The Experts below are selected from a list of 1344 Experts worldwide ranked by ideXlab platform
Mark J D Griffiths - One of the best experts on this subject based on the ideXlab platform.
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Strategies to reduce Ventilator-Associated Lung Injury (VALI).
Burns, 2012Co-Authors: David Salman, Simon J. Finney, Mark J D GriffithsAbstract:Abstract Optimal management of the acute respiratory distress syndrome (ARDS) requires prompt recognition, treatment of the underlying cause and the prevention of secondary Injury. Ventilator-Associated Lung Injury (VALI) is one of the several iatrogenic factors that can exacerbate Lung Injury and ARDS. Reduction of VALI by protective low tidal volume ventilation is one of the only interventions with a proven survival benefit in ARDS. There are, however, several factors inhibiting the widespread use of this technique in patients with established Lung Injury. Prevention of ARDS and VALI by detecting at-risk patients and implementing protective ventilation early is a feasible strategy. Detection of injurious ventilation itself is possible, and potential biological markers of VALI have been investigated. Finally, facilitation of protective ventilation, including techniques such as extracorporeal support, can mitigate VALI.
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ventilator associated Lung Injury
The Lancet, 2003Co-Authors: Liao Pinhu, Thomas Whitehead, T Evans, Mark J D GriffithsAbstract:Summary Mechanical ventilation is indispensable in support of patients with respiratory failure who are critically ill. However, use of this technique has adverse effects, including increased risk of pneumonia, impaired cardiac performance, and difficulties associated with sedation and paralysis. Moreover, application of pressure to the Lung, whether positive or negative, can cause damage known as Ventilator-Associated Lung Injury (VALI). Despite difficulties in distinguishing the effects of mechanical ventilation from those of the underlying disorder, VALI greatly assists patients with the most severe form of Lung Injury, acute respiratory distress syndrome (ARDS). Moreover, modification of mechanical ventilation so that VALI is kept to a minimum improves survival of patients with ARDS. Here, we outline the effects of mechanical ventilation on injured Lungs and explore the underlying mechanisms.
Paolo Pelosi - One of the best experts on this subject based on the ideXlab platform.
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C URRENT OPINION Pathophysiology of Ventilator-Associated Lung Injury
2020Co-Authors: Patricia R.m. Rocco, Claudia C. Dos Santos, Paolo PelosiAbstract:Summary How ventilation strategy, specific mechanisms of mechanotransduction, and their individual threshold values impact on VALI remains to be elucidated. In addition, clinical studies are required to evaluate the usefulness of individualized ventilator strategies based on Lung mechanics.
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Increased effort during partial ventilatory support is not associated with Lung damage in experimental acute Lung Injury.
Intensive Care Medicine Experimental, 2019Co-Authors: Dietrich Henzler, Haibo Zhang, Arthur S. Slutsky, Zhaolin Xu, Alf Schmidt, N. Ismaiel, Paolo PelosiAbstract:An on-going debate exists as to whether partial ventilatory support is Lung protective in an acute phase of ARDS. So far, the effects of different respiratory efforts on the development of Ventilator-Associated Lung Injury (VALI) have been poorly understood. To test the hypothesis whether respiratory effort itself promotes VALI, acute Lung Injury (ALI) was induced in 48 Sprague Dawley rats by hydrochloric acid aspiration model. Hemodynamics, gas-exchange, and respiratory mechanics were measured after 4 h of ventilation in pressure control (PC), assist-control (AC), or pressure support with 100% (PS100), 60% (PS60), or 20% (PS20) of the driving pressure during PC. VALI was assessed by histological analysis and biological markers. ALI was characterized by a decrease in PaO2/FiO2 from 447 ± 75 to 235 ± 90 mmHg (p
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positive end expiratory pressure titrated according to respiratory system mechanics or to ardsnetwork table did not guarantee positive end expiratory transpulmonary pressure in acute respiratory distress syndrome
Journal of Critical Care, 2018Co-Authors: Joerg Krebs, Patricia R.m. Rocco, Paolo Pelosi, Michael Hagmann, Thomas LueckeAbstract:Abstract Purpose Pulmonary recruitment and positive end-expiratory pressure (PEEP) titrated according to minimal static elastance of the respiratory system (PEEPEstat,RS) compared to PEEP set according to the ARDSNetwork table (PEEPARDSNetwork) as a strategy to prevent Ventilator-Associated Lung Injury (VALI) in patients with acute respiratory distress syndrome (ARDS) increases mortality. Alternatively, avoiding negative end-expiratory transpulmonary pressure has been discussed as superior PEEP titration strategy. Therefore, we tested whether PEEPEstat,RS or PEEPARDSNetwork prevent negative end-expiratory transpulmonary pressure in ARDS patients. Material and methods Thirteen patients with moderate to severe ARDS were studied at PEEPARDSNetwork versus PEEPEstat,RS. Patients were then grouped post hoc according to the end-expiratory transpulmonary pressure (positive or negative). Results 7 out of 13 patients showed negative end-expiratory transpulmonary pressures (Ptp−) with both strategies (PEEPARDSNetwork: - 5.4 ± 3.5 vs. 2.2 ± 3.7 cm H2O, p = .005; PEEPEstat,RS: - 3.6 ± 1.5 vs. 3.5 ± 3.3 cm H2O, p Conclusions In patients with moderate-to-severe ARDS, PEEP titrated according to the minimal static elastance of the respiratory system or according to the ARDSNetwork table did not prevent negative end-expiratory transpulmonary pressure.
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Ventilator-Associated Lung Injury during assisted mechanical ventilation.
Seminars in Respiratory and Critical Care Medicine, 2014Co-Authors: Felipe Saddy, Patricia R.m. Rocco, Yuda Sutherasan, Paolo PelosiAbstract:Assisted mechanical ventilation (MV) may be a favorable alternative to controlled MV at the early phase of acute respiratory distress syndrome (ARDS), since it requires less sedation, no paralysis and is associated with less hemodynamic deterioration, better distal organ perfusion, and Lung protection, thus reducing the risk of Ventilator-Associated Lung Injury (VALI). In the present review, we discuss VALI in relation to assisted MV strategies, such as volume assist–control ventilation, pressure assist–control ventilation, pressure support ventilation (PSV), airway pressure release ventilation (APRV), APRV with PSV, proportional assist ventilation (PAV), noisy ventilation, and neurally adjusted ventilatory assistance (NAVA). In summary, we suggest that assisted MV can be used in ARDS patients in the following situations: (1) Pa o 2 /F io 2 >150 mm Hg and positive end-expiratory pressure ≥ 5 cm H 2 O and (2) with modalities of pressure-targeted and time-cycled breaths including more or less spontaneous or supported breaths (A-PCV [assisted pressure-controlled ventilation] or APRV). Furthermore, during assisted MV, the following parameters should be monitored: inspiratory drive, transpulmonary pressure, and tidal volume (6 mL/kg). Further studies are required to determine the impact of novel modalities of assisted ventilation such as PAV, noisy pressure support, and NAVA on VALI.
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Advances in ventilator- associated Lung Injury: prevention is the target
Expert Review of Respiratory Medicine, 2014Co-Authors: Y. Sutherasan, Davide D'antini, Paolo PelosiAbstract:Mechanical ventilation (MV) is the main supportive treatment in respiratory failure due to different etiologies. However, MV might aggravate Ventilator-Associated Lung Injury (VALI). Four main mechanisms leading to VALI are: 1) increased stress and strain, induced by high tidal volume (VT); 2) increased shear stress, i.e. opening and closing, of previously atelectatic alveolar units; 3) distribution of perfusion and 4) biotrauma. In severe acute respiratory distress syndrome patients, low VT, higher levels of positive end expiratory pressure, long duration prone position and neuromuscular blockade within the first 48 hours are associated to a better outcome. VALI can also occur by using high VT in previously non injured Lungs. We believe that prevention is the target to minimize injurious effects of MV. This review aims to describe pathophysiology of VALI, the possible prevention and treatment as well as monitoring MV to minimize VALI.
James E. Baumgardner - One of the best experts on this subject based on the ideXlab platform.
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Influence of respiratory rate and end-expiratory pressure variation on cyclic alveolar recruitment in an experimental Lung Injury model
Critical Care, 2012Co-Authors: Erik K. Hartmann, James E. Baumgardner, Bastian Duenges, Stefan Boehme, Alexander H. Bentley, Klaus Ulrich Klein, Amelie Elsaesser, Matthias David, Klaus MarkstallerAbstract:Introduction Cyclic alveolar recruitment/derecruitment (R/D) is an important mechanism of Ventilator-Associated Lung Injury. In experimental models this process can be measured with high temporal resolution by detection of respiratory-dependent oscillations of the paO2 (ΔpaO2). A previous study showed that end-expiratory collapse can be prevented by an increased respiratory rate in saline-lavaged rabbits. The current study compares the effects of increased positive end-expiratory pressure (PEEP) versus an individually titrated respiratory rate (RRind) on intra-tidal amplitude of Δ paO2 and on average paO2 in saline-lavaged pigs.
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Spatial and temporal heterogeneity of Ventilator-Associated Lung Injury after surfactant depletion
Journal of Applied Physiology, 2008Co-Authors: Cynthia M Otto, Birgit Pfeiffer, Klaus Markstaller, Osamu Kajikawa, J. Karmrodt, Rebecca S. Syring, Virginia P. Good, Charles W. Frevert, James E. BaumgardnerAbstract:Volutrauma and atelectrauma have been proposed as mechanisms of Ventilator-Associated Lung Injury, but few studies have compared their relative importance in mediating Lung Injury. The objective of our study was to compare the Injury produced by stretch (volutrauma) vs. cyclical recruitment (atelectrauma) after surfactant depletion. In saline-lavaged rabbits, we used high tidal volume, low respiratory rate, and low positive end-expiratory pressure to produce stretch Injury in nondependent Lung regions and cyclical recruitment in dependent Lung regions. Tidal changes in shunt fraction were assessed by measuring arterial Po2 oscillations. After ventilating for times ranging from 0 to 6 h, Lungs were excised, sectioned gravitationally, and assessed for regional Injury by evaluation of edema formation, chemokine expression, upregulation of inflammatory enzyme activity, and alveolar neutrophil accumulation. Edema formation, Lung tissue interleukin-8 expression, and alveolar neutrophil accumulation progressed more rapidly in dependent Lung regions, whereas macrophage chemotactic protein-1 expression progressed more rapidly in nondependent Lung regions. Temporal and regional heterogeneity of Lung Injury were substantial. In this surfactant depletion model of acute Lung Injury, cyclical recruitment produced more Injury than stretch.
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Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage Lung Injury.
Journal of Applied Physiology, 2006Co-Authors: Rebecca S. Syring, Cynthia M Otto, Klaus Markstaller, Rebecca E. Spivack, James E. BaumgardnerAbstract:Cyclical recruitment of atelectasis with each breath is thought to contribute to Ventilator-Associated Lung Injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitm...
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Effects of respiratory rate, plateau pressure, and positive end-expiratory pressure on PaO2 oscillations after saline lavage.
American journal of respiratory and critical care medicine, 2002Co-Authors: James E. Baumgardner, Birgit Pfeiffer, Marcus Doebrich, Klaus Markstaller, Cynthia M OttoAbstract:One of the proposed mechanisms of Ventilator-Associated Lung Injury is cyclic recruitment of atelectasis. Collapse of dependent Lung regions with every breath should lead to large oscillations in PaO2 as shunt varies throughout the respiratory cycle. We placed a fluorescence-quenching PO2 probe in the brachiocephalic artery of six anesthetized rabbits after saline lavage. Using pressure-controlled ventilation with oxygen, ventilator settings were varied in random order over three levels of positive end-expiratory pressure (PEEP), respiratory rate (RR), and plateau pressure minus PEEP (Delta). Dependence of the amplitude of PaO2 oscillations on PEEP, RR, and Delta was modeled by multiple linear regression. Before lavage, arterial PO2 oscillations varied from 3 to 22 mm Hg. After lavage, arterial PO2 oscillations varied from 5 to 439 mm Hg. Response surfaces showed markedly nonlinear dependence of amplitude on PEEP, RR, and Delta. The large PaO2 oscillations observed provide evidence for cyclic recruitment in this model of Lung Injury. The important effect of RR on the magnitude of PaO2 oscillations suggests that the static behavior of atelectasis cannot be accurately extrapolated to predict dynamic behavior at realistic breathing frequencies.
Klaus Markstaller - One of the best experts on this subject based on the ideXlab platform.
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Influence of respiratory rate and end-expiratory pressure variation on cyclic alveolar recruitment in an experimental Lung Injury model
Critical Care, 2012Co-Authors: Erik K. Hartmann, James E. Baumgardner, Bastian Duenges, Stefan Boehme, Alexander H. Bentley, Klaus Ulrich Klein, Amelie Elsaesser, Matthias David, Klaus MarkstallerAbstract:Introduction Cyclic alveolar recruitment/derecruitment (R/D) is an important mechanism of Ventilator-Associated Lung Injury. In experimental models this process can be measured with high temporal resolution by detection of respiratory-dependent oscillations of the paO2 (ΔpaO2). A previous study showed that end-expiratory collapse can be prevented by an increased respiratory rate in saline-lavaged rabbits. The current study compares the effects of increased positive end-expiratory pressure (PEEP) versus an individually titrated respiratory rate (RRind) on intra-tidal amplitude of Δ paO2 and on average paO2 in saline-lavaged pigs.
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Ventilator-Associated Lung Injury Superposed to Oleic Acid Infusion or Surfactant Depletion: Histopathological Characteristics of Two Porcine Models of Acute Lung Injury
European Surgical Research, 2010Co-Authors: Hemei Wang, Marc Bodenstein, Bastian Duenges, S. Ganatti, Stefan Boehme, Y. Ning, B. Roehrig, Klaus MarkstallerAbstract:Background: The pathophysiological concept of acute Lung Injury (ALI) in combination with Ventilator-Associated Lung Injury (VALI) is still unclear. We characterized the histopathol
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Spatial and temporal heterogeneity of Ventilator-Associated Lung Injury after surfactant depletion
Journal of Applied Physiology, 2008Co-Authors: Cynthia M Otto, Birgit Pfeiffer, Klaus Markstaller, Osamu Kajikawa, J. Karmrodt, Rebecca S. Syring, Virginia P. Good, Charles W. Frevert, James E. BaumgardnerAbstract:Volutrauma and atelectrauma have been proposed as mechanisms of Ventilator-Associated Lung Injury, but few studies have compared their relative importance in mediating Lung Injury. The objective of our study was to compare the Injury produced by stretch (volutrauma) vs. cyclical recruitment (atelectrauma) after surfactant depletion. In saline-lavaged rabbits, we used high tidal volume, low respiratory rate, and low positive end-expiratory pressure to produce stretch Injury in nondependent Lung regions and cyclical recruitment in dependent Lung regions. Tidal changes in shunt fraction were assessed by measuring arterial Po2 oscillations. After ventilating for times ranging from 0 to 6 h, Lungs were excised, sectioned gravitationally, and assessed for regional Injury by evaluation of edema formation, chemokine expression, upregulation of inflammatory enzyme activity, and alveolar neutrophil accumulation. Edema formation, Lung tissue interleukin-8 expression, and alveolar neutrophil accumulation progressed more rapidly in dependent Lung regions, whereas macrophage chemotactic protein-1 expression progressed more rapidly in nondependent Lung regions. Temporal and regional heterogeneity of Lung Injury were substantial. In this surfactant depletion model of acute Lung Injury, cyclical recruitment produced more Injury than stretch.
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Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage Lung Injury.
Journal of Applied Physiology, 2006Co-Authors: Rebecca S. Syring, Cynthia M Otto, Klaus Markstaller, Rebecca E. Spivack, James E. BaumgardnerAbstract:Cyclical recruitment of atelectasis with each breath is thought to contribute to Ventilator-Associated Lung Injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitm...
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Effects of respiratory rate, plateau pressure, and positive end-expiratory pressure on PaO2 oscillations after saline lavage.
American journal of respiratory and critical care medicine, 2002Co-Authors: James E. Baumgardner, Birgit Pfeiffer, Marcus Doebrich, Klaus Markstaller, Cynthia M OttoAbstract:One of the proposed mechanisms of Ventilator-Associated Lung Injury is cyclic recruitment of atelectasis. Collapse of dependent Lung regions with every breath should lead to large oscillations in PaO2 as shunt varies throughout the respiratory cycle. We placed a fluorescence-quenching PO2 probe in the brachiocephalic artery of six anesthetized rabbits after saline lavage. Using pressure-controlled ventilation with oxygen, ventilator settings were varied in random order over three levels of positive end-expiratory pressure (PEEP), respiratory rate (RR), and plateau pressure minus PEEP (Delta). Dependence of the amplitude of PaO2 oscillations on PEEP, RR, and Delta was modeled by multiple linear regression. Before lavage, arterial PO2 oscillations varied from 3 to 22 mm Hg. After lavage, arterial PO2 oscillations varied from 5 to 439 mm Hg. Response surfaces showed markedly nonlinear dependence of amplitude on PEEP, RR, and Delta. The large PaO2 oscillations observed provide evidence for cyclic recruitment in this model of Lung Injury. The important effect of RR on the magnitude of PaO2 oscillations suggests that the static behavior of atelectasis cannot be accurately extrapolated to predict dynamic behavior at realistic breathing frequencies.
John J. Marini - One of the best experts on this subject based on the ideXlab platform.
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Advances in the support of respiratory failure: putting all the evidence together
Critical Care, 2015Co-Authors: John J. MariniAbstract:Considerable progress has been made recently in the understanding of how best to accomplish safe and effective ventilation of patients with acute Lung Injury. Mechanical and nonmechanical factors contribute to causation of Ventilator-Associated Lung Injury. Intervention timing helps determine the therapeutic efficacy and outcome, and the stage and severity of the disease process may determine the patient's vulnerability as well as an intervention's value. Reducing oxygen consumption and ventilatory demands are key to a successful strategy for respiratory support of acute respiratory distress syndrome. Results from major clinical trials can be understood against the background of the complex physiology of ventilator-induced Lung Injury.
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Bench-to-bedside review: microvascular and airspace linkage in ventilator-induced Lung Injury.
Critical Care, 2003Co-Authors: John J. Marini, John R. Hotchkiss, Alain F. BroccardAbstract:Experimental and clinical evidence point strongly toward the potential for microvascular stresses to influence the severity and expression of ventilator associated Lung Injury. Intense microvascular stresses not only influence edema but predispose to structural failure of the gas–blood barrier, possibly with adverse consequences for the Lung and for extrapulmonary organs. Taking measures to lower vascular stress may offer a logical, but as yet unproven, extension of a Lung-protective strategy for life support in ARDS.
