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      The immediate effect of soft tissue manual therapy intervention on lung function in severe chronic obstructive pulmonary disease

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          Abstract

          Background and objective

          In chronic obstructive pulmonary disease (COPD), accessory respiratory muscles are recruited as a compensatory adaptation to changes in respiratory mechanics. This results in shortening and overactivation of these and other muscles. Manual therapy is increasingly being investigated as a way to alleviate these changes. The aim of this study was to measure the immediate effect on lung function of a soft tissue manual therapy protocol (STMTP) designed to address changes in the accessory respiratory muscles and their associated structures in patients with severe COPD.

          Methods

          Twelve medically stable patients (n=12) with an existing diagnosis of severe COPD (ten: GOLD Stage III and two: GOLD Stage IV) were included. Residual volume, inspiratory capacity and oxygen saturation (SpO 2) were recorded immediately before and after administration of the STMTP. A Student’s t-test was used to determine the effect of the manual therapy intervention ( P<0.05).

          Results

          The mean age of the patients was 62.4 years (range 46–77). Nine were male. Residual volume decreased from 4.5 to 3.9 L ( P=0.002), inspiratory capacity increased from 2.0 to 2.1 L ( P=0.039) and SpO 2 increased from 93% to 96% ( P=0.001).

          Conclusion

          A single application of an STMTP appears to have the potential to produce immediate clinically meaningful improvements in lung function in patients with severe and very severe COPD.

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          Most cited references 28

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          Pulmonary hypertension in COPD.

          Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema. A small proportion of COPD patients may present with "out-of-proportion" pulmonary hypertension, defined by a mean pulmonary artery pressure >35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-of-proportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension. Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements. The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.
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            What Is Evidence-Based About Myofascial Chains: A Systematic Review.

            To provide evidence for the existence of 6 myofascial meridians proposed by Myers based on anatomic dissection studies.
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              Structure and function of the respiratory muscles in patients with COPD: impairment or adaptation?

              Respiratory muscles are essential to alveolar ventilation. These muscles work against increased mechanical loads due to airflow limitation and geometrical changes of the thorax derived from pulmonary hyperinflation. Respiratory muscle fibres show several degrees of impairment in cellular and subcellular structures which, in many cases, are proportional to the severity of the disease and accompanying conditions (ageing, deconditioning, starvation, comorbidity). This structural impairment translates, from the functional point of view, to a loss of strength (capacity to generate tension) and an increased susceptibility to failure in the face of a particular load (early onset of fatigue). On the other hand, there is accumulating evidence that the diaphragm and other respiratory muscles are also able to express adaptive changes in response to the chronic mechanical load imposed by the disease. In most cases, impairment and adaptation of the respiratory muscles reaches a balance that permits enough ventilation for patients' survival. However, this balance can be altered for additional increments of the mechanical or metabolic load on the muscles (e.g. abdominal or thoracic surgeries, pneumonia, pulmonary embolism, etc.). Moreover, loss of balance is not always associated with extreme situations. Many patients develop ventilatory failure and require hospital admission even if the cause of the exacerbation is less dramatic (bronchial infections, pain of any nature, electrolyte disturbances, etc.). Although the physiopathology of chronic obstructive pulmonary disease exacerbations is multifactorial, the above-mentioned fragility suggests the existence of a "fragile balance" between respiratory muscle overload and respiratory muscle adaptations. Assessment of respiratory muscle function through specific tests evaluating the strength and endurance could offer valuable information about this particular susceptibility to muscle imbalance. Identification of patients possessing a fragile respiratory muscle balance could have important implications for the application of specific strategies such as respiratory muscle training, nutrition, or anabolic treatment.
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                Author and article information

                Journal
                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
                1176-9106
                1178-2005
                2017
                21 February 2017
                : 12
                : 691-696
                Affiliations
                [1 ]Laboratory of Biomechanics and Kinesiology, San José Hospital, Santiago, Chile
                [2 ]Department of Physical Therapy, Faculty of Medicine, University of Chile, Santiago, Chile
                [3 ]Unit of Kinesiology and Physical Therapy, San José Hospital, Santiago, Chile
                [4 ]Departamento de Kinesiología, Universidad Metropolitana de Ciencias de la Educación, Santiago, Chile
                [5 ]Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
                [6 ]Department of Chiropractic, Macquarie University, Sydney, Australia
                Author notes
                Correspondence: Roger M Engel, Department of Chiropractic, Macquarie University, Sydney, NSW 2109, Australia, Tel +61 2 9850 6387, Fax +61 2 9850 9389, Email roger.engel@ 123456mq.edu.au
                Article
                copd-12-691
                10.2147/COPD.S127742
                5327901
                © 2017 Cruz-Montecinos et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). 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.

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