20 research outputs found
Lung stress, strain, and energy load: engineering concepts to understand the mechanism of ventilator-induced lung injury (VILI)
Excessive extracellular ATP desensitizes P2Y2 and P2X4 ATP receptors provoking surfactant impairment ending in ventilation-induced lung injury
Stretching the alveolar epithelial type I (AT I) cells controls the intercellular signaling for the exocytosis of surfactant by the AT II cells through the extracellular release of adenosine triphosphate (ATP) (purinergic signaling). Extracellular ATP is cleared by extracellular ATPases, maintaining its homeostasis and enabling the lung to adapt the exocytosis of surfactant to the demand. Vigorous deformation of the AT I cells by high mechanical power ventilation causes a massive release of extracellular ATP beyond the clearance capacity of the extracellular ATPases. When extracellular ATP reaches levels >100 ÎĽM, the ATP receptors of the AT II cells become desensitized and surfactant impairment is initiated. The resulting alteration in viscoelastic properties and in alveolar opening and collapse time-constants leads to alveolar collapse and the redistribution of inspired air from the alveoli to the alveolar ducts, which become pathologically dilated. The collapsed alveoli connected to these dilated alveolar ducts are subject to a massive strain, exacerbating the ATP release. After reaching concentrations >300 ÎĽM extracellular ATP acts as a danger-associated molecular pattern, causing capillary leakage, alveolar space edema, and further deactivation of surfactant by serum proteins. Decreasing the tidal volume to 6 mL/kg or less at this stage cannot prevent further lung injury
Ratchet recruitment in the acute respiratory distress syndrome: lessons from the newborn cry
Patients with acute respiratory distress syndrome (ARDS) have few treatment options other than supportive mechanical ventilation. The mortality associated with ARDS remains unacceptably high, and mechanical ventilation itself has the potential to increase mortality further by unintended ventilator-induced lung injury (VILI). Thus, there is motivation to improve management of ventilation in patients with ARDS. The immediate goal of mechanical ventilation in ARDS should be to prevent atelectrauma resulting from repetitive alveolar collapse and reopening. However, a long-term goal should be to re-open collapsed and edematous regions of the lung and reduce regions of high mechanical stress that lead to regional volutrauma. In this paper, we consider the proposed strategy used by the full-term newborn to open the fluid-filled lung during the initial breaths of life, by ratcheting tissues opened over a series of initial breaths with brief expirations. The newborn’s cry after birth shares key similarities with the Airway Pressure Release Ventilation (APRV) modality, in which the expiratory duration is sufficiently short to minimize end-expiratory derecruitment. Using a simple computational model of the injured lung, we demonstrate that APRV can slowly open even the most recalcitrant alveoli with extended periods of high inspiratory pressure, while reducing alveolar re-collapse with brief expirations. These processes together comprise a ratchet mechanism by which the lung is progressively recruited, similar to the manner in which the newborn lung is aerated during a series of cries, albeit over longer time scales
Surfactant delivery in rat lungs: Comparing 3D geometrical simulation model with experimental instillation
International audienceSurfactant Replacement Therapy (SRT), which involves instillation of a liquid-surfactant mixture directly into the lung airway tree, is a major therapeutic treatment in neonatal patients with respiratory distress syndrome (RDS). This procedure has proved to be remarkably effective in premature newborns, inducing a five-fold decrease of mortality in the past 35 years. Disappointingly, its use i
Reply to Drs. Monjezi and Jamaati: Dynamic alveolar mechanics are more than a soap bubble on a capillary tube
Acute lung injury: how to stabilize a broken lung
Abstract The pathophysiology of acute respiratory distress syndrome (ARDS) results in heterogeneous lung collapse, edema-flooded airways and unstable alveoli. These pathologic alterations in alveolar mechanics (i.e. dynamic change in alveolar size and shape with each breath) predispose the lung to secondary ventilator-induced lung injury (VILI). It is our viewpoint that the acutely injured lung can be recruited and stabilized with a mechanical breath until it heals, much like casting a broken bone until it mends. If the lung can be “casted” with a mechanical breath, VILI could be prevented and ARDS incidence significantly reduced
Certificat d'université en Building Information Modeling pour petites et moyennes structures - Rapport d'études
Le BIM (pour Building Information Model – Modeling – Management) acquiert une importance de plus en plus grande dans les secteurs de l’architecture et de la construction, comme en témoignent les nombreuses communications en la matière, qu’elles émanent de fournisseurs de logiciels, d’associations professionnelles ou de centres de recherches. Le BIM y est présenté comme une solution d’avenir permettant d’améliorer l’efficacité des processus de projet, le partage des données et la collaboration entre tous les acteurs du projet, autour de la maquette numérique 3D, avec des économies en termes de coût mais aussi de délais, supposées conséquentes à terme.
L’objectif du présent rapport d’études est d’abord de synthétiser les principaux acquis théoriques de la formation dispensée dans le cadre du « Certificat d’Université en Building Information Modeling pour Petites et Moyennes Structures ». Dans un domaine qui n’en est encore qu’à ses prémices, en particulier au niveau des retours d’expériences concrètes sur terrain, cette synthèse, documentée de références externes et de réflexions personnelles, propose de garder un regard critique sur le BIM et de placer au centre des réflexions les processus organisationnels et collaboratifs plutôt que la technologie.
Ces acquis théoriques sont ensuite mobilisés pour esquisser une première ébauche de plan d’implémentation du BIM à l’Administration des Ressources Immobilières de l’Université de Liège. Cette section commence par un état des lieux des missions, de l’organisation et des projets gérés par cette Administration. Le propos développé se structure ensuite par type de projets et vise à identifier les questions-clés sur lesquelles la réflexion devra être portée et concertée avec l’ensemble des acteurs, internes et externes à l’Administration concernée par ce processus.
L’implémentation doit ainsi être le fruit d’une réflexion partagée entre tous les acteurs, hors des recettes toutes faites et se faire progressivement, en plaçant la communication et la rationalisation des processus de projet au centre de la démarche. L’organisation, la rigueur et la planification sont essentiels à l’émergence d’une réelle culture de projets « BIM », efficace et partagée par tous
Last Word on Viewpoint: Looking beyond macrovenitlatory parameters and rethinking ventilator-induced lung injury
The role of high airway pressure and dynamic strain on ventilator-induced lung injury in a heterogeneous acute lung injury model
Abstract Background Acute respiratory distress syndrome causes a heterogeneous lung injury with normal and acutely injured lung tissue in the same lung. Improperly adjusted mechanical ventilation can exacerbate ARDS causing a secondary ventilator-induced lung injury (VILI). We hypothesized that a peak airway pressure of 40 cmH2O (static strain) alone would not cause additional injury in either the normal or acutely injured lung tissue unless combined with high tidal volume (dynamic strain). Methods Pigs were anesthetized, and heterogeneous acute lung injury (ALI) was created by Tween instillation via a bronchoscope to both diaphragmatic lung lobes. Tissue in all other lobes was normal. Airway pressure release ventilation was used to precisely regulate time and pressure at both inspiration and expiration. Animals were separated into two groups: (1) over-distension + high dynamic strain (OD + HDS, n = 6) and (2) over-distension + low dynamic strain (OD + LDS, n = 6). OD was caused by setting the inspiratory pressure at 40 cmH2O and dynamic strain was modified by changing the expiratory duration, which varied the tidal volume. Animals were ventilated for 6 h recording hemodynamics, lung function, and inflammatory mediators followed by an extensive necropsy. Results In normal tissue (NT), OD + LDS caused minimal histologic damage and a significant reduction in BALF total protein (p < 0.05) and MMP-9 activity (p < 0.05), as compared with OD + HDS. In acutely injured tissue (ALIT), OD + LDS resulted in reduced histologic injury and pulmonary edema (p < 0.05), as compared with OD + HDS. Conclusions Both NT and ALIT are resistant to VILI caused by OD alone, but when combined with a HDS, significant tissue injury develops