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Reduced exercise capacity has been reported previously in patients with OSA hypopnea syndrome (OSAHS), although the underlying mechanisms are unclear.

BackgroundInfections are considered as leading causes of acute exacerbations of chronic obstructive pulmonary disease (COPD). Non-infectious risk factors such as short-term air pollution exposure may play a clinically important role. We sought to estimate the relationship between short-term air pollutant exposure and exacerbations in Canadian adults living with mild to moderate COPD.MethodsIn this case-crossover study, exacerbations (‘symptom based’: ≥48 hours of dyspnoea/sputum volume/purulence; ‘event based’: ‘symptom based’ plus requiring antibiotics/corticosteroids or healthcare use) were collected prospectively from 449 participants with spirometry-confirmed COPD within the Canadian Cohort Obstructive Lung Disease. Daily nitrogen dioxide (NO2), fine particulate matter (PM2.5), ground-level ozone (O3), composite of NO2and O3(Ox), mean temperature and relative humidity estimates were obtained from national databases. Time-stratified sampling of hazard and control periods on day ‘0’ (day-of-event) and Lags (‘−1’ to ‘−6’) were compared by fitting generalised estimating equation models. All data were dichotomised into ‘warm’ (May–October) and ‘cool’ (November–April) seasons. ORs and 95% CIs were estimated per IQR increase in pollutant concentrations.ResultsIncreased warm season ambient concentration of NO2was associated with symptom-based exacerbations on Lag−3 (1.14 (1.01 to 1.29), per IQR), and increased cool season ambient PM2.5was associated with symptom-based exacerbations on Lag−1 (1.11 (1.03 to 1.20), per IQR). There was a negative association between warm season ambient O3and symptom-based events on Lag−3 (0.73 (0.52 to 1.00), per IQR).ConclusionsShort-term ambient NO2and PM2.5exposure were associated with increased odds of exacerbations in Canadians with mild to moderate COPD, further heightening the awareness of non-infectious triggers of COPD exacerbations.

In people with COPD, pulmonary gas-exchange efficiency may be impaired because of abnormal alveolar ventilation (V˙A), capillary perfusion (Q˙c), or both. Both have been reported in early and mild stages of the disease. Such derangements often accompany significant clinical consequences such as activity-related dyspnea and exercise intolerance. Although much attention has been paid to pharmacologic treatment of mechanical abnormalities in COPD (eg, bronchodilators to deflate the lungs), increasing neurochemical afferent activity, secondary to gas-exchange inefficiency, has remained elusive as a therapeutic target. Hence, in this invited review, we first summarize how dyspnea, leading to poor exercise tolerance in COPD, may be explained by an increased venous admixture resulting from low V˙A/Q˙c, or wasted ventilation related to high V˙A/Q˙c, or both. We review the conflicting evidence supporting current treatments for gas-exchange inefficiency and exercise tolerance that act primarily on V˙A (bronchodilators, antiinflammatory medications) or Q˙c (oral and inhaled vasodilators, almitrine, and supplemental oxygen). Finally, to address the current knowledge and health care gaps, we propose two independent clinical research foci that may lead to a better understanding of the role of pulmonary gas-exchange inefficiency and activity-related dyspnea in COPD: (1) enhanced and deeper phenotyping of patients with COPD with V˙A/Q˙c abnormalities and (2) evaluation of existing and novel pharmacologic treatments to improve gas-exchange inefficiency, exertional dyspnea, and exercise tolerance across the spectrum of COPD severity.

A cardiopulmonary exercise test (CPET) is ideally suited to quantify exercise tolerance and evaluate the pathophysiological mechanism(s) of dyspnea and exercise limitation in people with chronic respiratory disease. Although there are several statements on CPET and many outstanding resources detailing the cardiorespiratory and perceptual responses to exercise, limited information is available to support the health care provider in conducting a practical CPET evaluation. This article provides the health care provider with practical and timely information on how to use CPET data to understand dyspnea and exercise intolerance in people with chronic respiratory diseases. Information on CPET protocol, as well as how to evaluate maximal patient effort, peak rate of oxygen consumption, ventilatory demand, pulmonary gas exchange, ventilatory reserve, operating lung volumes, and exertional dyspnea, is presented. Two case examples are also described to highlight how these parameters are evaluated to provide a clinical interpretation of CPET data.

ABSTRACT: Although spirometry plays an important role in the evaluation of chronic obstructive pulmonary disease (COPD), it provides only a rough estimate of the patient's functional impairment. A variety of [...]

Objectives: Current criteria use FE[V.sub.1] to assess bronchodilator responsiveness, despite its insensitivity and inability to predict improvement in symptoms or exercise tolerance. Response in lung volumes remains largely unexplored even [...]

Ventilatory limitations in patients with chronic obstructive pulmonary disease cause intense breathlessness and severely restrict exercise capabilities. Therapeutic interventions that effectively reduce lung volumes during physical activity help to prevent dynamic lung hyperinflation and improve exercise tolerance in patients with chronic obstructive pulmonary disease.

Study objective: To explore mechanisms of relief of exertional breathlessness following surgery to reduce thoracic gas volume in patients with emphysema. Materials arid methods: We studied 8 patients with emphysema [...]

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality and functional disability in older adults. In its advanced stages, it is characterized by progressive breathlessness and serious exercise curtailment. Aerobic exercise training (EXT) is recommended for patients who remain breathless despite optimal pharmacologic treatment. Although the physiologic rationale for EXT in COPD patients remains controversial, it is generally accepted that even older incapacitated COPD sufferers who participate in an individualized training program show significant reductions in breathlessness, increased exercise capacity, and enhanced psychosocial function. An 8-week outpatient program that is carefully regulated and includes an educational component is recommended., Chronic obstructive pulmonary disease (COPD)--including chronic bronchitis and emphysema--is the fifth leading cause of death in the United States.|1~ Despite welcome trends in reduced tobacco consumption, mortality rates for COPD [...]

We wished to identify the physiologic abnormalities that distinguish severely breathless (SB) patients with chronic airflow limitation (CAL) from mildly breathless (MB) patients. Thirty-seven patients with stable, advanced CAL ([FEV.sub.1] [...]

International guidelines (1) have correctly highlighted dyspnea alleviation and improvement in exercise tolerance as being among the most important management goals in patients with COPD. Bronchodilator therapy is the first [...]

COPD is associated with nighttime respiratory symptoms, poor sleep quality, and increased risk of nocturnal death. Overnight deterioration of inspiratory capacity (IC) and FEV1have been documented previously. However, the precise nature of this deterioration and mechanisms by which evening bronchodilation may mitigate this occurrence have not been studied.

BackgroundExercise-induced hypoxaemia is a hallmark of chronic fibrotic interstitial lung disease (f-ILD). It remains unclear whether patients’ severe hypoxaemia may exaggerate locomotor muscle fatigue and, if so, to what extent oxygen (O2) supplementation can ameliorate these abnormalities.MethodsFifteen patients (12 males, 9 with idiopathic pulmonary fibrosis) performed a constant-load (60% peak work rate) cycle test to symptom limitation (Tlim) while breathing medical air. Fifteen age-matched and sex-matched controls cycled up to patients’ Tlim. Patients repeated the exercise test on supplemental O2(42%±7%) for the same duration. Near-infrared spectroscopy assessed vastus lateralis oxyhaemoglobin concentration ((HbO2)). Pre-exercise to postexercise variation in twitch force (Tw) induced by femoral nerve magnetic stimulation quantified muscle fatigue.ResultsPatients showed severe hypoxaemia (lowest O2saturation by pulse oximetry=80.0%±7.6%) which was associated with a blunted increase in muscle (HbO2)during exercise vs controls (+1.3±0.3 µmol vs +4.4±0.4 µmol, respectively; p<0.001). Despite exercising at work rates ∼ one-third lower than controls (42±13 W vs 66±13 W), Tw was greater in patients (Tw/external work performed by the leg muscles=−0.59±0.21 %/kJ vs −0.25±0.19 %/kJ; p<0.001). Reversal of exertional hypoxaemia with supplemental O2was associated with a significant increase in muscle (HbO2), leading to a reduced decrease in Tw in patients (−0.33±0.19 %/kJ; p<0.001 vs air). Supplemental O2significantly improved leg discomfort (p=0.005).ConclusionO2supplementation during exercise improves leg muscle oxygenation and fatigue in f-ILD. Lessening peripheral muscle fatigue to enhance exercise tolerance is a neglected therapeutic target that deserves clinical attention in this patient population.

IntroductionRespiratory-related morbidity and mortality were evaluated in relation to incident prescription oral synthetic cannabinoid (nabilone, dronabinol) use among older adults with chronic obstructive pulmonary disease (COPD).MethodsThis was a retrospective, population-based, data-linkage cohort study, analysing health administrative data from Ontario, Canada, from 2006 to 2016. We identified individuals aged 66 years and older with COPD, using a highly specific, validated algorithm, excluding individuals with malignancy and those receiving palliative care (n=185 876 after exclusions). An equivalent number (2106 in each group) of new cannabinoid users (defined as individuals dispensed either nabilone or dronabinol, with no dispensing for either drug in the year previous) and controls (defined as new users of a non-cannabinoid drug) were matched on 36 relevant covariates, using propensity scoring methods. Cox proportional hazard regression was used.ResultsRate of hospitalisation for COPD or pneumonia was not significantly different between new cannabinoid users and controls (HR 0.87; 95% CI 0.61–1.24). However, significantly higher rates of all-cause mortality occurred among new cannabinoid users compared with controls (HR 1.64; 95% CI 1.14–2.39). Individuals receiving higher-dose cannabinoids relative to controls were observed to experience both increased rates of hospitalisation for COPD and pneumonia (HR 2.78; 95% CI 1.17–7.09) and all-cause mortality (HR 3.31; 95% CI 1.30–9.51).ConclusionsNew cannabinoid use was associated with elevated rates of adverse outcomes among older adults with COPD. Although further research is needed to confirm these observations, our findings should be considered in decisions to use cannabinoids among older adults with COPD.

Up-to-date normative reference sets for cardiopulmonary exercise testing (CPET) are important to aid in the accurate interpretation of CPET in clinical or research settings.

Massively obese subjects frequently undergo pulmonary function tests nowadays. Obesity-associated decreases in key operating lung volumes (reduced inspiratory capacity and reduced vital capacity) are particularly concerning because they may shorten the “room” for tidal volume expansion with negative physiologic and sensory consequences.

The lung function laboratory frequently provides relevant information to the practice of pulmonology. Clinical interpretation of pulmonary function and exercise tests, however, has been complicated more recently by temporal changes in demographic characteristics (higher life expectancy), anthropometric attributes (increased obesity prevalence), and the surge of polypharmacy in a sedentary population with multiple chronic degenerative diseases. In this narrative review, we concisely discuss some key challenges to test interpretation that have been affected by these epidemiologic shifts: (a) the confounding effects of advanced age and severe obesity, (b) the contemporary controversies in the diagnosis of obstruction (including asthma and/or COPD), (c) the importance of considering the diffusing capacity of the lung for carbon monoxide (Dlco)/”accessible” alveolar volume (carbon monoxide transfer coefficient) in association with Dlcoto uncover the causes of impaired gas exchange, and (d) the modern role of the pulmonary function laboratory (including cardiopulmonary exercise testing) in the investigation of undetermined dyspnea. Following a Bayesian perspective, we suggest interpretative algorithms that consider the pretest probability of abnormalities as indicated by additional clinical information. We, therefore, adopt a pragmatic approach to help the practicing pulmonologist to apply the information provided by the lung function laboratory to the care of individual patients.

Lung function testing has undisputed value in the comprehensive assessment and individualized management of chronic obstructive pulmonary disease, a pathologic condition in which a functional abnormality, poorly reversible expiratory airway obstruction, is at the core of its definition. After an overview of the physiologic underpinnings of the disease, the authors outline the role of lung function testing in this disease, including diagnosis, assessment of severity, and indication for and responses to pharmacologic and nonpharmacologic interventions. They discuss the current controversies surrounding test interpretation with these purposes in mind and provide balanced recommendations to optimize their usefulness in different clinical scenarios.

A review of contemporary exercise models and data acquisition and analysis techniques for evaluation of muscle blood-flow dynamics at exercise onset is presented together with a summary of the available information on exercising muscle blood-flow dynamics based on the forearm exercise model. Preliminary findings indicate that the major characteristics differentiating the limbs reflect a sensitivity of the forearm vasculature to aging and chronic obstructive pulmonary disease (COPD) that is not demonstrated by the leg vasculature.

COPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the relationship between subjective sleep quality and risk of COPD exacerbations.

FVC may underestimate the slow vital capacity (SVC) due to early closure of the small airways at low lung volumes in the forced maneuver. It remains unclear whether using SVC instead of FVC in the FEV1/vital capacity (VC) ratio increases the yield of spirometry in detecting airflow limitation or, alternatively, leads to a false-positive finding for obstruction.

Unexplained dyspnea presents a significant diagnostic challenge. Dyspnea arises when inspiratory neural drive (IND) to the respiratory muscles is increased and the respiratory system fails to meet this increased demand. Cardiopulmonary exercise testing (CPET) is a valuable tool to unravel the causes of exertional dyspnea in the individual. Moreover, analysis of breathing pattern, operating lung volumes and flow-volume loops allows characterization of abnormal dynamic mechanical response to increased IND - an important source of breathing discomfort. We illustrate the clinical utility of this approach which examines respiratory sensation, ventilatory control, respiratory mechanics and cardio-circulatory responses in cases of unexplained dyspnea.

Dyspnea, the most common symptom in chronic obstructive pulmonary disease (COPD), often becomes disabling in advanced stages of the disease. Chronic dyspnea erodes perceived health status and diminishes engagement in physical activity, often leading to skeletal muscle deconditioning, anxiety, depression, and social isolation. Broader understanding of the pathophysiologic underpinnings of dyspnea has allowed us to formulate a sound rationale for individualized management. This review examines recent research and provides historical context. The overarching objectives are to consider current constructs of the physiologic mechanisms of activity-related dyspnea and identify specific targets amenable to therapeutic manipulation in patients with COPD.

Chronic obstructive pulmonary disease (COPD) and heart failure with reduced ejection fraction (HF) frequently coexist in the elderly. Expiratory flow limitation and lung hyperinflation due to COPD may adversely affect central hemodynamics in HF. Low lung compliance, increased alveolar-capillary membrane thickness, and abnormalities in pulmonary perfusion because of HF further deteriorates lung function in COPD. We discuss how those negative cardiopulmonary interactions create challenges in clinical interpretation of pulmonary function and cardiopulmonary exercise tests in coexisting COPD-HF. In the light of physiologic concepts, we also discuss the influence of COPD or HF on the current medical treatment of each disease.

Lung diffusing capacity for carbon monoxide (Dlco) remains the only noninvasive pulmonary function test to provide an integrated picture of gas exchange efficiency in human lungs. Due to its critical dependence on the accessible “alveolar” volume (Va), there remains substantial misunderstanding on the interpretation of Dlcoand the diffusion coefficient (Dlco/Va ratio, Kco). This article presents the physiologic and methodologic foundations of Dlcomeasurement. A clinically friendly approach for Dlcointerpretation that takes those caveats into consideration is outlined. The clinical scenarios in which Dlcocan effectively assist the chest physician are discussed and illustrative clinical cases are presented.

Is Spirometry Useful? Bronchodilator therapy in COPD is deemed successful if it improves ventilatory mechanics to a degree where effective symptom alleviation and increased exercise capacity are achieved. A greater [...]

CT imaging is a readily quantifiable tool that can provide in-vivo assessments of lung structure in conditions such as chronic obstructive pulmonary disease (COPD). The information extracted from these data has been used in many clinical, epidemiological, and genetic investigations for patient stratification and prognostication, and to determine intermediate endpoints for clinical trials. Although these efforts have informed our understanding of the heterogeneity of pulmonary disease in smokers, they have not yet translated into new treatments for COPD or the personalisation of patient care. There are a multitude of potential reasons for this, including the lack of insight that static imaging provides for lung function and dysfunction, the limited resolution of clinical CT scanning for microscopic changes to the lung architecture, and the challenges that the biomedical community faces when trying to translate discovery to therapy. Such limitations might be addressed through novel image analysis techniques, up-and-coming CT-based and MRI-based technologies, closer ties between academia and industry, and an expanded endeavour to share data across the biomedical community.

ABSTRACTRATIONALE: Since the last published Canadian Thoracic Society (CTS) COPD guideline in 2007 and the 2008 update – highlights for primary care, many new clinical trials have challenged COPD treatment practices. The current Canadian position statement provides the reader with an update on pharmacotherapy of patients with COPD as reviewed by the CTS.OBJECTIVES: The objectives of this position statement are: 1) to summarize the literature on topics relevant to the pharmacological therapy of patients with stable COPD; and 2) to provide clinical guidance with evidence-based recommendations and expert-informed key messages for the pharmacological therapy for patients with stable COPD.METHODS: The authors systematically reviewed the relevant literature focusing on randomized controlled trials and when available, systematic reviews of randomized controlled trials. The proposed key messages, based on scientific evidence and expert-informed opinion, were agreed upon by a majority consensus.MAIN RESULTS: There is typically a significant delay in seeking medical care by patients with dyspnea, often waiting until symptoms affect the performance of activities of daily living. The diagnosis of COPD requires spirometry to confirm the presence of airflow obstruction in any patient presenting with symptoms and/or risk factors of COPD. An effective management plan for individuals with COPD should include: smoking cessation, vaccination and education. A number of non-pharmacological treatments are available for COPD patients with symptoms to improve outcomes such as self-management with coaching from a health care professional; pulmonary rehabilitation; supplemental oxygen in selected patients; and surgery.Current pharmacotherapy for COPD has been shown to alleviate symptoms and prevent exacerbations and related complications such as hospital admissions. In symptomatic patients with stable COPD not having or having infrequent exacerbation, treatment should be started with inhaled LAMA or LABA monotherapy, and if experiencing persistent or increased dyspnea, exercise intolerance, and/or reduced health status despite use of monotherapy, patients should be considered for treatment “step up”with an inhaled LAMA plus LABA dual therapy. In this situation, the use of a single inhaler would be preferred to simplify the treatment regimen and minimize the cost. In patients with stable COPD experiencing exacerbations despite the use of LAMA or LABA monotherapy, treatment “step up”with inhaled LAMA plus LABA dual therapy should be considered unless a patient has concomitant asthma (Asthma/COPD overlap (ACO)). There has been recent interest in using biomarkers to identify patients who are more likely to respond to ICS. Most of the studies have demonstrated that high blood eosinophils could be valuable to predict an increase response in terms of reduction of exacerbation rate when treated with combination ICS/LABA; there is still uncertainty about the exact cut-off level of blood eosinophils having potential therapeutic value. If a patient is still experiencing exacerbations despite the use of LAMA and LABA dual therapy, treatment “step up”with LAMA plus ICS/LABA triple therapy can be considered. Because the superiority of inhaled triple or dual therapy may not be achieved in every patient, the notion of treatment “step down”may be a consideration in some patients. These patients would be those not demonstrating expected benefits or having side effects exceeding benefits. In any circumstance, when a physician decides using a treatment “step down”, this approach should be undertaken under close medical supervision.Individuals with ACO are a population of medical interest, however, the paucity of original studies precluded evidence-based recommendations. The position statement, therefore, presents key messages from a survey which at best reflects the practice in our Canadian community and academic respirologists on assessment, diagnosis, and pharmacotherapy of ACO patients.CONCLUSIONS: This position statement is an evolution towards personalized treatment, compared to the previous published CTS COPD guideline. It promotes approaches to match treatment decisions based on symptom burden and risk of future exacerbations. Personalized medicine becomes increasingly possible, but to make future progress, we will need clinical research to be more specific, including greater focus on or defining better subsets of patients that are characterized by specific biomarkers and disease severity.RÉSUMÉJUSTIFICATION: Depuis les dernières lignes directrices publiées par la Société canadienne de thoracologie (SCT) en 2007 et actualisées pour le médecin de famille en 2008, de nombreux essais cliniques ont remis en question les pratiques relatives au traitement de la MPOC. Cet énoncé de position canadien présente au lecteur les plus récentes informations concernant la pharmacothérapie destinée aux patients souffrant de MPOC, telle que revue par la SCT.OBJECTIFS: Les objectifs de cet énoncé de position sont : 1) résumer la littérature sur les sujets pertinents au traitement pharmacologique des patients souffrant d'une MPOC stable; et 2) présenter des directives comprenant des recommandations fondées sur les données probantes et des messages-clés fondés sur l'avis d'experts pour le traitement pharmacologique des patients souffrant d'une MPOC stable.MÉTHODES: Les auteurs ont revu la littérature pertinente de manière systématique en privilégiant les essais contrôlés randomisés et, lorsque disponibles, les revues systématiques d'essais randomisés. Les messages-clés proposés, qui se fondent sur les données probantes et sur l'opinion d'experts, ont été approuvés par consensus obtenu à la majorité.PRINCIPAUX RÉSULTATS: Les patients souffrant de dyspnée retardent généralement leur quête de soins médicaux jusqu'au moment où les symptômes commencent à affecter leurs activités quotidiennes. Le diagnostic de MPOC nécessite une spirométrie pour confirmer la présence d'une obstruction des voies respiratoires chez un patient qui présente des symptômes ou des facteurs de risque de MPOC. Un plan de prise en charge efficace pour les individus souffrant de MPOC devrait comprendre : la cessation du tabagisme, la vaccination et l’éducation. Un certain nombre de traitements non pharmacologiques sont disponibles pour les patients atteints de MPOC symptomatique afin d'optimiser les résultats, dont l'auto-prise en charge accompagnée des conseils d'un professionnel de la santé; la réadaptation pulmonaire; l'oxygène d'appoint chez certains patients; et la chirurgie.Il a été démontré que la pharmacothérapie actuelle pour la MPOC soulage les symptômes et prévient les exacerbations ainsi que les complications qui en découlent, comme les hospitalisations. Chez les patients atteints de MPOC symptomatique stable avec ou sans exacerbations occasionnelles, le traitement devrait commencer par l'inhalation d'un anticholinergique à longue durée d'action (ACLA) ou d'un Beta2agoniste à longue durée d'action (BALA) en monothérapie, et dans les cas où la dyspnée, l'intolérance à l'exercice et la détérioration de l’état de santé persistent ou augmentent, une intensification  du traitement devrait être envisagée pour ces patients en combinant l'inhalation d'un ACLA à celle d'un BALA en double thérapie. Dans une telle situation, l'usage d'un seul inhalateur devrait être privilégié afin de simplifier le régime de traitement et minimiser les coûts. Chez les patients atteints de MPOC stable qui ont des exacerbations malgré l'utilisation d'un ACLA ou d'un BALA en monothérapie, l'intensification du traitement par l'inhalation d'un ACLA associé au BALA en double thérapie devrait être envisagée, sauf dans les cas où le patient souffre d'asthme concomitant (chevauchement asthme/MPOC). Récemment, on assiste à un accroissement de l'intérêt pour l'utilisation de biomarqueurs afin de déterminer les patients qui sont les plus susceptibles de répondre aux CSI. La plupart des études ont démontré qu'un nombre élevé d’éosinophiles dans le sang pourrait être utile pour prédire une meilleure réponse en ce qui a trait à la réduction du taux d'exacerbation lorsque traité par une combinaison de CSI et de BALA; toutefois, l'incertitude demeure quant au seuil d’éosinophiles dans le sang pouvant avoir une valeur thérapeutique. Si le patient connaît encore des exacerbations malgré un double traitement par ACLA et BALA, l'intensification du traitement par l'ajout d'un ACLA au traitement CSI/BALA en trithérapie peut être envisagé. Puisque la supériorité du traitement par inhalation double ou triple pourrait ne pas être réalisable pour chaque patient, la notion de « diminution graduelle » du traitement pourrait être envisagée pour certains patients. Ces patients seraient ceux qui ne démontrent pas les bénéfices attendus ou qui ont des effets secondaires qui dépassent les bénéfices. Dans toute circonstance, lorsqu'un médecin décide d'avoir recours à une « diminution graduelle » du traitement, cette approche devrait être entreprise sous supervision médicale étroite.Les personnes souffrants de chevauchement asthme/MPOC sont une population de grand intéretê médical. Toutefois, le nombre limité d’études originales empêche la formulation de recommandations fondées sur des données probantes. Cet énoncé de position présente donc des messages-clés issus d'une enquête qui, au mieux, reflète la pratique dans notre communauté canadienne et chez les pneumologues universitaires en ce qui concerne l'evaluation, le diagnostic et la pharmacothérapie dans le cas des patients souffrant de chevauchement asthma/MPOC.CONCLUSION: Cet énoncé de position constitue une évolution vers le traitement personnalisé, comparativement aux lignes directrices de la SCT relatives à la MPOC publiées précédemment. Il favorise les approches qui visent à établir une correspondance entre les décisions thérapeutiques fondées sur le fardeau des symptômes et le risque d'exacerbations futures. La médecine personnalisée devient de plus en plus possible, mais pour progresser, la recherche clinique doit être plus spécifique, notamment en ciblant ou en définissant plus clairement des sous-ensembles de patients caractérisés par des biomarqueurs précis et par le degré de gravité de leur maladie.

Single-point measurements of maximal inspiratory pressure (MIP) are frequently used to suggest muscle weakness in clinical practice. Although there is a large variability in “mean” predicted MIP depending on the chosen reference values, it remains unclear whether those discrepancies actually impact on the prevalence of weakness, that is, MIP below the lower limit of normal.

BackgroundSome patients with COPD report frequent acute exacerbations (AECOPD) of the disease (FE), whereas others suffer them infrequently (IE). Because the current diagnosis of exacerbation relies on patient's perception of increased symptoms (mostly dyspnoea), we hypothesised that dyspnoea perception might be different in COPD patients with FE (≥2 exacerbations or 1 hospitalisation due to AECOPD in the previous year) or IE (≤1 exacerbation in the previous year), AECOPD being defined by the institution antibiotics and/or steroids treatment, or hospital admission.ObjectiveTo test the hypothesis that dyspnoea perception is increased in FE and/or decreased in IE with COPD.MethodsWe compared the perception of dyspnoea (Borg scale), mouth occlusion pressure 0.1 s after the onset of inspiration (P0.1) and ventilatory response to hypercapnia (ΔVE/ΔPETCO2) in 34 clinically stable COPD patients with FE (n=14) or IE (n=20), with similar age, gender, body mass index and degree of airflow limitation. As a reference, we studied a group of age-matched healthy volunteers (n=10) with normal spirometry.ResultsAt rest, P0.1was higher in FE than IE and controls (p<0.01). Compared with controls, the ventilatory response to hypercapnia was equally blunted both in FE and IE (p<0.001). Despite similar spirometry, during rebreathing peak Borg score and ΔBorg were higher (p<0.01) in FE and lower (p<0.01) in IE, than in controls.ConclusionsDyspnoea perception during CO2rebreathing is enhanced in FE and blunted in IE. These differences may contribute to the differential rate of reported exacerbations in FE and IE.Trial registration numberNCT02113839.

The COPD Assessment Test (CAT) is a valid disease-specific questionnaire measuring health status. However, knowledge concerning its use regarding patient and disease characteristics remains limited. Our main objective was to assess the degree to which the CAT score varies and can discriminate between specific patient population groups.

A 56-year-old white woman was referred to the pulmonary clinic for evaluation of unexplained shortness of breath. She enjoyed good health until 3 months prior to this visit when she reported experiencing recurrent episodes of shortness of breath and oppressive retrosternal chest discomfort with radiation to the neck. Episodes lasting 5 to 10 min often occurred at rest and were inconsistently related to physical activity. These symptoms became progressively worse and were often associated with light-headedness and presyncope. Her past medical history was uneventful apart from a prior diagnosis of breast cysts and suspected prolactinoma. Her symptoms escalated to such a level that she was forced to seek urgent medical attention at our institutional ED on two separate occasions in the preceding weeks. These visits precipitated a number of investigations and, eventually, a referral to the pulmonary clinic.

Smokers with persistent cough and sputum production (chronic bronchitis [CB]) represent a distinct clinical phenotype, consistently linked to negative clinical outcomes. However, the mechanistic link between physiologic impairment, dyspnea, and exercise intolerance in CB has not been studied, particularly in those with mild airway obstruction. We, therefore, compared physiologic abnormalities during rest and exercise in CB to those in patients without symptoms of mucus hypersecretion (non-CB) but with similar mild airway obstruction.

Dyspnea is the most prevalent symptom among patients with cardiac and respiratory diseases. It is an independent predictor of mortality in patients with heart disease, COPD, and the elderly. Studies using naloxone to block opioid-receptor signaling demonstrate that endogenous opioids modulate dyspnea in patients with COPD. Neuroimaging studies support a cortical-limbic network for dyspnea perception. A 2012 American Thoracic Society statement recommended that dyspnea be considered across three different constructs: sensory (intensity), affective (distress), and impact on daily activities. The 2013 GOLD (Global Initiative for Chronic Obstructive Lung Disease) executive summary recommended a treatment paradigm for patients with COPD based on the modified Medical Research Council dyspnea score. The intensity and quality of dyspnea during exercise in patients with COPD is influenced by the time to onset of critical mechanical volume constraints that are ultimately dictated by the magnitude of resting inspiratory capacity. Long-acting bronchodilators, either singly or in combination, provide sustained bronchodilation and lung deflation that contribute to relief of dyspnea in those with COPD. Opioid medications reduce breathing discomfort by decreasing respiratory drive (and associated corollary discharge), altering central perception, and/or decreasing anxiety. For individuals suffering from refractory dyspnea, a low dose of an opioid is recommended initially, and then titrated to achieve the lowest effective dose based on patient ratings. Acupuncture, bronchoscopic volume reduction, and noninvasive open ventilation are experimental approaches shown to ameliorate dyspnea in patients with COPD, but require confirmatory evidence before clinical use.

To better understand the interrelationships among disease severity, inspiratory capacity (IC), breathing pattern, and dyspnea, we studied responses to symptom-limited cycle exercise in a large cohort with COPD.

Both chronic airway obstruction and obesity are increasing in prevalence but the effect of their combination on pulmonary function parameters across the range of airway obstruction is unknown.

Obese individuals have impaired respiratory function relative to their normal-weight counterparts. Despite these negative effects, obesity is paradoxically associated with better survival in individuals with chronic obstructive pulmonary disease (COPD). The purpose of this review is to describe this ‘obesity paradox’, to discuss the effects of obesity on respiratory function, and to speculate as to whether obesity-related alterations in respiratory mechanics can influence the natural history of COPD.

The purpose of this review is to identify new advances in our understanding of dyspnea in patients with chronic obstructive pulmonary disease (COPD). Specifically, we highlight new scientific discoveries concerning the language of dyspnea, its underlying mechanisms and its clinical management.

O’DONNELL, E. D. Ventilatory limitations in chronic obstructive pulmonary disease. Med. Sci. Sports Exerc.,Vol. 33, No. 7, Suppl., pp. S647–S655, 2001. Chronic obstructive pulmonary disease (COPD) is a heterogeneous disorder characterized by dysfunction of the small and large airways, as well as by destruction of the lung parenchyma and vasculature, in highly variable combinations. Breathlessness and exercise intolerance are the most common symptoms in COPD and progress relentlessly as the disease advances. Exercise intolerance is multifactorial, but in more severe disease, ventilatory limitation is often the proximate exercise-limiting event. Multiple factors determine ventilatory limitation and include integrated abnormalities in ventilatory mechanics and ventilatory muscle function as well as increased ventilatory demands (as a result of gas exchange abnormalities) and alterations in the neuroregulatory control of breathing. Despite its heterogeneity, the pathophysiological hallmark of COPD is expiratory flow limitation. When ventilation increases in flow-limited patients during exercise, air trapping is inevitable and causes further dynamic lung hyperinflation (DH) above the already increased resting volumes. DH causes elastic and inspiratory threshold loading of inspiratory muscles already burdened with increased resistive work. It seriously constrains tidal volume expansion during exercise. DH compromises the ability of the inspiratory muscles to generate pressure, and the positive intrathoracic pressures likely contribute to cardiac impairment during exercise. Progressive DH hastens the development of critical ventilatory constraints that limit exercise and, by causing serious neuromechanical uncoupling, contributes importantly to the quality and intensity of breathlessness. The corollary of this is that therapeutic interventions that reduce operational lung volumes during exercise, by improving lung emptying or by reducing ventilatory demand (which delays the rate of DH), result in clinically meaningful improvement of exercise endurance and symptoms in disabled COPD patients.

We mimicked important mechanical and ventilatory aspects of restrictive lung disorders by employing chest wall strapping (CWS) and dead space loading (DS) in normal subjects to gain mechanistic insights into dyspnea causation and exercise limitation. We hypothesized that thoracic restriction with increased ventilatory stimulation would evoke exertional dyspnea that was similar in nature to that experienced in such disorders. Twelve healthy young men [28 ± 2 (SE) yr of age] completed pulmonary function tests and maximal cycle exercise tests under four conditions, in randomized order: 1) control, 2) CWS to 60% of vital capacity, 3) added DS of 600 ml, and 4) CWS + DS. Measurements during exercise included cardiorespiratory parameters, esophageal pressure, and Borg scale ratings of dyspnea. Compared with control, CWS significantly reduced the tidal volume response to exercise, increased dyspnea intensity at any given work rate or ventilation, and thus limited exercise performance. DS stimulated ventilation but had minimal effects on dyspnea and exercise performance. Adding DS to CWS further increased dyspnea by 1.7 ± 0.6 standardized Borg units (P= 0.012) and decreased exercise performance (total work) by 21 ± 6% (P= 0.003) over CWS alone. Across conditions, increased dyspnea intensity correlated best with decreased resting inspiratory reserve volume (r= −0.63, P< 0.0005). Dyspnea during CWS was described primarily as “inspiratory difficulty” and “unsatisfied inspiration,” similar to restrictive disorders. In conclusion, severe dyspnea and exercise intolerance were provoked in healthy normal subjects when tidal volume responses were constrained in the face of increased ventilatory drive during exercise.

We compared qualitative and quantitative aspects of perceived exertional dyspnea in patients with interstitial lung disease (ILD) and normal subjects and sought a physiological rationale for their differences. Twelve patients with ILD [forced vital capacity = 64 ± 4 (SE) %predicted] and 12 age-matched normal subjects performed symptom-limited incremental cycle exercise tests with measurements of dyspnea intensity (Borg scale), ventilation, breathing pattern, operational lung volumes, and esophageal pressures (Pes). Qualitative descriptors of dyspnea were selected at exercise cessation. Both groups described increased “work and/or effort” and “heaviness” of breathing; only patients with ILD described “unsatisfied inspiratory effort” (75%), “increased inspiratory difficulty” (67%), and “rapid breathing” (58%) (P< 0.05 patients with ILD vs. normal subjects). Borg-O2uptake (V˙o2) and Borg-ventilation slopes were significantly greater during exercise in patients with ILD (P< 0.01). At peak exercise, when dyspnea intensity and inspiratory effort (Pes-to-maximal inspiratory pressure ratio) were similar, the distinct qualitative perceptions of dyspnea in patients with ILD were attributed to differences in dynamic ventilatory mechancis, i.e., reduced inspiratory capacity, heightened Pes-to-tidal volume ratio, and tachypnea. Factors contributing to dyspnea intensity in both groups were also different: the best correlate of the Borg-V˙o2slope in patients with ILD was the resting tidal volume-to-inspiratory capacity ratio (r= 0.58,P< 0.05) and in normal subjects was the slope of Pes-to-maximal inspiratory pressure ratio overV˙o2(r= 0.60,P< 0.05).