Project description:This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2020. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2020. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.
Project description:ObjectivesLung- and diaphragm-protective ventilation is a novel concept that aims to limit the detrimental effects of mechanical ventilation on the diaphragm while remaining within limits of lung-protective ventilation. The premise is that low breathing effort under mechanical ventilation causes diaphragm atrophy, whereas excessive breathing effort induces diaphragm and lung injury. In a proof-of-concept study, we aimed to assess whether titration of inspiratory support based on diaphragm effort increases the time that patients have effort in a predefined "diaphragm-protective" range, without compromising lung-protective ventilation.DesignRandomized clinical trial.SettingMixed medical-surgical ICU in a tertiary academic hospital in the Netherlands.PatientsPatients (n = 40) with respiratory failure ventilated in a partially-supported mode.InterventionsIn the intervention group, inspiratory support was titrated hourly to obtain transdiaphragmatic pressure swings in the predefined "diaphragm-protective" range (3-12 cm H2O). The control group received standard-of-care.Measurements and main resultsTransdiaphragmatic pressure, transpulmonary pressure, and tidal volume were monitored continuously for 24 hours in both groups. In the intervention group, more breaths were within "diaphragm-protective" range compared with the control group (median 81%; interquartile range [64-86%] vs 35% [16-60%], respectively; p < 0.001). Dynamic transpulmonary pressures (20.5 ± 7.1 vs 18.5 ± 7.0 cm H2O; p = 0.321) and tidal volumes (7.56 ± 1.47 vs 7.54 ± 1.22 mL/kg; p = 0.961) were not different in the intervention and control group, respectively.ConclusionsTitration of inspiratory support based on patient breathing effort greatly increased the time that patients had diaphragm effort in the predefined "diaphragm-protective" range without compromising tidal volumes and transpulmonary pressures. This study provides a strong rationale for further studies powered on patient-centered outcomes.
Project description:BackgroundWe hypothesized that a decrease in frequency of controlled breaths during biphasic positive airway pressure (BIVENT), associated with an increase in spontaneous breaths, whether pressure support (PSV)-assisted or not, would mitigate lung and diaphragm damage in mild experimental acute respiratory distress syndrome (ARDS).Materials and methodsWistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24 hours, animals were randomly assigned to: 1) BIVENT-100+PSV0%: airway pressure (Phigh) adjusted to VT = 6 mL/kg and frequency of controlled breaths (f) = 100 bpm; 2) BIVENT-50+PSV0%: Phigh adjusted to VT = 6 mL/kg and f = 50 bpm; 3) BIVENT-50+PSV50% (PSV set to half the Phigh reference value, i.e., PSV50%); or 4) BIVENT-50+PSV100% (PSV equal to Phigh reference value, i.e., PSV100%). Positive end-expiratory pressure (Plow) was equal to 5 cmH2O. Nonventilated animals were used for lung and diaphragm histology and molecular biology analysis.ResultsBIVENT-50+PSV0%, compared to BIVENT-100+PSV0%, reduced the diffuse alveolar damage (DAD) score, the expression of amphiregulin (marker of alveolar stretch) and muscle atrophy F-box (marker of diaphragm atrophy). In BIVENT-50 groups, the increase in PSV (BIVENT-50+PSV50% versus BIVENT-50+PSV100%) yielded better lung mechanics and less alveolar collapse, interstitial edema, cumulative DAD score, as well as gene expressions associated with lung inflammation, epithelial and endothelial cell damage in lung tissue, and muscle ring finger protein 1 (marker of muscle proteolysis) in diaphragm. Transpulmonary peak pressure (Ppeak,L) and pressure-time product per minute (PTPmin) at Phigh were associated with lung damage, while increased spontaneous breathing at Plow did not promote lung injury.ConclusionIn the ARDS model used herein, during BIVENT, the level of PSV and the phase of the respiratory cycle in which the inspiratory effort occurs affected lung and diaphragm damage. Partitioning of inspiratory effort and transpulmonary pressure in spontaneous breaths at Plow and Phigh is required to minimize VILI.
Project description:ObjectiveTo evaluate the accuracy of respiratory mechanics using dynamic signal analysis during noninvasive pressure support ventilation (PSV).MethodsA Respironics V60 ventilator was connected to an active lung simulator to model normal, restrictive, obstructive, and mixed obstructive and restrictive profiles. The PSV was adjusted to maintain tidal volumes (VT) that achieved 5.0, 7.0, and 10.0 mL/kg body weight, and the positive end-expiration pressure (PEEP) was set to 5 cmH2O. Ventilator performance was evaluated by measuring the flow, airway pressure, and volume. The system compliance (Crs) and airway resistance (inspiratory and expiratory resistance, Rinsp and Rexp, respectively) were calculated.ResultsUnder active breathing conditions, the Crs was overestimated in the normal and restrictive models, and it decreased with an increasing pressure support (PS) level. The Rinsp calculated error was approximately 10% at 10.0 mL/kg of VT, and similar results were obtained for the calculated Rexp at 7.0 mL/kg of VT.ConclusionUsing dynamic signal analysis, appropriate tidal volume was beneficial for Rrs, especially for estimating Rexp during assisted ventilation. The Crs measurement was also relatively accurate in obstructive conditions.
Project description:The significant mortality rate and prolonged ventilator days associated with invasive mechanical ventilation (IMV) in patients with severe COVID-19 have incited a debate surrounding the use of noninvasive respiratory support (NIRS) (i.e., HFNC, CPAP, NIV) as a potential treatment strategy. Central to this debate is the role of NIRS in preventing intubation in patients with mild respiratory disease and the potential beneficial effects on both patient outcome and resource utilization. However, there remains valid concern that use of NIRS may prolong time to intubation and lung protective ventilation in patients with more advanced disease, thereby worsening respiratory mechanics via self-inflicted lung injury. In addition, the risk of aerosolization with the use of NIRS has the potential to increase healthcare worker (HCW) exposure to the virus. We review the existing literature with a focus on rationale, patient selection and outcomes associated with the use of NIRS in COVID-19 and prior pandemics, as well as in patients with acute respiratory failure due to different etiologies (i.e., COPD, cardiogenic pulmonary edema, etc.) to understand the potential role of NIRS in COVID-19 patients. Based on this analysis we suggest an algorithm for NIRS in COVID-19 patients which includes indications and contraindications for use, monitoring recommendations, systems-based practices to reduce HCW exposure, and predictors of NIRS failure. We also discuss future research priorities for addressing unanswered questions regarding NIRS use in COVID-19 with the goal of improving patient outcomes.
Project description:In patients with post-extubation respiratory distress, delayed reintubation may worsen clinical outcomes. Objective measures of extubation failure at the bedside are lacking, therefore clinical parameters are currently used to guide the need of reintubation. Electrical activity of the diaphragm (EAdi) provides clinicians with valuable, objective information about respiratory drive and could be used to monitor respiratory effort.We describe the case of a patient with Chronic Obstructive Pulmonary Disease (COPD), from whom we recorded EAdi during four different ventilatory conditions: 1) invasive mechanical ventilation, 2) spontaneous breathing trial (SBT), 3) unassisted spontaneous breathing, and 4) Noninvasive Positive Pressure Ventilation (NPPV). The patient had been intubated due to an exacerbation of COPD, and after four days of mechanical ventilation, she passed the SBT and was extubated. Clinical signs of respiratory distress were present immediately after extubation, and EAdi increased compared to values obtained during mechanical ventilation. As we started NPPV, EAdi decreased substantially, indicating muscle unloading promoted by NPPV, and we used the EAdi signal to monitor respiratory effort during NPPV. Over the next three days, she was on NPPV for most of the time, with short periods of spontaneous breathing. EAdi remained considerably lower during NPPV than during spontaneous breathing, until the third day, when the difference was no longer clinically significant. She was then weaned from NPPV and discharged from the ICU a few days later.EAdi monitoring during NPPV provides an objective parameter of respiratory drive and respiratory muscle unloading and may be a useful tool to guide post-extubation ventilatory support. Clinical studies with continuous EAdi monitoring are necessary to clarify the meaning of its absolute values and changes over time.
Project description:Mechanical ventilation is used to sustain respiratory function in patients with acute respiratory failure. To aid clinicians in consistently selecting lung- and diaphragm-protective ventilation settings, a physiology-based decision support system is needed. To form the foundation of such a system, a comprehensive physiological model which captures the dynamics of ventilation has been developed. The Lung and Diaphragm Protective Ventilation (LDPV) model centers around respiratory drive and incorporates respiratory system mechanics, ventilator mechanics, and blood acid-base balance. The model uses patient-specific parameters as inputs and outputs predictions of a patient's transpulmonary and esophageal driving pressures (outputs most clinically relevant to lung and diaphragm safety), as well as their blood pH, under various ventilator and sedation conditions. Model simulations and global optimization techniques were used to evaluate and characterize the model. The LDPV model is demonstrated to describe a CO2 respiratory response that is comparable to what is found in literature. Sensitivity analysis of the model indicate that the ventilator and sedation settings incorporated in the model have a significant impact on the target output parameters. Finally, the model is seen to be able to provide robust predictions of esophageal pressure, transpulmonary pressure and blood pH for patient parameters with realistic variability. The LDPV model is a robust physiological model which produces outputs which directly target and reflect the risk of ventilator-induced lung and diaphragm injury. Ventilation and sedation parameters are seen to modulate the model outputs in accordance with what is currently known in literature.