Dynamic predictors of VILI risk: beyond the driving pressure

Marini, John J.; Jaber, Samir

doi:10.1007/s00134-016-4534-x

Cited by 70 publications

(62 citation statements)

References 10 publications

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“…To the best of our knowledge, this was the first study to investigate the impact of different V T levels, under the same low mechanical power, on lung function, DAD score, ultrastructural analysis of pulmonary parenchyma and gene expression of different biomarkers of VILI in experimental ARDS. We calculated the mechanical power by using a simplified equation to allow possible extrapolation of results to the clinical scenario (Marini and Jaber, 2016 ). PEEP was kept constant throughout the experiment; thus, different V T levels led only to dynamic energy changes.…”

Section: Discussionmentioning

confidence: 99%

“…Transpulmonary pressure (P, L ) was calculated as the difference between the Paw and Pes, whereas transpulmonary driving pressure (ΔP, L ) was the difference between the transpulmonary pressure during end-inspiration (post-inspiratory pause) and end-expiration. The mechanical energy (Energy, L ) was calculated based on the equation described by Guerin et al ( 2016 ) and Marini and Jaber ( 2016 ) (simplified formula), as Energy, L = Δ

/Est, L , where Est, L is the static lung elastance. Energy, L = Δ

/(ΔP, L /V T ) = ΔP, L xV T , which is the area of rectangle (see Supplementary Figure 1 ).…”

Section: Methodsmentioning

confidence: 99%

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Impact of Different Tidal Volume Levels at Low Mechanical Power on Ventilator-Induced Lung Injury in Rats

et al. 2018

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Tidal volume (VT) has been considered the main determinant of ventilator-induced lung injury (VILI). Recently, experimental studies have suggested that mechanical power transferred from the ventilator to the lungs is the promoter of VILI. We hypothesized that, as long as mechanical power is kept below a safe threshold, high VT should not be injurious. The present study aimed to investigate the impact of different VT levels and respiratory rates (RR) on lung function, diffuse alveolar damage (DAD), alveolar ultrastructure, and expression of genes related to inflammation [interleukin (IL)-6], alveolar stretch (amphiregulin), epithelial [club cell secretory protein (CC)16] and endothelial [intercellular adhesion molecule (ICAM)-1] cell injury, and extracellular matrix damage [syndecan-1, decorin, and metalloproteinase (MMP)-9] in experimental acute respiratory distress syndrome (ARDS) under low-power mechanical ventilation. Twenty-eight Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 h, 21 animals were randomly assigned to ventilation (2 h) with low mechanical power at three different VT levels (n = 7/group): (1) VT = 6 mL/kg and RR adjusted to normocapnia; (2) VT = 13 mL/kg; and 3) VT = 22 mL/kg. In the second and third groups, RR was adjusted to yield low mechanical power comparable to that of the first group. Mechanical power was calculated as [(ΔP,L2/Est,L)/2]× RR (ΔP,L = transpulmonary driving pressure, Est,L = static lung elastance). Seven rats were not mechanically ventilated (NV) and were used for molecular biology analysis. Mechanical power was comparable among groups, while VT gradually increased. ΔP,L and mechanical energy were higher in VT = 22 mL/kg than VT = 6 mL/kg and VT = 13 mL/kg (p < 0.001 for both). Accordingly, DAD score increased in VT = 22 mL/kg compared to VT = 6 mL/kg and VT = 13 mL/kg [23(18.5–24.75) vs. 16(12–17.75) and 16(13.25–18), p < 0.05, respectively]. VT = 22 mL/kg was associated with higher IL-6, amphiregulin, CC16, MMP-9, and syndecan-1 mRNA expression and lower decorin expression than VT = 6 mL/kg. Multiple linear regression analyses indicated that VT was able to predict changes in IL-6 and CC16, whereas ΔP,L predicted pHa, oxygenation, amphiregulin, and syndecan-1 expression. In the model of ARDS used herein, even at low mechanical power, high VT resulted in VILI. VT control seems to be more important than RR control to mitigate VILI.

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Section: Discussionmentioning

confidence: 99%

/Est, L , where Est, L is the static lung elastance. Energy, L = Δ

/(ΔP, L /V T ) = ΔP, L xV T , which is the area of rectangle (see Supplementary Figure 1 ).…”

Section: Methodsmentioning

confidence: 99%

Impact of Different Tidal Volume Levels at Low Mechanical Power on Ventilator-Induced Lung Injury in Rats

et al. 2018

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“…Although the concept of mechanical power may appeal as a unifying variable with which to track VILI risk (both during controlled and spontaneously assisted breathing), several challenges must be met before it can be implemented in practice: first, power must be normalized either for a standard lung volume or for the amount of aerated lung tissue [68, 69]; and second, the relationship between the power delivered to the whole respiratory system and that actually delivered to the lung (using the transpulmonary pressure) must be differentiated. In particular, the impact of inspiratory flow and tissue resistance should be better defined.…”

Section: The Future Of Mechanical Ventilationmentioning

confidence: 99%

The future of mechanical ventilation: lessons from the present and the past

et al. 2017

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The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonary pressure-related side effects primarily account for ventilator-induced lung injury (VILI) while the pleural pressure-related side effects primarily account for hemodynamic alterations. The changes of transpulmonary pressure and pleural pressure resulting from a given applied driving pressure depend on the relative elastances of the lung and chest wall. The term ‘volutrauma’ should refer to excessive strain, while ‘barotrauma’ should refer to excessive stress. Strains exceeding 1.5, corresponding to a stress above ~20 cmH2O in humans, are severely damaging in experimental animals. Apart from high tidal volumes and high transpulmonary pressures, the respiratory rate and inspiratory flow may also play roles in the genesis of VILI. We do not know which fraction of mortality is attributable to VILI with ventilation comparable to that reported in recent clinical practice surveys (tidal volume ~7.5 ml/kg, positive end-expiratory pressure (PEEP) ~8 cmH2O, rate ~20 bpm, associated mortality ~35%). Therefore, a more complete and individually personalized understanding of ARDS lung mechanics and its interaction with the ventilator is needed to improve future care. Knowledge of functional lung size would allow the quantitative estimation of strain. The determination of lung inhomogeneity/stress raisers would help assess local stresses; the measurement of lung recruitability would guide PEEP selection to optimize lung size and homogeneity. Finding a safety threshold for mechanical power, normalized to functional lung volume and tissue heterogeneity, may help precisely define the safety limits of ventilating the individual in question. When a mechanical ventilation set cannot be found to avoid an excessive risk of VILI, alternative methods (such as the artificial lung) should be considered.

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“…For example, minute ventilation can be considered an intensity variable that determines whether an identical driving pressure for ventilation may cause injury or be well tolerated. The total power that lung tissue must endure is determined by the frequency of breathing as well as the conformation of the individual tidal cycle [ 26 , 27 ]. The flow profile of each individual breath determines the rate at which alveolar pressure develops, and experimentally has been shown to be important in minimizing ventilator-induced lung injury [ 28 , 29 ].…”

Section: Timing Issues In Critical Illnessmentioning

confidence: 99%

Time-sensitive therapeutics

Marini

2017

Crit Care

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Much of what we now do in Critical Care carries an air of urgency, a pressing need to discover and act, with priorities biased toward a reactive response. However, efficacy often depends not simply upon what we do, but rather on whether, when, and how persistently we intervene. The practice of medicine is based upon diagnosis, integration of multiple sources of information, keen judgment, and appropriate intervention. Timing may not be everything, as the well-known adage suggests, but in the intensive care unit (ICU) timing issues clearly deserve more attention than they are currently given. Successfully or not, the patient is continually attempting to adapt and re-adjust to acute illness, and this adaptive process takes time. Knowing that much of what we do carries potential for unintended harm as well as benefit, the trick is to decide whether the patient is winning or losing the adaptive struggle and whether we can help. Costs of modern ICU care is enormous and the trend line shows no encouraging sign of moderation. To sharpen our effectiveness, reduce hazard, and pare cost we must learn to time our interventions, help the patient adapt, and at times withhold treatment rather than jump in on the impulse to rescue and/or to alter the natural course of disease. Indeed, much of the progress made in our discipline has resulted both from timely intervention when called for and avoidance or moderation of hazardous treatments when not. Time-sensitive ICU therapeutics requires awareness of trends in key parameters, respect for adaptive chronobiology, level-headed evaluation of the need to intervene, and awareness of the costs of disrupting a potentially constructive natural response to illness.

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Dynamic predictors of VILI risk: beyond the driving pressure

Cited by 70 publications

References 10 publications

Impact of Different Tidal Volume Levels at Low Mechanical Power on Ventilator-Induced Lung Injury in Rats

Impact of Different Tidal Volume Levels at Low Mechanical Power on Ventilator-Induced Lung Injury in Rats

The future of mechanical ventilation: lessons from the present and the past

Time-sensitive therapeutics

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