference was not considered clinically relevant. Additionally, we observed that each 5% increase in Tslope time corresponded to a decrease in mechanical power values by approximately 1 J/min.ConclusionsThe differences between mechanical power values calculated using the MPdyn and MPLM equations at various Tslope durations were determined to lack clinical significance. Consequently, for practical and continuous mechanical power estimation in Pressure-Controlled Ventilation (PCV) mode, the MPdyn equation presents itself as a viable option. It is important to note that as Tslope times increased, the calculated mechanical power exhibited a clinically relevant decrease.

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Driving pressure and mechanical power: new targets for VILI prevention.

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