Respiratory care
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Editorial Comment
Weakness and Fluid Overload Hinder Weaning. Or Do They?
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Controlled mechanical ventilation is characterized by a fixed breathing frequency and tidal volume. Physiological and mathematical models have demonstrated the beneficial effects of varying tidal volume and/or inspiratory pressure during positive-pressure ventilation. The addition of noise (random changes) to a monotonous nonlinear biological system, such as the lung, induces stochastic resonance that contributes to the recruitment of collapsed alveoli and atelectatic lung segments. In this article, we review the mechanism of physiological pulmonary variability, the principles of noise and stochastic resonance, and the emerging understanding that there are beneficial effects of variability during mechanical ventilation.
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Pulmonary rehabilitation programs document outcomes to prepare for program certification, to demonstrate the value of the program to upper management, and to provide feedback to pulmonary rehabilitation staff regarding the efficacy of the program. The overall goal of this study was to evaluate the feasibility of using non-research-generated clinical data to report long-term outcomes following a pulmonary rehabilitation program. ⋯ This study demonstrated the ability of one pulmonary rehabilitation program to accurately monitor extended long-term follow-up after pulmonary rehabilitation. Implementing this long-term monitoring methodology consistently in pulmonary rehabilitation programs could contribute to evaluation of the comparative effectiveness of various treatment options.
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We present 2 cases of severe re-expansion pulmonary edema (RPE) after one-lung ventilation (OLV) for thoracic surgery. A 32-y-old woman with multiple lung metastases developed severe RPE after OLV during lung resection surgery. ⋯ The levels of interleukin-8 and monocyte chemotactic protein-1, which are thought to play important roles in the development of lung injury, in bronchial secretions were extremely high after the onset of RPE. These results suggest that the pathogenesis of RPE shares, at least in part, a common pathophysiology of acute lung injury.