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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.

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          Most cited references 21

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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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              Diaphragm activation during exercise in chronic obstructive pulmonary disease.

              Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V E) was 12.2 +/- 1.9 L/min (mean +/- SD) at rest, and increased progressively (p < 0.001) to 31.0 +/- 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 +/- 3% of TLC at end-exercise. Pdi at rest was 9.4 +/- 3.2 cm H(2)O and increased during the first two thirds of exercise (p < 0.001) to plateau at about 13 cm H(2)O. EAdi was 24 +/- 6% of voluntary maximal at rest and increased progressively during exercise (p < 0.001) to reach 81 +/- 7% at end-exercise. In conclusion, dynamic hyperinflation during exhaustive exercise in patients with COPD reduces diaphragm pressure-generating capacity, promoting high levels of diaphragm activation.
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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
                © 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.

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