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Background and Objective: Persistent dyspnoea is a public health issue for which the therapeutic arsenal is limited. This study tested high‐flow nasal cannula therapy (HFNT) as a means to alleviate experimental dyspnoea. Methods: Thirty‐two healthy subjects underwent an experimental dyspnoea induced by thoracoabdominal elastic loading. HFNT was administered with alternately FiO2 of 100% (HFNT100) or 21% (HFNT21). The sensory (S‐VAS) and affective (A‐VAS) components of dyspnoea, transcutaneous CO2 pressure (PtcCO2), pulse‐oximetry oxygen saturation (SpO2), heart rate, respiratory rate and skin galvanometry were monitored continuously. Three experimental sessions of 8 min were conducted: the first session consisted in familiarization with the experimental dyspnoea and the next two sessions tested the effects of HFNT100 and HFNT21 alternatively in a randomized order. Results: HFNT21 and HFNT100 significantly reduced dyspnoea, respectively of ∆A‐VAS = 0.80 cm [−0.02–1.5]; p = 0.007 and ∆A‐VAS = 1.00 cm [0.08–1.75]; p < 0.0001; ∆S‐VAS = 0.70 cm [−0.15–1.98]), p < 0.0001 and ∆S‐VAS = 0.70 cm [0.08–1.95]), p = 0.0002) with no significant difference between HFNT21 and HFNT100. HFNT did not significantly alter the respiratory rate or the heart rate, reduced PtcCO2 only on room air and GSR under both experimental conditions. Conclusion: HFNT was associated with a statistically significant reduction in the intensity of the sensory and affective components of dyspnoea, independent of oxygen addition. This relief of laboratory dyspnoea could result from a reduction of afferent‐reafferent mismatch. High‐flow nasal cannula therapy relieves acute experimental breathlessness induced by thoracoabdominal elastic loading in healthy subjects, independent of oxygen addition. Modulation of the central integration of respiratory afferences may be involved in the dyspnoea alleviation. [ABSTRACT FROM AUTHOR]

Background: More than a symptom, dyspnoea is an existential experience shaping the lives of those afflicted, particularly when its persistence despite maximal pathophysiological treatments makes it pervasive. It is, however, insufficiently appreciated by concerned people themselves, family members, healthcare professionals and the public (dyspnoea invisibility), limiting access to appropriate care and support. Aim: To provide a better understanding of dyspnoea experiences and its invisibility. Design: Interpretative phenomenological analysis of data collected prospectively through in-depth semi-structured interviews. Setting/Participants: Pulmonary rehabilitation facility of a tertiary care university hospital; 11 people (six men, five women) with severe chronic obstructive pulmonary disease (stages 3 and 4 of the 4-stage international GOLD classification) admitted for immediate post-exacerbation rehabilitation. Results: We identified several types of dyspnoea invisibility depending on temporality and interlocutors: (1) invisibility as a symptom to oneself; (2) invisibility as a symptom to others; (3) invisibility as an experience that cannot be shared; (4) invisibility as an experience detached from objective measurements; (5) invisibility as an experience that does not generate empathic concern. The notion of invisibility was present in all the identified experiential dimensions of dyspnoea. It was seen as worsening the burden of the disease and as self-aggravating through self-isolation and self-censorship. Conclusions: The study confirmed that dyspnoea invisibility is a reality for people with advanced chronic obstructive pulmonary disease. It shows dyspnoea invisibility to be a multifaceted burden. Future research should aim at identifying individual and collective measures to overcome dyspnoea invisibility. [ABSTRACT FROM AUTHOR]

Highlights: [•] Dyspnoea has antinociceptive effects in humans. [•] This is true for both air hunger and the sensation of excessive respiratory work/effort. [•] Spinal inhibition (diffuse nociceptive inhibitory controls) is one of the mechanisms of dyspnoea-pain counter-irritation. [•] Yet spinal inhibition does not occur in response to experimental air hunger in normal humans (this study). [•] The analgesic effects of air hunger therefore probably proceed from central phenomena. [ABSTRACT FROM AUTHOR]

The article report that, in almost half of their patients with chronic obstructive pulmonary disease (COPD), an electroencephalogram (EEG)recorded during spontaneous breathing at rest showed cortical activation linked to respiration, in conjunction with a higher rating of excessive respiratory work dyspnoea compared to age-matched controls. The condition has been explored for potentially significant advances in the field.

Background Dyspnoea is a distressing and debilitating symptom with a major impact on quality of life. Alleviation of dyspnoea therefore constitutes a major clinical challenge. When causative physiological disorders cannot be corrected (“persistent dyspnoea”), nonspecific treatment must be considered. Morphine alleviates dyspnoea but has numerous side-effects including ventilatory depression, which justifies looking for alternatives. Certain forms of dyspnoea involve C-fibres, and can be attenuated by C-fibres blockade. We hypothesised that nefopam, a non-sedative benzoxazocine analgesic known to block the transient receptor potential vanilloid subtype 1 abundantly present on C-fibres, would attenuate dyspnoea. Methods We conducted a randomised, double-blind, placebo-controlled crossover study of nefopam in healthy subjects submitted to experimental work/effort dyspnoea by inspiratory threshold loading (15 healthy male volunteers; age 23–41). We studied a perceptual outcome (dyspnoea visual analogue scale —D-VAS—) and a neurophysiological outcome (effect of nefopam on dyspnoea-pain counter-irritation as assessed by laser-evoked potentials; an effect of nefopam on dyspnoea was hypothetised to reduce the ability of dyspnoea to inhibit pain). Somaesthetic evoked potentials (SEPs) were studied as a control. Results A statistically significant decrease in LEP amplitude was observed in response to loading with nefopam (F = 19.1; p < 0.001) and placebo (F = 5.73 and p < 0.001), with no significant difference between nefopam and placebo and no change in SEP characteristics. Conclusions In this study, nefopam did not exhibit any effects on dyspnoea. [ABSTRACT FROM AUTHOR]