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...

The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG).An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects.All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.740.29 mV (meanSD) for ES and 0.760.30 mV for UMS with maximal power output, and for the left side 0.880.33 mV for ES and 0.800.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.00.8 ms and 6.90.8 ms, respectively, and for the left side 7.81.2 ms and 7.71.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT.The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time. Eur Respir J 1999; 13: 385±390. Measuring the phrenic nerve conduction time (PNCT) and the diaphragm electromyogram (EMG) in response to phrenic nerve stimulation provides useful information for the assessment of diaphragm function and in the diagnosis of neuromuscular disease. PNCT measured with conventional electrical stimulation (ES) of phrenic nerves is a well-established technique [1±3]. However, this measurement is not widely used because ES can be technically difficult [4±6]. To overcome the problems of ES, cervical magnetic stimulation (CMS) [5,6] and unilateral magnetic stimulation (UMS) of the phrenic nerve [4] have been developed. These techniques are both painless and easy to apply. However, the latencies [6,7] and amplitudes [5] of the diaphragm compound muscle action potential (CMAP) measured with CMS are variable and different to those produced by ES. To evaluate the technique of UMS chest wall surface electrodes have previously been used to record the CMAP, and the PNCT was found to be shorter than that measured with ES [4]. The PNCT measured with an oesophageal electrode using UMS has not been reported, although it is considered that the diaphragm EMG recorded from an oesophageal electrode is more specific than when using surface electrodes [1]. The diaphragm EMG recorded from chest wall electrodes can be contaminated by extradiaphragmatic muscle activity [2]; therefore, the PNC...

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