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      International Journal of COPD (submit here)

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      Correlation and compatibility between surface respiratory electromyography and transesophageal diaphragmatic electromyography measurements during treadmill exercise in stable patients with COPD

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          Abstract

          Purpose

          To evaluate the compatibility and correlation between noninvasive surface respiratory electromyography and invasive transesophageal diaphragmatic electromyography measurements as facilitating indicators of neural respiratory drive (NRD) evaluation during treadmill exercise.

          Patients and methods

          Transesophageal diaphragmatic electromyogram activity (EMGdi,es) and surface inspiratory electromyogram (EMG) activity, including surface diaphragmatic EMG activity (EMGdi,sur), surface parasternal intercostal muscle EMG activity (EMGpara), and surface sternocleidomastoid EMG activity (EMGsc), were detected simultaneously during increasing exercise capacity in 20 stable patients with COPD. EMGdi,es, EMGdi,sur, EMGpara, and EMGsc were quantified using the root mean square (RMS) and were represented as RMSdi,es, RMSdi,sur, RMSpara, and RMSsc, respectively.

          Results

          There was a significant association between EMGdi,es and EMGdi,sur ( r=0.966, p<0.01), EMGpara ( r=0.967, p<0.01), and EMGsc ( r=0.956, p<0.01) in the COPD patients during exercise. Bland-Altman plots showed that the lowest mean bias value was between EMGdi,es and EMGpara compared with the bias values between EMGdi,es and the other two EMG parameters. In comparing the estimation of EMGdi,es, we observed the lowest bias values (−1%) and the lowest limits of agreement values (−10% to −12%). Intraclass correlation coefficient (ICC) between EMGdi,es and EMGdi,sur was 0.978 ( p<0.01), between EMGdi,es and EMGpara was 0.980 ( p<0.01), and between EMGdi,es and EMGsc was 0.868 ( p<0.01).

          Conclusion

          RMSdi,sur, RMSpara, and RMSsc could provide useful physiological markers of NRD in COPD. RMSpara shows the best compatibility and correlation with transesophageal diaphragmatic electromyography during treadmill exercise in stable patients with COPD.

          Most cited references21

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          Patient-ventilator trigger asynchrony in prolonged mechanical ventilation.

          To investigate patient-ventilator trigger asynchrony (TA), its prevalence, physiologic basis, and clinical implications in patients requiring prolonged mechanical ventilation (PMV). Descriptive and prospective cohort study. Barlow Respiratory Hospital (BRH), a regional weaning center. Two hundred consecutive ventilator-dependent patients, transferred to BRH over an 18-month period for attempted weaning from PMV. Patients were assessed clinically for TA within the first week of hospital admission, or once they were in hemodynamically stable condition, by observation of uncoupling of accessory respiratory muscle efforts and onset of machine breaths. Patients were excluded if they had weaned by the time of assessment or if they never achieved hemodynamic stability. Ventilator mode was patient triggered, flow control, volume cycled, with a tidal volume of 7 to 10 mL/kg. Esophageal pressure (Peso), airway-opening pressure, and airflow were measured in patients with TA who consented to esophageal catheter insertion. Attempts to decrease TA in each patient included application of positive end-expiratory pressure (PEEP) stepwise to 10 cm H2O, flow triggering, and reduction of ventilator support in pressure support (PS) mode. Patients were followed up until hospital discharge, when outcomes were scored as weaned (defined as >7 days of ventilator independence), failed to wean, or died. Of the 200 patients screened, 26 were excluded and 19 were found to have TA. Patients with TA were older, carried the diagnosis of COPD more frequently, and had more severe hypercapnia than their counterparts without TA. Only 3 of 19 patients (16%), all with intermittent TA, weaned from mechanical ventilation, after 70, 72, and 108 days, respectively. This is in contrast to a weaning success rate of 57%, with a median (range) time to wean of 33 (3 to 182) days in patients without TA. Observation of uncoupling of accessory respiratory muscle movement and onset of machine breaths was accurate in identifying patients with TA, which was confirmed in all seven patients consenting to Peso monitoring. TA appeared to result from high auto-PEEP and severe pump failure. Adjusting trigger sensitivity and application of flow triggering were unsuccessful in eliminating TA; external PEEP improved but rarely led to elimination of TA that was transient in duration. Reduction of ventilator support in PS mode, with resultant increased respiratory pump output and lower tidal volumes, uniformly succeeded in eliminating TA. However, this approach imposed a fatiguing load on the respiratory muscles and was poorly tolerated. TA can be easily identified clinically, and when it occurs in the patient in stable condition with PMV, is associated with poor outcome.
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            Inspiratory pressure support prevents diaphragmatic fatigue during weaning from mechanical ventilation.

            Persistent inability to tolerate discontinuation from mechanical ventilation is frequently encountered in patients recovering from acute respiratory failure. We studied the ability of inspiratory pressure support, a new mode of ventilatory assistance, to promote a nonfatiguing respiratory muscle activity in eight patients unsuccessful at weaning from mechanical ventilation. During spontaneous breathing, seven of the eight patients demonstrated electromyographic signs of incipient diaphragmatic fatigue. During ventilation with pressure support at increasing levels, the work of breathing gradually decreased (p less than 0.02) as well as the oxygen consumption of the respiratory muscles (p less than 0.01), and electrical signs suggestive of diaphragmatic fatigue were no longer present. In addition, intrinsic positive end-expiratory pressure was progressively reduced. For each patient an optimal level of pressure support was found (as much as 20 cm H2O), identified as the lowest level maintaining diaphragmatic activity without fatigue. Above this level, diaphragmatic activity was further reduced and untoward effects such as hyperinflation and apnea occurred. When electrical diaphragmatic fatigue occurred, the activity of the sternocleidomastoid muscle was markedly increased, whereas it was minimal when the optimal level was reached. We conclude that in patients demonstrating difficulties in weaning from the ventilator: (1) pressure support ventilation can assist spontaneous breathing and avoid diaphragmatic fatigue (pressure support allows adjustment of the work of each breath to provide an optimal muscle load); (2) clinical monitoring of sternocleidomastoid muscle activity allows the required level of pressure support to be determined to prevent fatigue.
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              Neural respiratory drive and breathlessness in COPD.

              The aim of this study was to test the hypothesis that neural respiratory drive, measured using diaphragm electromyogram (EMGdi) activity expressed as a percentage of maximum (EMGdi%max), is closely related to breathlessness in chronic obstructive pulmonary disease. We also investigated whether neuroventilatory uncoupling contributes significantly to breathlessness intensity over an awareness of levels of neural respiratory drive alone. EMGdi and ventilation were measured continuously during incremental cycle and treadmill exercise in 12 chronic obstructive pulmonary disease patients (forced expiratory volume in 1 s±sd was 38.7±14.5 % pred). EMGdi was expressed both as EMGdi%max and relative to tidal volume expressed as a percentage of predicted vital capacity to quantify neuroventilatory uncoupling. EMGdi%max was closely related to Borg breathlessness in both cycle (r=0.98, p=0.0001) and treadmill exercise (r=0.94, p=0.005), this relationship being similar to that between neuroventilatory uncoupling and breathlessness (cycling r=0.94, p=0.005; treadmill r=0.91, p=0.01). The relationship between breathlessness and ventilation was poor when expansion of tidal volume became limited. In chronic obstructive pulmonary disease the intensity of exertional breathlessness is closely related to EMGdi%max. These data suggest that breathlessness in chronic obstructive pulmonary disease can be largely explained by an awareness of levels of neural respiratory drive, rather than the degree of neuroventilatory uncoupling. EMGdi%max could provide a useful physiological biomarker for breathlessness in chronic obstructive pulmonary disease.
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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
                06 November 2017
                : 12
                : 3273-3280
                Affiliations
                [1 ]Guangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University
                [2 ]Department of Respiratory Medicine, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China
                Author notes
                Correspondence: Luqian Zhou; Rongchang Chen, Guangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, 151 Yan Jiang Road, Guangzhou, China, Tel +86 137 6338 3160; +86 131 6338 3160, Fax +86 208 306 2882; +86 208 306 2882, Email zhlx09@ 123456163.com ; chenrc_vip@ 123456163.com
                [*]

                These authors contributed equally to this work

                Article
                copd-12-3273
                10.2147/COPD.S148980
                5683626
                9a42ebd8-c29e-4dcc-8dfe-1af0cab1d244
                © 2017 Wu 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.

                History
                Categories
                Original Research

                Respiratory medicine
                neural respiratory drive,transesophageal diaphragmatic emg,surface diaphragmatic emg,surface sternocleidomastoid emg,surface parasternal intercostal muscle emg

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