2018
DOI: 10.1183/13993003.01726-2017
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Neurophysiological mechanisms of exertional dyspnoea in fibrotic interstitial lung disease

Abstract: Our understanding of the mechanisms of dyspnoea in fibrotic interstitial lung disease (ILD) is incomplete. The aims of this study were two-fold: 1) to determine whether dyspnoea intensity is better predicted by neural respiratory drive (NRD) or neuromechanical uncoupling (NMU) of the respiratory system in fibrotic ILD, and 2) to examine the effect of breathing 60% oxygen on NRD, NMU and dyspnoea ratings.Fourteen patients with fibrotic ILD were included. Visit 1 comprised a familiarisation incremental cycle exe… Show more

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Cited by 31 publications
(24 citation statements)
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“…In chronic obstructive pulmonary disease (COPD), resting IND is increased 2-fold (EMGdi %max >20%) vs. age-matched health ( 39 , 90 ). Similar magnitudes of increase are seen in interstitial lung disease (ILD) ( 55 , 102 ) and cystic fibrosis ( 49 ). This is linked to pathophysiologic alterations in mechanical and chemical factors ( 103 ) and can already appear in very early disease, as detailed in the accompanying review by ( 104 ): “Dyspnea and Exercise Limitation in COPD: the value of CPET.”…”
Section: Neural Drive In the Evaluation Of The Breathless Patientmentioning
confidence: 60%
“…In chronic obstructive pulmonary disease (COPD), resting IND is increased 2-fold (EMGdi %max >20%) vs. age-matched health ( 39 , 90 ). Similar magnitudes of increase are seen in interstitial lung disease (ILD) ( 55 , 102 ) and cystic fibrosis ( 49 ). This is linked to pathophysiologic alterations in mechanical and chemical factors ( 103 ) and can already appear in very early disease, as detailed in the accompanying review by ( 104 ): “Dyspnea and Exercise Limitation in COPD: the value of CPET.”…”
Section: Neural Drive In the Evaluation Of The Breathless Patientmentioning
confidence: 60%
“…A growing body of research has shown that pulmonary gas-exchange abnormalities and ventilatory inefficiency (i.e., elevated V E /V CO 2 slope and nadir) are key mechanisms of dyspnea and exercise intolerance in patients with interstitial lung disease (ILD; Faisal et al, 2016;Schaeffer et al, 2018). The increased V E /V CO 2 during exercise in ILD appears to be due to the combination of increased dead space and hyperventilation (Agusti et al, 1991;Faisal et al, 2016).…”
Section: Interstitial Lung Diseasementioning
confidence: 99%
“…The increased V E /V CO 2 during exercise in ILD appears to be due to the combination of increased dead space and hyperventilation (Agusti et al, 1991;Faisal et al, 2016). During exercise in patients with ILD, dynamic restrictive mechanical constraints, secondary to increased lung elastic recoil, increase inspiratory elastic loading, and patients often adopt a more rapid and shallow breathing pattern during exercise to minimize the inspiratory elastic work of breathing (Faisal et al, 2016;Schaeffer et al, 2018). Although the reduction in tidal volume is an effective strategy to minimize the elastic work of breathing during exercise, the compensatory tachypnea increases anatomical dead space and, ultimately, V E /V CO 2 (Faisal et al, 2016;Schaeffer et al, 2018).…”
Section: Interstitial Lung Diseasementioning
confidence: 99%
“…This notion is supported by the fact that when patients with ILD are given supplemental oxygen during constant-load exercise, the neural respiratory drive to the diaphragm decreases along with their perception of dyspnea (Schaeffer et al, 2017b). Neural respiratory drive to the diaphragm can be estimated during CPET using esophageal electromyography (Faisal et al, 2016;Schaeffer et al, 2018). Given that ILD primarily affects the lungs, it is logical to assume that ventilatory factors would lead to the increased perception of exertional dyspnea.…”
Section: Sensory Responsesmentioning
confidence: 99%
“…During incremental exercise, patients with ILD report higher levels of dyspnea than healthy individuals for a given absolute exercise intensity or V̇ E ( O’Donnell et al, 1998 ; Faisal et al, 2016 ). The increased dyspnea is thought to reflect the awareness of an increased neural respiratory drive necessitated by the aforementioned pathophysiological alterations in respiratory mechanics and pulmonary gas exchange efficiency ( Schaeffer et al, 2018 ). This notion is supported by the fact that when patients with ILD are given supplemental oxygen during constant-load exercise, the neural respiratory drive to the diaphragm decreases along with their perception of dyspnea ( Schaeffer et al, 2017b ).…”
Section: Introductionmentioning
confidence: 99%