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Mechanical power thresholds during mechanical ventilation: An experimental study.

ABSTRACT: The extent of ventilator-induced lung injury may be related to the intensity of mechanical ventilation--expressed as mechanical power. In the present study, we investigated whether there is a safe threshold, below which lung damage is absent. Three groups of six healthy pigs (29.5 ± 2.5 kg) were ventilated prone for 48 h at mechanical power of 3, 7, or 12 J/min. Strain never exceeded 1.0. PEEP was set at 4 cmH₂ O. Lung volumes were measured every 12 h; respiratory, hemodynamics, and gas exchange variables every 6. End-experiment histological findings were compared with a control group of eight pigs which did not undergo mechanical ventilation. Functional residual capacity decreased by 10.4% ± 10.6% and 8.1% ± 12.1% in the 7 J and 12 J groups (p = 0.017, p < 0.001) but not in the 3 J group (+1.7% ± 17.7%, p = 0.941). In 3 J group, lung elastance, PaO₂ and PaCO₂ were worse compared to 7 J and 12 J groups (all p < 0.001), due to lower ventilation-perfusion ratio (0.54 ± 0.13, 1.00 ± 0.25, 1.78 ± 0.36 respectively, p < 0.001). The lung weight was lower (p < 0.001) in the controls (6.56 ± 0.90 g/kg) compared to 3, 7, and 12 J groups (12.9 ± 3.0, 16.5 ± 2.9, and 15.0 ± 4.1 g/kg, respectively). The wet-to-dry ratio was 5.38 ± 0.26 in controls, 5.73 ± 0.52 in 3 J, 5.99 ± 0.38 in 7 J, and 6.13 ± 0.59 in 12 J group (p = 0.03). Vascular congestion was more extensive in the 7 J and 12 J compared to 3 J and control groups. Mechanical ventilation (with anesthesia/paralysis) increase lung weight, and worsen lung histology, regardless of the mechanical power. Ventilating at 3 J/min led to better anatomical variables than at 7 and 12 J/min but worsened the physiological values.

SUBMITTER: Romitti F

PROVIDER: S-EPMC8957661 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Mechanical power thresholds during mechanical ventilation: An experimental study.

Romitti Federica F Busana Mattia M Palumbo Maria Michela MM Bonifazi Matteo M Giosa Lorenzo L Vassalli Francesco F Gatta Alessandro A Collino Francesca F Steinberg Irene I Gattarello Simone S Lazzari Stefano S Palermo Paola P Nasr Ahmed A Gersmann Ann-Kathrin AK Richter Annika A Herrmann Peter P Moerer Onnen O Saager Leif L Camporota Luigi L Marini John J JJ Quintel Michael M Meissner Konrad K Gattinoni Luciano L

Physiological reports 20220301 6

The extent of ventilator-induced lung injury may be related to the intensity of mechanical ventilation--expressed as mechanical power. In the present study, we investigated whether there is a safe threshold, below which lung damage is absent. Three groups of six healthy pigs (29.5 ± 2.5 kg) were ventilated prone for 48 h at mechanical power of 3, 7, or 12 J/min. Strain never exceeded 1.0. PEEP was set at 4 cmH<sub>2</sub> O. Lung volumes were measured every 12 h; respiratory, hemodynamics, and g ...[more]

PMID: 35340133

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Project description:BackgroundThe individual components of mechanical ventilation may have distinct effects on kidney perfusion and on the risk of developing acute kidney injury; we aimed to explore ventilatory predictors of acute kidney failure and the hemodynamic changes consequent to experimental high-power mechanical ventilation.MethodsSecondary analysis of two animal studies focused on the outcomes of different mechanical power settings, including 78 pigs mechanically ventilated with high mechanical power for 48 h. The animals were categorized in four groups in accordance with the RIFLE criteria for acute kidney injury (AKI), using the end-experimental creatinine: (1) NO AKI: no increase in creatinine; (2) RIFLE 1-Risk: increase of creatinine of > 50%; (3) RIFLE 2-Injury: two-fold increase of creatinine; (4) RIFLE 3-Failure: three-fold increase of creatinine; RESULTS: The main ventilatory parameter associated with AKI was the positive end-expiratory pressure (PEEP) component of mechanical power. At 30 min from the initiation of high mechanical power ventilation, the heart rate and the pulmonary artery pressure progressively increased from group NO AKI to group RIFLE 3. At 48 h, the hemodynamic variables associated with AKI were the heart rate, cardiac output, mean perfusion pressure (the difference between mean arterial and central venous pressures) and central venous pressure. Linear regression and receiving operator characteristic analyses showed that PEEP-induced changes in mean perfusion pressure (mainly due to an increase in CVP) had the strongest association with AKI.ConclusionsIn an experimental setting of ventilation with high mechanical power, higher PEEP had the strongest association with AKI. The most likely physiological determinant of AKI was an increase of pleural pressure and CVP with reduced mean perfusion pressure. These changes resulted from PEEP per se and from increase in fluid administration to compensate for hemodynamic impairment consequent to high PEEP.

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 ventilation, a crucial intervention for acute respiratory distress syndrome (ARDS), can lead to ventilator-induced lung injury (VILI). This study focuses on individualizing mechanical power (MP) in mechanically ventilated patients to minimize VILI and reduce ICU mortality.MethodsA retrospective analysis was conducted using the Amsterdam University Medical Centers Database (AmsterdamUMCdb) data. The study included patients aged 18 and older who needed at least 48 hours of pressure-controlled mechanical ventilation. Patients who died or were extubated within 48 hours and those with inadequate data were excluded. Patients were categorized into hypoxemia groups based on their PaO2/FiO2 ratio. MP was calculated using a surrogate formula and normalized to ideal body weight (IBW). Statistical analyses and machine learning models, including logistic regression and random forest, were used to predict ICU mortality and establish safe upper limits for IBW-adjusted MP.ResultsOut of 23,106 admissions, 2,338 met the criteria. Nonsurvivors had a significantly higher time-weighted average MP (TWA-MP) than survivors. Safe upper limits for IBW-adjusted MP varied across hypoxemia groups. The XGBoost model showed the highest predictive accuracy for ICU mortality. An individualization method for mechanical ventilation settings, based on real-time physiological variables, demonstrated reduced predicted mortality in a subset of patients.DiscussionElevated TWA-MP is associated with increased ICU mortality, underscoring the need for personalized mechanical ventilation strategies. The study highlights the complexity of VILI and the multifactorial nature of ICU mortality. Further studies to define a safe upper limit for IBW-adjusted MP may help clinicians optimize mechanical ventilation settings and decrease the risk of VILI and mortality.ConclusionsDespite the fact that the study's retrospective design and reliance on a single-center database may limit the generalizability of findings, this study offers valuable insights into the relationship between mechanical power and ICU mortality, emphasizing the need for individualized mechanical ventilation strategies. The findings suggest a potential for more personalized, data-driven approach in managing mechanically ventilated patients, which could improve patient outcomes in critical care settings.

Project description:BACKGROUND:Adaptive mechanical ventilation automatically adjusts respiratory rate (RR) and tidal volume (VT) to deliver the clinically desired minute ventilation, selecting RR and VT based on Otis' equation on least work of breathing. However, the resulting VT may be relatively high, especially in patients with more compliant lungs. Therefore, a new mode of adaptive ventilation (adaptive ventilation mode 2, AVM2) was developed which automatically minimizes inspiratory power with the aim of ensuring lung-protective combinations of VT and RR. The aim of this study was to investigate whether AVM2 reduces VT, mechanical power, and driving pressure (ΔPstat) and provides similar gas exchange when compared to adaptive mechanical ventilation based on Otis' equation. METHODS:A prospective randomized cross-over study was performed in 20 critically ill patients on controlled mechanical ventilation, including 10 patients with acute respiratory distress syndrome (ARDS). Each patient underwent 1 h of mechanical ventilation with AVM2 and 1 h of adaptive mechanical ventilation according to Otis' equation (adaptive ventilation mode, AVM). At the end of each phase, we collected data on VT, mechanical power, ΔP, PaO2/FiO2 ratio, PaCO2, pH, and hemodynamics. RESULTS:Comparing adaptive mechanical ventilation with AVM2 to the approach based on Otis' equation (AVM), we found a significant reduction in VT both in the whole study population (7.2 ± 0.9 vs. 8.2 ± 0.6 ml/kg, p < 0.0001) and in the subgroup of patients with ARDS (6.6 ± 0.8 ml/kg with AVM2 vs. 7.9 ± 0.5 ml/kg with AVM, p < 0.0001). Similar reductions were observed for ΔPstat (whole study population: 11.5 ± 1.6 cmH2O with AVM2 vs. 12.6 ± 2.5 cmH2O with AVM, p < 0.0001; patients with ARDS: 11.8 ± 1.7 cmH2O with AVM2 and 13.3 ± 2.7 cmH2O with AVM, p = 0.0044) and total mechanical power (16.8 ± 3.9 J/min with AVM2 vs. 18.6 ± 4.6 J/min with AVM, p = 0.0024; ARDS: 15.6 ± 3.2 J/min with AVM2 vs. 17.5 ± 4.1 J/min with AVM, p = 0.0023). There was a small decrease in PaO2/FiO2 (270 ± 98 vs. 291 ± 102 mmHg with AVM, p = 0.03; ARDS: 194 ± 55 vs. 218 ± 61 with AVM, p = 0.008) and no differences in PaCO2, pH, and hemodynamics. CONCLUSIONS:Adaptive mechanical ventilation with automated minimization of inspiratory power may lead to more lung-protective ventilator settings when compared with adaptive mechanical ventilation according to Otis' equation. TRIAL REGISTRATION:The study was registered at the German Clinical Trials Register ( DRKS00013540 ) on December 1, 2017, before including the first patient.

Project description:BackgroundVolume-controlled ventilation has been suggested to optimize lung deposition during nebulization although promoting spontaneous ventilation is targeted to avoid ventilator-induced diaphragmatic dysfunction. Comparing topographic aerosol lung deposition during volume-controlled ventilation and spontaneous ventilation in pressure support has never been performed. The aim of this study was to compare lung deposition of a radiolabeled aerosol generated with a vibrating-mesh nebulizer during invasive mechanical ventilation, with two modes: pressure support ventilation and volume-controlled ventilation.MethodsSeventeen postoperative neurosurgery patients without pulmonary disease were randomly ventilated in pressure support or volume-controlled ventilation. Diethylenetriaminepentaacetic acid labeled with technetium-99m (2 mCi/3 mL) was administrated using a vibrating-mesh nebulizer (Aerogen Solo(®), provided by Aerogen Ltd, Galway, Ireland) connected to the endotracheal tube. Pulmonary and extrapulmonary particles deposition was analyzed using planar scintigraphy.ResultsLung deposition was 10.5 ± 3.0 and 15.1 ± 5.0 % of the nominal dose during pressure support and volume-controlled ventilation, respectively (p < 0.05). Higher endotracheal tube and tracheal deposition was observed during pressure support ventilation (27.4 ± 6.6 vs. 20.7 ± 6.0 %, p < 0.05). A similar penetration index was observed for the right (p = 0.210) and the left lung (p = 0.211) with both ventilation modes. A high intersubject variability of lung deposition was observed with both modes regarding lung doses, aerosol penetration and distribution between the right and the left lung.ConclusionsIn the specific conditions of the study, volume-controlled ventilation was associated with higher lung deposition of nebulized particles as compared to pressure support ventilation. The clinical benefit of this effect warrants further studies. Clinical trial registration NCT01879488.

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Mechanical power thresholds during mechanical ventilation: An experimental study.

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Mechanical power thresholds during mechanical ventilation: An experimental study.

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