Do we “drive” dyspnoea?

Abstract

@ERSpublicationsChanges between neural drive and dyspnoea were determined during exercise in severe COPD patients by measuring EMGdi http://ow.ly/FCAs3Electromyography (EMG) measures neural drive, and is routinely used to investigate movement control and pathophysiology in human subjects. The electrical signals recorded from a muscle indicate the recruitment and discharge of spinal motor neurones by voluntary and reflex activation. EMG recordings are typically made with surface electrodes placed on the skin over the muscle of interest, or intramuscular needle or wire electrodes inserted into the muscle of interest. There are advantages and disadvantages of both techniques [1] but the disadvantages are somewhat amplified for EMG recordings from the respiratory muscles. As many respiratory muscles are small and located close to one other, often in layers of muscle with different functions (e.g. the external and internal intercostal muscles), surface recordings are easily contaminated by activity from neighbouring muscles. Intramuscular recordings are more selective but the risks associated with needle use are more serious for the respiratory muscles because of the underlying lung. In saying that, inspiratory muscle surface EMG recordings are possible [2,3] and electrode position can be optimised for the diaphragm [4] for some protocols. With intramuscular electrodes, the risk of pneumothorax can be minimised by using ultrasound to visualise the muscle and lung and estimate maximal insertion depth prior to recordings [5], and on-line audio and visual feedback of EMG activity during recordings [6]. Intramuscular recordings have been used to assess diaphragm activity with three-fold increases in minute ventilation (V´E) associated with hypercapnia [7] but have not been used in exercise protocols, potentially due to the high risk of pneumothorax with large changes in lung volume. As surface and intramuscular EMG recordings from the respiratory muscles are complicated by their anatomy, alternative measures, such as V´E and intrathoracic pressures, have been used as surrogates to assess respiratory neural drive, particularly in clinical populations.Much of the insight into the pathophysiology of exertional dyspnoea in respiratory disease, including chronic obstructive pulmonary disease (COPD), asthma and pulmonary arterial hypertension, has come from studies using pressure measurements, V´E and lung volumes to assess respiratory mechanics [8][9][10][11][12][13]. Neurophysiologically, increased perceived breathing effort is believed to reflect the awareness of increased motor command output to the respiratory muscles ("neural respiratory drive") and increased central corollary discharge from the respiratory motor centres to the somatosensory cortex [8]. It cannot be neglected that when the spontaneous increase in tidal volume (VT) is constrained (either volitionally or by external imposition) in the face of increased chemostimulation, respiratory discomfort (specifically, air hunger or unsatisfied inspiration) arises [8]...

Blunted perception of neural respiratory drive and breathlessness in patients with cystic fibrosis

“…In response to H udson and L aveneziana [27], our data confirm that in cystic fibrosis NRD to obligatory muscles, i.e. the parasternal intercostal muscles (sEMG para ) is correlated to dyspnoea sensation.…”

Modulation of Respiratory Neural Drive by Physiological Loads in COVID-19 Patients with Dyspnea

“…Additionally, patients who have recovered from COVID-19 may suffer from persistent dyspnea due to diaphragm dysfunction. In critically ill patients with novel Coronavirus disease, diaphragm dysfunction may occur due to critical illness myopathy or ventilator-induced diaphragm damage due to blunted ventilation [76] [77]. Also, the significance of corticospinal input to the respiratory centers has been highlighted for contributing to neural drive during the waking state [78].…”

The clinical relevance of the emphysema-hyperinflated phenotype in COPD

“…In COPD patients with hyperinflation, emphysema decreases lung elastic recoil pressure and causes a reset of functional residual capacity, or EELV, at a higher absolute lung volume. The difference between expected (long-dashed lines) and observed EELV (short-dashed lines) represent static hyperinflation increases shortness of breath [48][49][50], and a mechanical dyspnoea threshold is reached when inspiratory reserve volume (IRV) decreases to approximately 0.6-0.4 L [51]. Further increase in minute ventilation will preferentially be accomplished by increased respiratory rate, with consequently deceased expiratory time, which aggravates DH to a greater extent.…”