Articles: mechanical-ventilation.
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Intensive Care Med Exp · Dec 2014
Genetic and pharmacologic inhibition of Tpl2 kinase is protective in a mouse model of ventilator-induced lung injury.
Mechanical stress induced by injurious ventilation leads to pro-inflammatory cytokine production and lung injury. The extracellular-signal-regulated-kinase, ERK1/2, participates in the signaling pathways activated upon mechanical stress in the lungs to promote the inflammatory response. Tumor progression locus 2 (Tpl2) is a MAP3kinase that activates ERK1/2 upon cytokine or TLR signaling, to induce pro-inflammatory cytokine production. The role of Tpl2 in lung inflammation, and specifically in the one caused by mechanical stress has not been investigated. The aim of the study was to examine if genetic or pharmacologic inhibition of Tpl2 could ameliorate ventilator-induced lung injury. ⋯ Genetic and pharmacologic inhibition of Tpl2 is protective in a mouse model of ventilator-induced lung injury, ameliorating both high-permeability pulmonary edema and lung inflammation.
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Nursing in critical care · Nov 2014
Complications related to early mobilization of mechanically ventilated patients on Intensive Care Units.
To compare international literature on the detection of complications associated with early mobilization of mechanically ventilated patients in intensive care units (ICUs). ⋯ Despite a low complication rate, a frame for safety during early mobilization including team training and adapted criteria is recommended.
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Emerg. Med. Clin. North Am. · Nov 2014
ReviewLung-protective Ventilation Strategies and Adjunctive Treatments for the Emergency Medicine Patient with Acute Respiratory Failure.
Respiratory failure is a frequent disease process encountered in the emergency department. There is significant need for improvement in the care of patients on mechanical ventilation. If not contraindicated, lung-protective ventilation strategies should be used. It is important to consider pathophysiology (shunting, dead space ventilation, and low venous admixture) when formulating treatment strategies in patients who are difficult to oxygenate or ventilate or when Pao2, Paco2, and pH can only be maintained at unsafe ventilator settings.
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Editorial Randomized Controlled Trial Multicenter Study
THE ASSOCIATION BETWEEN PHYSIOLOGIC DEAD-SPACE FRACTION AND MORTALITY IN PATIENTS WITH THE ACUTE RESPIRATORY DISTRESS SYNDROME ENROLLED INTO A PROSPECTIVE MULTI-CENTERED CLINICAL TRIAL.
We tested the association between pulmonary dead-space fraction (ratio of dead space to tidal volume [V(D)/V(T)]) and mortality in subjects with ARDS (Berlin definition, P(aO2)/F(IO2) ≤ 300 mm Hg; PEEP ≥ 5 cm H2O) enrolled into a clinical trial incorporating lung-protective ventilation. ⋯ Markedly elevated V(D)/V(T) (≥ 0.60) in early ARDS is associated with higher mortality. Measuring V(D)/V(T) may be useful in identifying ARDS patients at increased risk of death who are enrolled into a therapeutic trial.