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      Can resistive breathing injure the lung? Implications for COPD exacerbations

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          In obstructive lung diseases, airway inflammation leads to bronchospasm and thus resistive breathing, especially during exacerbations. This commentary discusses experimental evidence that resistive breathing per se (the mechanical stimulus) in the absence of underlying airway inflammation leads to lung injury and inflammation (mechanotransduction). The potential implications of resistive breathing-induced mechanotrasduction in COPD exacerbations are presented along with the available clinical evidence.

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          Most cited references 32

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          Chronic obstructive pulmonary disease.

           Chris Barnes (2000)
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            The pathology of chronic obstructive pulmonary disease.

            The pathogenesis of chronic obstructive pulmonary disease (COPD) is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although tobacco smoking is the primary cause of this inhalation injury, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue-repair and -remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The common form of emphysema observed in smokers begins in the respiratory bronchioles near the thickened and narrowed small bronchioles that become the major site of obstruction in COPD. The mechanism(s) that allow small airways to thicken in such close proximity to lung tissue undergoing emphysematous destruction remains a puzzle that needs to be solved.
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              The tension-time index and the frequency/tidal volume ratio are the major pathophysiologic determinants of weaning failure and success.

              We have previously shown (Am. J. Respir. Crit. Care Med. 1995;152:1248-1255) that in patients needing mechanical ventilation, the load imposed on the inspiratory muscles is excessive relative to their neuromuscular capacity. We have therefore hypothesized that weaning failure may occur because at the time of the trial of spontaneous breathing there is insufficient reduction of the inspiratory load. We therefore prospectively studied patients who initially had failed to wean from mechanical ventilation (F) but had successful weaning (S) on a later occasion. Compared with S, during F patients had greater intrinsic positive end-expiratory pressure (6. 10 +/- 2.45 versus 3.83 +/- 2.69 cm H2O), dynamic hyperinflation (327 +/- 180 versus 213 +/- 175 ml), total resistance (Rmax, 14.14 +/- 4.95 versus 11.19 +/- 4.01 cm H2O/L/s), ratio of mean to maximum inspiratory pressure (0.46 +/- 0.1 versus 0.31 +/- 0.08), tension time index (TTI, 0.162 +/- 0.032 versus 0.102 +/- 0.023) and power (315 +/- 153 versus 215 +/- 75 cm H2O x L/min), less maximum inspiratory pressure (42.3 +/- 12.7 versus 53.8 +/- 15.1 cm H2O), and a breathing pattern that was more rapid and shallow (ratio of frequency to tidal volume, f/VT 98 +/- 38 versus 62 +/- 21 breaths/min/L). To clarify on pathophysiologic grounds what determines inability to wean from mechanical ventilation, we performed multiple logistic regression analysis with the weaning outcome as the dependent variable. The TTI and the f/VT ratio were the only significant variables in the model. We conclude that the TTI and the f/VT are the major pathophysiologic determinants underlying the transition from weaning failure to weaning success.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                26 September 2016
                : 11
                : 2377-2384
                Pulmonary and Critical Care Medicine, Medical School, National and Kapodistrian University of Athens, Greece
                Author notes
                Correspondence: Theodoros Vassilakopoulos, Pulmonary and Critical Care Medicine, Medical School, National and Kapodistrian University of Athens, Evangelismos Hospital, 45-47 Ipsilandou St, Athens 10676, Greece, Tel +30 210 720 1952, Fax +30 210 720 1951, Email tvassil@
                © 2016 Vassilakopoulos and Toumpanakis. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.


                Respiratory medicine

                inflammation, bronchoconstriction, mechanotransduction, copd, resistive breathing


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