The aim of the present study was to use the diaphragm electromyogram (EMGdi) to compare levels of neural respiratory drive (NRD) in a cohort of healthy subjects and chronic obstructive pulmonary disease (COPD) patients, and to investigate the relationship between NRD and pulmonary function in COPD.EMGdi was recorded at rest and normalised to peak EMGdi recorded during maximum inspiratory manoeuvres (EMGdi % max) in 100 healthy subjects and 30 patients with COPD, using a multipair oesophageal electrode. EMGdi was normalised to the amplitude of the diaphragm compound muscle action potential (CMAPdi,MS) in 64 healthy subjects.The mean¡SD EMGdi % max was 9.0¡3.4% in healthy subjects and 27.9¡9.9% in COPD patients, and correlated with percentage predicted forced expiratory volume in one second, vital capacity and inspiratory capacity in patients. EMGdi % max was higher in healthy subjects aged 51-80 yrs than in those aged 18-50 yrs (11.4¡3.4 versus 8.2¡2.9%, respectively). Observations in the healthy group were similar when peak EMGdi or CMAPdi,MS were used to normalise EMGdi.Levels of neural respiratory drive were higher in chronic obstructive pulmonary disease patients than healthy subjects, and related to disease severity. Diaphragm compound muscle action potential could be used to normalise diaphragm electromyogram if volitional inspiratory manoeuvres could not be performed, allowing translation of the technique to critically ill and ventilated patients.KEYWORDS: Chronic obstructive pulmonary disease, electromyography, respiratory diaphragm O bjective markers of disease severity that reflect the physiological load on the respiratory system in chronic obstructive pulmonary disease (COPD) are currently lacking. Although COPD severity is categorised in terms of forced expiratory volume in one second (FEV1) in management guidelines [1], correlations between FEV1 and breathlessness [2] or quality of life are modest [3], and reported relationships between FEV1 and prognosis are inconsistent [4][5][6]. Two small studies confirm that neural respiratory drive (NRD) is increased in COPD [7] and relates to symptoms [8], but the use of measurements of NRD to assess disease severity in COPD has not been fully investigated, in part because there are no data to define ranges of NRD within the healthy population.In COPD, mechanical abnormalities including airflow obstruction, static and dynamic hyperinflation and intrinsic positive end-expiratory pressure increase the load on the respiratory muscles. The translation of inspiratory muscle contraction into negative intrathoracic pressure, and of pressure changes to ventilation, is impaired as a consequence of muscle shortening, increased velocity of contraction, alteration in geometry and reduced compliance of the respiratory system. This results in high NRD in COPD, and disproportionate increases whenever airways obstruction worsens (and hyperinflation increases) or ventilatory requirements increase. The neural output of the brainstem respiratory centre cannot easily be...
Background Neural respiratory drive (NRD) measured from the diaphragm electromyogram (EMGdi) reflects the load/capacity balance of the respiratory muscle pump and is a marker of lung disease severity. EMGdi measurement is invasive, but recording the EMG from the parasternal intercostal muscles using surface electrodes (sEMGpara) could provide a non-invasive method of assessing NRD and disease severity. Objectives To test the hypothesis that NRD measured by sEMGpara correlates with EMGdi, to provide an index of disease severity in cystic fibrosis (CF) and to relate to exercise-induced breathlessness. Methods 15 patients with CF (mean forced expiratory volume in 1 s (FEV 1 ) 53.5% predicted) and 15 age-matched healthy controls were studied. sEMGpara and EMGdi were recorded at rest and during exercise. sEMGpara was recorded using surface electrodes and EMGdi using a multipair oesophageal electrode catheter. Signals were normalised using the peak EMG recorded during maximum respiratory manoeuvres and expressed as EMG%max. The respiratory pattern, metabolic data, oesophageal and gastric pressures and Borg scores were also recorded. Results Mean (SD) resting sEMGpara%max and EMGdi %max were higher in patients with CF than in controls (13.1 (7)% and 18.5 (7.5)% vs 5.8 (3)% and 7.5 (2)%, respectively, p<0.001). In the patients with CF, resting sEMGpara%max and EMGdi%max were related to the degree of airways obstruction (FEV 1 ) (r¼À0.91 and r¼À0.82, both p<0.001), hyperinflation (r¼0.63 and r¼0.56, both p<0.001) and dynamic lung compliance (r¼À0.53 and r¼À0.59, both p<0.001). During exercise, sEMGpara%max and EMGdi%max were strongly correlated with breathlessness in the patients with CF before (r¼0.906, p<0.001) and after (r¼0.975, p<0.001) the onset of neuromechanical dissociation. Conclusion sEMGpara%max provides a non-invasive marker of neural drive, which reflects disease severity and exercise-induced breathlessness in CF.
Background Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. Patients and methods We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (P L ) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory P L volume curves were measured. Results The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m 2 , and the normal group had a BMI of 23.2 (1.6) kg/m 2 ( p=0.001). Obese and normals were matched for age ( p=0.233), gender ( p=0.637) and height ( p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) % predicted, p=0.033; FEV 1 /FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H 2 O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H 2 O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs −2.0 (3.5) cm H 2 O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H 2 O, p=0.008). BMI correlated with end-expiratory gastric (seated R 2 =0.43, supine R 2 =0.66, p<0.01) and oesophageal pressures (seated R 2 =0.51, supine R 2 =0.62, p<0.01). Conclusions Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing.
In a randomized trial involving children who had been born extremely prematurely, those who had undergone HFOV, as compared with those who had received conventional ventilation, had superior lung function at 11 to 14 years of age, with no evidence of poorer functional outcomes. (Funded by the National Institute for Health Research Health Technology Assessment Programme and others.).
Ultrasound provides clinical utility for assessing the trajectory of change in peripheral skeletal muscle architecture during critical illness, supplementing more detailed characterization, albeit rarely used, from muscle biopsy analysis. Adoption of standardized operating protocols for measurement will facilitate future meta-analysis of data.
Lung function deteriorated with increasing age in SCD children and the rate of decline was greater in younger children in whom ACS episodes were more common. Pediatr Pulmonol. 2016;51:717-723. © 2015 Wiley Periodicals, Inc.
Fat-free mass measured by impedance correlated better with pulmonary and respiratory muscle function and exercise capacity than BMI.
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