Chronic obstructive pulmonary disease (COPD) remains a major public health problem. It is the fourth leading cause of chronic morbidity and mortality in the United States, and is projected to rank fifth in 2020 in burden of disease worldwide, according to a study published by the World Bank/World Health Organization. Yet, COPD remains relatively unknown or ignored by the public as well as public health and government officials. In 1998, in an effort to bring more attention to COPD, its management, and its prevention, a committed group of scientists encouraged the U.S. National Heart, Lung, and Blood Institute and the World Health Organization to form the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Among the important objectives of GOLD are to increase awareness of COPD and to help the millions of people who suffer from this disease and die prematurely of it or its complications. The first step in the GOLD program was to prepare a consensus report, Global Strategy for the Diagnosis, Management, and Prevention of COPD, published in 2001. The present, newly revised document follows the same format as the original consensus report, but has been updated to reflect the many publications on COPD that have appeared. GOLD national leaders, a network of international experts, have initiated investigations of the causes and prevalence of COPD in their countries, and developed innovative approaches for the dissemination and implementation of COPD management guidelines. We appreciate the enormous amount of work the GOLD national leaders have done on behalf of their patients with COPD. Despite the achievements in the 5 years since the GOLD report was originally published, considerable additional work is ahead of us if we are to control this major public health problem. The GOLD initiative will continue to bring COPD to the attention of governments, public health officials, health care workers, and the general public, but a concerted effort by all involved in health care will be necessary.

https://www.who.int/respiratory/copd/GOLD_WR_06.pdf

Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary.

Representatives from many countries serve as a network for the dissemination and implementation of programs for diagnosis, management, and prevention of COPD. The GOLD Board of Directors is grateful to the many GOLD National Leaders who participated in discussions of concepts that appear in GOLD reports.

Global initiative for chronic obstructive lung disease.

The aim of this study was to test the hypothesis that use of tiotropium, a new long-acting anticholinergic bronchodilator, would be associated with sustained reduction in lung hyperinflation and, thereby, would improve exertional dyspnoea and exercise performance in patients with chronic obstructive pulmonary disease. A randomised, double-blind, placebo-controlled, parallel-group study was conducted in 187 patients (forced expiratory volume in one second 44 +/- 13% pred): 96 patients received 18 microg tiotropium and 91 patients received placebo once daily for 42 days. Spirometry, plethysmographic lung volumes, cycle exercise endurance and exertional dyspnoea intensity at 75% of each patient's maximal work capacity were compared. On day 42, the use of tiotropium was associated with the following effects at pre-dose and post-dose measurements as compared to placebo: vital capacity and inspiratory capacity (IC) increased, with inverse decreases in residual volume and functional residual capacity. Tiotropium increased post-dose exercise endurance time by 105 +/- 40 s (21%) as compared to placebo on day 42. At a standardised time near end-exercise (isotime), IC, tidal volume and minute ventilation all increased, whilst dyspnoea decreased by 0.9 +/- 0.3 Borg scale units. In conclusion, the use of tiotropium was associated with sustained reductions of lung hyperinflation at rest and during exercise. Resultant increases in inspiratory capacity permitted greater expansion of tidal volume and contributed to improvements in both exertional dyspnoea and exercise endurance.

https://erj.ersjournals.com/content/erj/23/6/832.full.pdf

Effects of tiotropium on lung hyperinflation, dyspnoea and exercise tolerance in COPD.

Pulmonary rehabilitation, a multidisciplinary and structured intervention for patients with chronic pulmonary diseases, has been shown to improve exercise tolerance, reduce dyspnea and improve health-related quality of life. Pulmonary rehabilitation appears to be cost-effective, since it reduces health care utilization. Exercise training represents the cornerstone of every pulmonary rehabilitation program. To obtain clinically relevant effects, training should closely supervised, of high intensity, lasting 30-45 min for at least 3 days/week. Patients should undertake a minimum of 20 sessions, but longer programs result in larger and more long-lasting effects. Education and self-management programs have been shown to result in a substantial reduction in hospital admissions. Nutritional intervention should be considered for patients who are underweight or those with body composition abnormalities. Patients reporting fear and anxiety may benefit from psychosocial support, and the integration of occupational therapy in a pulmonary rehabilitation program can improve independence in activity. Multidisciplinary pulmonary rehabilitation is preferably implemented in an outpatient hospital- or community-based setting. Inpatient programs are suited for patients with limited transportation capabilities or severe deconditioning. The most convincing effects of home-based rehabilitation are in maintaining the improvements obtained in an outpatient setting.

Pulmonary Rehabilitation in Chronic Obstructive Pulmonary Disease

Effective management of dyspnea in chronic obstructive pulmonary disease (COPD) requires a clearer understanding of its underlying mechanisms. This roundtable reviews what is currently known about the neurophysiology of dyspnea with the aim of applying this knowledge to the clinical setting. Dyspnea is not a single sensation, having multiple qualitative descriptors. Primary sources of dyspnea include: (1) inputs from multiple somatic proprioceptive and bronchopulmonary afferents, and (2) centrally generated signals related to inspiratory motor command output or effort. Respiratory disruption that causes a mismatch between medullary respiratory motor discharge and peripheral mechanosensor afferent feedback gives rise to a distressing urge to breathe which is independent of muscular effort. Recent brain imaging studies have shown increased limbic system activation in response to various dyspneogenic stimuli and emphasize the affective dimension of this symptom. All of these mechanisms are likely instrumental in exertional dyspnea causation in COPD. Increased central motor drive (and effort) is required to increase ventilation during activity because the inspiratory muscles become acutely overloaded and functionally weakened. Abnormal dynamic ventilatory mechanics and excessive chemostimulation during exercise also result in a widening disparity between escalating central neural drive and restricted thoracic volume displacement. This neuromechanical uncoupling may form the basis for the distressing sensation of unsatisfied inspiration. Interventions that alleviate dyspnea in COPD do so by improving ventilatory mechanics, reducing central neural drive, or both-thereby partially restoring neuromechanical coupling of the respiratory system. Self-management strategies address the affective aspect of dyspnea and are essential to successful treatment.

Pathophysiology of dyspnea in chronic obstructive pulmonary disease: a roundtable.

The mechanisms of exertional dyspnea relief in response to supplemental oxygen (O2) in chronic airflow limitation (CAL) are not precisely known and are likely multifactorial. To explore factors contributing to the relief of dyspnea after oxygen administration, 11 patients with severe CAL (FEV1.0 = 39 +/- 3% predicted, mean +/- SEM) and mild hypoxemia (resting PaO2 = 74 +/- 2 mm Hg) breathed room air (RA) and 60% O2 during exercise at approximately 50% of their maximal incremental exercise capacity. Breathlessness ratings (Borg scale), endurance time, respiratory drive (change in mouth occlusion pressure over the first 0.1 s of inspiration, P0.1), ventilation (VE), breathing pattern, operational lung volumes, gas exchange, and metabolic parameters were compared during RA and 60% O2. PaO2 at exercise cessation during RA and 60% O2 was 65 +/- 3 mm Hg and 226 +/- 12 mm Hg, respectively (p < 0.001). With 60% O2, the mean of individual Borg/time slopes fell significantly (p < 0.05) by 23 +/- 12% and was associated with a 35 +/- 11% increase (p < 0.01) in endurance time (r = -0.64, p < 0.05). During 60% O2, slopes of P0.1 and lactate over time also fell significantly (p < 0.05), whereas delta PaCO2/time did not change significantly. At a standardized time near end-exercise, Borg, VE, and P0.1 changed during 60% O2 by -0.8 +/- 0.3 (p < 0.05), -4.1 +/- 2.0 L/min (p = 0.07), and -1.3 +/- 0.5 cm H2O/s (p < 0.05), respectively. Slopes of Borg/VE, Borg/lactate, and VE/lactate were essentially superimposable during tests on RA and O2: Borg, lactate, and VE all fell proportionally during hyperoxia. In patients with CAL and mild exercise hypoxemia, relief of exertional breathlessness during hyperoxia is explained by reduced ventilatory demand in association with reduced blood lactate levels.

Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation.

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Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation.