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Static and Dynamic Contributors to Ventilator-induced Lung Injury in Clinical Practice. Pressure, Energy, and Power.

ABSTRACT: Ventilation is inherently a dynamic process. The present-day clinical practice of concentrating on the static inflation characteristics of the individual tidal cycle (plateau pressure, positive end-expiratory pressure, and their difference [driving pressure, the ratio of Vt to compliance]) does not take into account key factors shown experimentally to influence ventilator-induced lung injury (VILI). These include rate of airway pressure change (influenced by flow amplitude, inspiratory time fraction, and inspiratory inflation contour) and cycling frequency. Energy must be expended to cause injury, and the product of applied stress and resulting strain determines the energy delivered to the lungs per breathing cycle. Understanding the principles of VILI energetics may provide valuable insights and guidance to intensivists for safer clinical practice. In this interpretive review, we highlight that the injuring potential of the inflation pattern depends upon tissue vulnerability, the number of intolerable high-energy cycles applied in unit time (mechanical power), and the duration of that exposure. Yet, as attractive as this energy/power hypothesis for encapsulating the drivers of VILI may be for clinical applications, we acknowledge that even these all-inclusive and measurable ergonomic parameters (energy per cycle and power) are still too bluntly defined to pinpoint the precise biophysical link between ventilation strategy and tissue injury.

SUBMITTER: Marini JJ

PROVIDER: S-EPMC7124710 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundHigh rates of inflation energy delivery coupled with transpulmonary tidal pressures of sufficient magnitude may augment the risk of damage to vulnerable, stress-focused units within a mechanically heterogeneous lung. Apart from flow amplitude, the clinician-selected flow waveform, a relatively neglected dimension of inflation power, may distribute inflation energy of each inflation cycle non-uniformly among alveoli with different mechanical properties over the domains of time and space. In this initial step in modeling intracycle power distribution, our primary objective was to develop a mathematical model of global intracycle inflation power that uses clinician-measurable inputs to allow comparisons of instantaneous ICP profiles among the flow modes commonly encountered in clinical practice: constant, linearly decelerating, exponentially decelerating (pressure control), and spontaneous (sinusoidal).MethodsWe first tested the predictions of our mathematical model of passive inflation with the actual physical performance of a mechanical ventilator-lung system that simulated ventilation to three types of patients: normal, severe ARDS, and severe airflow obstruction. After verification, model predictions were then generated for 5000 'virtual ARDS patients'. Holding constant the tidal volume and inflation time between modes, the validated model then varied the flow profile and quantitated the resulting intensity and timing of potentially damaging 'elastic' energy and intracycle power (pressure-flow product) developed in response to random combinations of machine settings and severity levels for ARDS.ResultsOur modeling indicates that while the varied flow patterns ultimately deliver similar total amounts of alveolar energy during each breath, they differ profoundly regarding the potentially damaging pattern with which that energy distributes over time during inflation. Pressure control imposed relatively high maximal intracycle power.ConclusionsFlow amplitude and waveform may be relatively neglected and modifiable determinants of VILI risk when ventilating ARDS.

Project description: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 VT?=?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.

Project description: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 [(?[Formula: see text]/Est,L)/2]× RR (?P,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. ?P,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 ?P,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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Static and Dynamic Contributors to Ventilator-induced Lung Injury in Clinical Practice. Pressure, Energy, and Power.

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