Neural Respiratory Drive and Neuromuscular Coupling During CO2 Rebreathing in Patients with Chronic Interstitial Lung Disease

Gorini, Massimo; Spinelli, Andrea; Ginanni, Roberta; Duranti, Roberto; Gigliotti, Francesco; Arcangeli, P; Scano, Giorgio

doi:10.1378/chest.96.4.824

Cited by 28 publications

(20 citation statements)

References 31 publications

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“…reduced PImax) [28][29][30], while others have reported preserved PImax (as in the present study) [3,8,9,31]. These disparate findings might be explained by the fact that the degree of restrictive lung function impairment varies greatly amongst ILD patients (mean vital capacity ranged from 63% to 77% predicted), whereby disease severity probably represents an important confounding factor for the interpretation of data gained by volitional measurements.…”

Section: Discussioncontrasting

confidence: 66%

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Respiratory muscle function in interstitial lung disease

et al. 2012

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Section: Discussioncontrasting

confidence: 66%

“…However, diaphragmatic electromyography revealed that P0.1 does not adequately reflect the neural output to the inspiratory muscles in ILD patients [30]. Thus, care must be taken when respiratory drive is estimated by P0.1 in the presence of inspiratory muscle dysfunction [30].…”

Section: Respiratory Drive and Load Imposed On Inspiratory Muscles Inmentioning

confidence: 99%

Respiratory muscle function in interstitial lung disease

et al. 2012

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“…An association was also observed between P0.1 and KCO in patients with ILD, suggesting that impaired gas exchange contributes to ventilatory drive [98]. Diaphragm activation is increased in IPF in comparison with healthy subjects, both during carbon dioxide rebreathing [99] and at exercise [38], consistent with the preservation of the command of ventilation in this disease.…”

Section: Central Control Of Ventilationmentioning

confidence: 65%

Physiology of the lung in idiopathic pulmonary fibrosis

et al. 2018

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The clinical expression of idiopathic pulmonary fibrosis (IPF) is directly related to multiple alterations in lung function. These alterations derive from a complex disease process affecting all compartments of the lower respiratory system, from the conducting airways to the lung vasculature. In this article we review the profound alterations in lung mechanics (reduced lung compliance and lung volumes), pulmonary gas exchange (reduced diffusing capacity, increased dead space ventilation, chronic arterial hypoxaemia) and airway physiology (increased cough reflex and increased airway volume), as well as pulmonary haemodynamics related to IPF. The relative contribution of these alterations to exertional limitation and dyspnoea in IPF is discussed.

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“…In previous papers, we have thoroughly criticized the use of either surface or oesophageal EMG recording to assess respiratory drive in humans [9,15,19,[33][34][35][36]. Nonetheless, many data in normal and in disease state support the contention that the slope of the moving time average (Edi/TI) is a reliable measure of the respiratory centre activity [9,[11][12][13][14][15][16][17][18][19][20][21][33][34][35][36]. In the present study, chemoresponsiveness, expressed in terms of Edi response slope (∆XP/TI/∆PCO 2 ), increased from C to A (p<0.028 KWAV).…”

Section: Discussionmentioning

confidence: 99%

Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Scano¹,

Spinelli²,

Duranti³

et al. 1995

Eur Respir J

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C Ca ar rb bo on n d di io ox xi id de e r re es sp po on ns si iv ve en ne es ss s i in n C CO OP PD D p pa at ti ie en nt ts s w wi it th h a an nd d w wi it th ho ou ut t c ch hr ro on ni ic c h hy yp pe er rc ca ap pn ni ia a G. Scano*, A. Spinelli*, R. Duranti*, M. Gorini**, F. Gigliotti**, P. Goti*, J. Milic-Emili † Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia. G. Scano, A. Spinelli, R. Duranti, M. Gorini, F. Gigliotti, P. Goti, J. Milic-Emili. ©ERS Journals Ltd 1995. ABSTRACT: To ascertain whether and to what extent the reduced ventilatory response to a hypercapnic stimulus in chronic obstructive pulmonary disease (COPD) patients depends on a blunted chemoresponsiveness of central origin or to mechanical impairment, we studied two groups of COPD patients without (group A) and with (group B) chronic hypercapnia, but with similar degrees of airway obstruction and hyperinflation.The study was performed on 17 patients (9 normocapnic and 8 hypercapnic). Six age-matched normal subjects (group C) were also studied as a control. During a CO 2 rebreathing test, ventilation (VE), mouth occlusion pressure (P0.1), and the electromyographic activity of diaphragm (Edi) were recorded and then plotted against end-tidal carbon dioxide tension (PCO 2 ).Inspiratory muscle strength was significantly lower in the hypercapnic group (group B) compared to normocapnic group (A), and in these groups compared to the control group (C). Both patient groups exhibited significantly lower ∆VE/∆PCO 2 than the control group. In hypercapnics, ∆P0.1/∆PCO 2 was significantly lower than in normocapnics and control group, whilst mouth occlusion pressure as % of maximal inspiratory pressure ∆P0.1(%MIP)/∆PCO 2 did not differ significantly among the three groups. ∆Edi/∆PCO 2 increased from C to A. At a PCO 2 of 8.65 kPa, VE was similar in the normocapnic and control group, but lower in hypercapnics; Edi was similar in hypercapnic and control group; but greater in normocapnics. P0.1(%MIP) did not differ significantly among groups.Although these data seem to suggest that CO 2 chemoresponsiveness was normal in hypercapnic and increased in normocapnic COPD patients, the lower VE at a PCO 2 of 8.65 kPa casts doubts about the adequacy of chemoresponsiveness in the hypercapnic group. In the latter, the reduced P0.1 response in face of normal P0.1(MIP) and Edi responses to carbon dioxide stimulation could suggest an impairment in inspiratory muscle function. Mechanical impairment and inadequate chemoresponsiveness are both likely to contribute to the low ventilatory response to CO 2 stimulation in chronic hypercapnic COPD patients. Eur Respir J., 1995, 8, 78-85

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Neural Respiratory Drive and Neuromuscular Coupling During CO2 Rebreathing in Patients with Chronic Interstitial Lung Disease

Cited by 28 publications

References 31 publications

Respiratory muscle function in interstitial lung disease

Respiratory muscle function in interstitial lung disease

Physiology of the lung in idiopathic pulmonary fibrosis

Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

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