For updates on diagnosis and management of coexisting conditions during the coronavirus disease 2019 (COVID-19) pandemic, see our topic "Management of coexisting conditions in the context of COVID-19". For details on the management of alpha-1 antitrypsin deficiency, please see our topic "Alpha-1 antitrypsin deficiency." The ultimate goals of treatment of COPD are to prevent and control symptoms, to reduce the severity and number of exacerbations, to improve respiratory
capacity for increased exercise tolerance, and to reduce mortality.[1] One systematic review looking at 9 studies found that, compared with placebo, pharmacologic treatment for COPD can reduce the rate of decline in FEV1. Overall, the systematic review showed a reduction in the rate of
decline in FEV1 of 5.0 mL/year for active treatment arms compared with placebo. For studies with inhaled corticosteroid-containing treatment arms, the difference in decline was 7.3 mL/year compared with placebo, whereas the difference between treatment arms containing long-acting bronchodilator and placebo was 4.9 mL/year.[57] However, further research is needed to find out which patients are most likely to benefit. There is a stepwise approach to therapy and treatment should be individualized for general health status and comorbid conditions. The therapeutic approach involves reducing risk factor exposure, appropriate assessment of disease, patient education, pharmacologic and nonpharmacologic management of stable COPD, and prevention and treatment of acute COPD
exacerbations. The World Health Organization (WHO) has specified a minimum set of interventions for the management of stable COPD in primary care. WHO: package of essential noncommunicable (PEN) disease interventions for primary health care Opens in new window Ongoing monitoring and assessment in COPD ensures that the goals of treatment are being met. Quality of life and patients' sense of wellbeing will improve, and hospital admissions will be significantly decreased, when self- or professional monitoring of disease is being utilized.[58] Such assessment of the medical history should include: Exposure to risk factors and preventive measures: Tobacco smoke Indoor and outdoor air pollution Occupational exposures (fumes, dust, etc.) Influenza and pneumococcal vaccination. Disease progression and development of complications: Decline in exercise tolerance Increased symptoms Worsened sleep quality Missed work or other activities. Pharmacotherapy and other medical treatment: How often rescue inhaler is used Any new medicines Compliance with medical regimen Ability to use inhalers properly Adverse effects. Exacerbation history: Urgent care or emergency room visits Recent oral corticosteroid bursts Frequency, severity, and likely causes of exacerbations should be evaluated. Comorbidities:
In addition, objective assessment of lung function should be obtained yearly, or more frequently if there is a substantial increase in symptoms. One Cochrane review found that integrated disease management (IDM), in which several healthcare providers
(physical therapist, pulmonologist, nurse, etc.) work together with patients, probably results in improvement in disease‐specific quality of life, exercise capacity, hospital admissions, and hospital days per
person.[59] [ Acute exacerbationsAn exacerbation of COPD is defined as an event characterized by a change in the patient's baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations and is acute in onset. See our topic on Acute exacerbation of chronic obstructive pulmonary disease for further information. Chronic management: stepwise therapy according to GOLD groupThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommend that initial treatment is determined by the patient’s GOLD group at diagnosis:[1]
[Figure caption and citation for the preceding image starts]: Initial pharmacologic management of COPDGlobal Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2021 report); used with permission [Citation
ends]. Before any adjustment in treatment, patients should be reviewed for symptoms and exacerbation risk, and their inhaler technique and treatment adherence should be assessed. The role of non-pharmacologic treatment should also be assessed.[1] If the patient’s response to initial treatment is appropriate, then the initial treatment can be maintained. Adjustment of pharmacologic treatment can consist of escalation or de-escalation of therapy, as well as switching inhaler devices or molecules within the same drug class. If treatment is changed, then clinicians should review the patient for a clinical response, and for any potential side effects.[1] Recommended escalation therapy for patients with persistent dyspnea/exercise limitation after initial therapy is as follows:[1]
Recommended escalation therapy for patients with persistent exacerbations after initial therapy is as follows:[1]
All patients are candidates for education, vaccination, and smoking
cessation interventions.[Figure caption and citation for the preceding image starts]: Escalation therapy for patients with COPDGlobal Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2021 report). Reproduced with permission [Citation ends]. BronchodilatorsBeta-2 agonists are widely used in the treatment of COPD. They increase intracellular cAMP, leading to respiratory smooth muscle relaxation and reduced airway resistance. Muscarinic antagonists (anticholinergics) act as bronchodilators by blocking the cholinergic receptors on the respiratory smooth muscle. This causes muscle relaxation and reduces airflow limitation. Beta agonists and muscarinic antagonists, therefore, provide bronchodilator effects through different pathways. Both are available as short-acting and long-acting preparations. Short-acting beta-2 agonists (e.g., albuterol, levalbuterol) and short-acting muscarinic antagonists (e.g., ipratropium) improve lung function and breathlessness and quality of life. Ipratropium may have a small benefit over short-acting beta-2 agonists in improving health-related quality of life.[77] These agents can be used as rescue therapy when the patient is using long-acting bronchodilator therapy and may be used as initial treatment for patients in GOLD group A if patients only have occasional dyspnea.[1][78] However, regular use of short-acting bronchodilators is not generally recommended. Tiotropium, a LAMA, has been shown to reduce risk of exacerbation versus placebo or other maintenance
treatments.[79] [ LABAs and LAMAs both significantly improve lung function, dyspnea, and health status and reduce exacerbation rates. [ A LABA/LAMA combination may provide a better therapeutic effect without increasing the adverse effects of each
class.[85][88][89][90][91] Combination therapy with a LABA/LAMA reduces exacerbation rate compared with
monotherapy. Once-daily LABA/LAMA delivered via a combination inhaler is more associated with a clinically significant improvement in lung function and health-related quality of life in patients with mild/moderate COPD, compared with
placebo.[92] [ Umeclidinium/vilanterol, glycopyrrolate/formoterol, tiotropium/olodaterol, and aclidinium/formoterol are LABA/LAMA combinations approved for use in COPD. Umeclidinium/vilanterol decreases the risk of exacerbations in patients with mild/moderate
COPD.[92] [ As outlined above, GOLD makes recommendations on the initial agent based on the patient’s risk group (A, B, C, or D).[1] American Thoracic Society guidelines recommend initiating LABA/LAMA dual therapy in preference to monotherapy in patients with COPD who have dyspnea or exercise intolerance.[75] UK guidelines recommend initiating dual therapy with a LABA/LAMA or LABA/ICS if a patient has symptoms or exacerbations despite nonpharmacologic treatment and using a short-acting bronchodilator as needed. The choice of initial drug regimen in the UK guidance is based on whether or not the patient has features of asthma or features suggesting corticosteroid responsiveness.[2] Inhaled corticosteroidsWhen indicated in patients with COPD, ICS should always be prescribed in combination with long-acting bronchodilators. ICS are
believed to be effective because of their anti-inflammatory effects. Long-term ICS use reduces the need to use rescue therapy and reduces exacerbations, and may also decrease
mortality.[95][96][97] [
The effect of treatment regimens containing ICS is higher in patients at higher risk of exacerbations (two or more exacerbations and/or one hospitalization for an exacerbation in the previous year).[68][70][98] Blood eosinophil count may predict the effectiveness of adding ICS to regular long-acting bronchodilator treatment to prevent exacerbations.[99][63][64] Little or no effect is seen at blood eosinophil counts of <100 cells/microliter, while maximal effect is seen at blood eosinophil counts of >300 cells/microliter.[62][73] These thresholds indicate approximate cut-off values which may help clinicians predict the likelihood of a treatment benefit.[1] Former smokers are more corticosteroid-responsive than current smokers at any eosinophil count.[99] Both current and former smokers with COPD can benefit from ICS in terms of lung function and rates of exacerbations, although the effect is smaller for heavy or current smokers compared with light or former smokers.[70][100] Short-term ICS use (≤1 year) may be associated with greater improvements in FEV1 than long-term use, although further studies are needed to better understand the effect of treatment on lung function.[101] Several studies have pointed to an increased risk of pneumonia in patients with COPD taking ICS.[102] This risk is higher for fluticasone in comparison with budesonide.[103][104][105] A study in a large cohort of Danish patients found the risk of acquiring Pseudomonas aeruginosa, a common cause of hospital-acquired pneumonia, to be dose-dependent, with high-dose ICS associated with the greatest risk. The study also found that patients with P aeruginosa were more likely to have a lower BMI and FEV1 than P aeruginosa-negative patients.[106] A systematic review and meta-analysis found that, despite a significant increase in unadjusted risk of pneumonia associated with use of ICS, pneumonia fatality and overall mortality were not increased in randomized controlled trials and were decreased in observational studies.[107] Therefore, an individualized treatment approach that assesses a patient's risk of pneumonia versus the benefit of decreased exacerbations should be implemented.[102][108][109] Concern is also raised with regards to increased risk of tuberculosis and influenza in adult patients with COPD who are on ICS therapy, although one meta-analysis found that less than 1% of all assessed tuberculosis cases were attributable to ICS exposure.[110][111] ICS may also cause oropharyngeal candidiasis and hoarseness.[102] Although there have been reports of ICS use either increasing or decreasing the risk of lung cancer, the available data do not appear to support either conclusion; further studies are needed.[1] Clinicians should weigh the potential benefits and risks of prescribing ICS and discuss these with the patient.[2] A history of hospitalization(s) for exacerbations of COPD, two or more moderate exacerbations per year despite regular long-acting bronchodilators, blood eosinophils of ≥300 cells/microliter, and/or previous or concomitant asthma all strongly favor initiating ICS.[112] Repeated episodes of pneumonia, blood eosinophils <100 cells/microliter, and/or history of mycobacterial infection are all factors against the use of ICS.[112] Use of ICS can be considered in patients with one moderate exacerbation of COPD per year despite regular long-acting bronchodilator therapy and/or peripheral eosinophils 100-300 cells/microliter.[112] The European Respiratory Society has produced a guideline on the withdrawal of inhaled corticosteroids in COPD.[113] Long-term use of oral corticosteroids in COPD is not recommended.[75] Some patients with severe disease are unable to completely stop treatment after starting oral corticosteroids for an acute exacerbation. In this case, the dose should be kept as low as possible and consideration given to osteoporosis prophylaxis.[2] Combined bronchodilator and corticosteroid preparationsA combination preparation of a long-acting bronchodilator and an ICS may be used for patients who require both these
agents. [ Multiple studies support triple therapy with LABA/LAMA/ICS as being superior to single- or double-agent therapy with LABA/LAMA or LABA/ICS regarding rate of moderate to severe COPD exacerbations and rate of hospitalization.[66][67][68][69][70][71][72][73][74] Use of ICS also slows the rate of decline in lung function following an exacerbation in patients with mild to moderate COPD and elevated blood eosinophils.[117] One randomized controlled trial has reported a reduction in all-cause mortality in patients with FEV1 <50% and at least one exacerbation in the past year who take fluticasone furoate/umeclidinium/vilanterol, compared with patients taking umeclidinium/vilanterol. Patients with mild COPD and at least two moderate or one severe exacerbations in the last year also had reduced all-cause mortality when taking fluticasone furoate/umeclidinium/vilanterol, compared with umeclidinium/vilanterol.[118] Another randomized controlled trial had similar findings in terms of mortality in the triple therapy arm (budesonide/glycopyrrolate/formoterol), but only at the higher dose of ICS.[74][119] The same study showed that increasing the dose of budesonide in triple therapy does not decrease the rate of exacerbations, compared with standard dose triple therapy.[74] For both studies, there were no differences in mortality compared with LABA/ICS.[74][118][119] A post hoc pooled analysis of three trials of triple therapy in patients with COPD and severe airflow limitation and a history of exacerbations showed a non-significant trend for lower mortality with triple therapy compared with non-ICS treatments.[120] These results are strengthened by findings from a meta-analysis of over 200 studies: triple therapy provided a significant reduction in mortality versus dual therapy, although was associated with greater risk of pneumonia. No differences were observed between regimens in lung function or health-related quality of life.[121] Before prescribing triple therapy, clinicians should assess whether another physical or mental condition could be causing the patient’s symptoms. UK guidelines advise clinicians to review patients taking triple therapy for relief of daily symptoms after 3 months. Treatment should be changed to LABA/LAMA if the patient’s symptoms have not improved.[2] The ICS may be withdrawn if the patient has had no exacerbations in the past year.[75] One systematic review of data from real-world studies found little to no evidence of worsened outcomes when ICS was withdrawn and followed by appropriate pharmacologic management in patients with moderate to severe COPD.[122] Phosphodiesterase-4 inhibitorsRoflumilast is an oral phosphodiesterase-4 inhibitor which inhibits the breakdown of cAMP. It may be considered in patients with FEV1 <50% predicted and chronic bronchitis who are taking LABA/LAMA/ICS,
particularly if they have had at least one hospitalization for an exacerbation in the last year.[1] Roflumilast offers benefit in improving lung function and reducing the likelihood of exacerbations. However, it has little impact on quality of life or
symptoms.[123] [ AntibioticsProphylactic antibiotics, such as macrolides, may be considered for reducing the risk of acute exacerbation, particularly in patients who have frequent exacerbations and are refractory to standard
therapy.[124][125][126][127] A Cochrane review ranked macrolides first in reducing exacerbations and serious adverse events, and improving quality of life, above fluoroquinolones and
tetracyclines.[127] Use of prophylactic macrolide antibiotics decreases the frequency of exacerbations in patients with COPD but long-term azithromycin use is associated with clinically significant hearing loss, which in many cases was
reversible.[128] [ Azithromycin therapy is believed to be most effective in preventing acute exacerbation, with greater efficacy seen in older patients and milder GOLD stages. Little evidence of treatment benefit is seen in current smokers.[129] Azithromycin increases the risk of colonization with macrolide-resistant organisms and should not be prescribed for patients with hearing impairment, resting tachycardia, or apparent risk of QTc prolongation.[130] Azithromycin should be considered preferentially, but not only, in former smokers with persistent exacerbations despite appropriate therapy.[1] UK guidelines advise that prophylactic azithromycin could be considered for patients who have more than three acute exacerbations requiring corticosteroid therapy and at least one exacerbation requiring hospitalization per year.[131] Before starting prophylactic antibiotics, baseline ECG and liver function tests should be performed, a sputum sample obtained for culture and sensitivity (including tuberculosis testing), the patient’s sputum clearance technique should be optimised, and bronchiectasis should be excluding with a CT scan.[2][131] ECG and liver tests should be repeated after 1 month of treatment. A head-to-head comparison of fluoroquinolones, tetracyclines, and macrolides given for 12 to 13 weeks to people with COPD did not identify a difference in efficacy or safety between antibiotic classes, but the sample sizes of included studies were small and the studies were of short duration; further research is required in this area.[132] Prophylactic antibiotic therapy should be reviewed at 6 and 12 months to determine whether there is a benefit in terms of exacerbation rates.[131] If antibiotic therapy is not effective it should be stopped. MethylxanthinesTheophylline (a methylxanthine agent) is a bronchodilator that acts by increasing cAMP and subsequent respiratory smooth muscle relaxation. It is not commonly used because of limited potency, narrow therapeutic window, high risk profile, and frequent drug-drug interactions. Theophylline is indicated for persistent symptoms if inhaled therapy is insufficient to relieve airflow obstruction. Theophylline has modest effects on lung function in moderate to severe COPD.[133] A large randomized controlled trial found no effect of oral theophylline alone or with prednisone on exacerbations of severe COPD.[134] GOLD advise that theophylline should only be used if other long-term bronchodilator treatments are unavailable or unaffordable.[1] Experts may prescribe theophylline after a patient has exhausted all options for inhaled therapies. Patient education and self-managementAll patients should be well educated about the disease course and symptoms of exacerbation or decompensation. Their expectation of the disease, treatment, and prognosis should be realistic. It is important to remember that no medication has been shown to modify the long-term decline in lung function, and the primary goal of pharmacotherapy is to control symptoms and prevent complications. One Cochrane review found that self-management interventions that include an action plan for acute exacerbations of COPD are associated with improvements in health-related quality of life and fewer admissions to the hospital for respiratory problems. An exploratory analysis found a small, but significantly higher, respiratory-related mortality rate for self-management compared to usual care, although no excess risk of all-cause mortality was seen.[135] A randomized controlled trial showed that a 3-month program of self-management started in patients with COPD exacerbations recently discharged from hospital led to increases in COPD-related hospitalizations and emergency department visits over 6 months.[136] Self-management plans should include personalized advice on: breathlessness and stress management techniques, energy conservation, avoiding aggravating factors, how to monitor symptoms, how to manage worsening symptoms, and contact information to use in the event of an exacerbation.[1] Helping patients to self-manage should ideally address psychosocial concerns and patients’ personal beliefs about COPD and its management. Many patients report losses and limitations on their lifestyle and social interaction after a diagnosis of COPD. It is estimated that patients with COPD are 1.9 times more likely to commit suicide than those without COPD, and symptoms of anxiety, depression, and frustration are common.[137][138] Studies have found a beneficial effect of cognitive behavioral therapy (CBT) on outcomes including symptoms of depression and anxiety, quality of life, and frequency of emergency department visits.[139][140][141] Further research is warranted into the effects of high-resource-intensive versus low-resource-intensive CBT.[141] One randomized controlled trial found that a telephone health coaching intervention to promote behavior change in patients with mild COPD in primary care led to improvements in self-management activities, but did not improve health-related quality of life.[142] A meta-analysis found that health coaching that included goal setting, motivational interviewing, and COPD-related health education significantly improved health-related quality of life and reduced hospital admissions for an exacerbation of COPD, but did not decrease all-cause hospital admissions.[143] Patients who use inhaled therapies should receive training on inhaler device technique. The majority of patients make at least one error in using their inhaler and incorrect inhaler use is associated with worse disease control.[144][145] Poor technique is more likely when patients are using multiple devices or have never received inhaler technique training.[146] Demonstration of inhaler use by a clinician, device selection, and reviewing technique at subsequent appointments can improve inhaler technique.[147] Demonstration using a placebo device may be most effective for teaching inhaler technique to adults ages ≥65 years.[148] Patients should be asked to bring their inhalers to clinic to facilitate a review of inhaler use.[1] Pharmacist-led interventions and lay health coaching can improve inhaler technique and adherence in patients with COPD.[149][150] Inhaler device attributes such as rapid onset of symptom relief and small size have been recorded in patient preference studies.[151][152] Physical activity is recommended for all patients with COPD.[1] One systematic review and meta-analysis of randomized controlled trials found that exercise training on its own can improve physical activity in COPD, and greater improvements can be made with the addition of physical activity counseling.[153] Another systematic review and meta-analysis found that a combination of aerobic exercise and strength training was more effective than strength training or endurance training alone in increasing the 6-minute walking distance.[154] Other studies have demonstrated improvements in peak oxygen uptake, perceived fatigue, and health-related quality of life following adherence to supervised and unsupervised exercise programmes.[155][156][157] A Cochrane review found limited evidence for improvement in physical activity with physical activity counseling, exercise training, and pharmacologic management of COPD. The authors commented that assessment of quality had been limited by lack of methodologic detail and the diverse range of interventions had primarily been assessed in single studies.[158] The optimal timing, components, duration, and models for improving physical activity remain unclear. Meta-analyses suggest that yoga, Qigong, and other home-based breathing exercises can improve exercise capacity and pulmonary function in patients with COPD.[159][160][161] Tai Chi has been shown to improve exercise capacity compared with usual care.[162] Dietary advice and oral supplements have been found to improve body weight, quality of life, respiratory muscle strength, and 6-minute walk distance.[163][164] However, nutritional support has not been consistently found to improve lung function.[164] Smoking cessation and vaccinationSmoking cessation should be encouraged in all patients, in addition to guidance on avoiding exposure to occupational or environmental tobacco smoke and other irritants.[1][2] Smoking cessation significantly reduces the rate of progression of COPD and risk of malignancies. It also reduces the risk of coronary and cerebrovascular diseases. Among different therapeutic modalities in COPD, the only two factors that improve survival are smoking cessation and oxygen supplementation. Usual smoking cessation programs include counseling, group meetings, and drug therapy.[165] Some patients may need frequent referrals to achieve success. Smoking cessation that includes pharmacotherapy and intensive counseling has a higher success rate and is cost effective in COPD, with low costs per quality-adjusted life year.[166][167][168] The effectiveness and safety of e-cigarettes/vaping as an aid to smoking cessation is uncertain.[1] Depending on local guidelines, patients should be vaccinated against influenza virus, Streptococcus pneumoniae, pertussis (whooping cough), varicella-zoster virus (shingles), and coronavirus disease 2019 (COVID-19).[1][169] Vaccination against influenza is associated with fewer exacerbations of
COPD.[170][171] [ The CDC also recommends the tetanus/diphtheria/pertussis vaccine in people with COPD who were not vaccinated in adolescence, and varicella-zoster virus (shingles) for adults with COPD ages 50 years and over.[169] MucolyticsPatients with the chronic bronchitis phenotype of COPD often produce thick sputum on a frequent basis. Mucolytic agents are not associated with an increase in adverse effects and may be beneficial during exacerbations of COPD. [ Pulmonary rehabilitationPulmonary rehabilitation compromises aerobic exercise, strength training, and education. It should be initiated for patients who remain symptomatic despite bronchodilator therapy and is recommended to start early in the course of the disease, when they start feeling shortness of breath with regular activity and walking on a level surface. GOLD guidelines recommend pulmonary rehabilitation for patient groups B to D.[1] Pulmonary rehabilitation relieves dyspnea and fatigue, improves emotional function, and
enhances a sense of control to a moderately large and clinically significant extent.[176] Extensive pulmonary rehabilitation following hospital admission with an acute exacerbation of COPD decreases the risk of readmission, improves health-related quality of life, and reduces
mortality. [ A large US cohort study found that initiation of pulmonary rehabilitation within 90 days of hospital discharge was significantly associated with lower mortality risk at 1 year and fewer rehospitalizations at 1 year.[179][180] Less than 2% of the patient cohort initiated rehabilitation within this timeframe, highlighting the need to develop more effective strategies to encourage patient participation.[179] However, starting pulmonary rehabilitation before hospital discharge could be associated with a higher 12-month mortality, so is not recommended.[181] Pulmonary rehabilitation also decreases the depression and anxiety related to COPD, and reduces hospitalization.[182] The benefit of pulmonary rehabilitation appears to subside after termination of the course unless patients follow a home exercise schedule.[183] Maintenance pulmonary rehabilitation, defined as ongoing supervised exercise at a lower frequency than the original rehabilitation program, may have a role in preserving the benefits of pulmonary rehabilitation over time. Findings from a Cochrane review indicate that supervised maintenance programs may improve health-related quality of life and exercise capacity at 6 to 12 months compared with usual care.[184] Benefits of home- or community-based pulmonary rehabilitation on respiratory symptoms and quality of life in patients with COPD can match those of the hospital-based rehabilitation programs.[185][186][187] A Cochrane review concluded that both primary and maintenance telerehabilitation achieved similar outcomes to in-person rehabilitation with no safety issues. Limitations of the review include small patient numbers and heterogeneity in telerehabilitation models.[188] Oxygen therapy and ventilatory supportGOLD guidelines recommend long-term oxygen therapy in stable patients who have:[1]
Guidelines from the American Thoracic Society (ATS) recommend prescribing long-term oxygen therapy for at least 15 hours per day in adults with COPD who have severe chronic resting room air hypoxemia. The ATS defines severe hypoxemia as either:[189]
For patients prescribed home oxygen therapy, the ATS recommends that the patient and their caregivers should receive instruction and training on the use and maintenance of all oxygen equipment and education on oxygen safety, including smoking cessation, fire prevention, and tripping hazards.[189] Supplemental oxygen should be titrated to achieve SaO₂ ≥90%.[1] The patient should be reassessed after 60 to 90 days to determine whether oxygen is still indicated and is therapeutic.[1] Among different therapeutic modalities in COPD, the only two factors that improve survival are smoking cessation and oxygen supplementation. Oxygen therapy helps minimize pulmonary hypertension by decreasing pulmonary artery pressure, and improves exercise tolerance and quality of life. It has been shown to improve survival.[1][46] There is some evidence that oxygen can relieve breathlessness when given during exercise to mildly hypoxemic and nonhypoxemic people with COPD who do not otherwise qualify for home oxygen therapy.[190] The ATS suggests prescribing ambulatory oxygen (oxygen delivered during exercise or activities of daily living) in adults with COPD who have severe exertional room air hypoxemia.[189] However, the ATS suggests not prescribing long-term oxygen therapy in adults with COPD who have moderate chronic resting room air hypoxemia (SpO₂ of 89%-93%).[189] Air travel is safe for most patients receiving long-term oxygen therapy.[1] Patients with SaO₂ >95% at sea level and SaO₂ ≥84% after a 6-minute walk test may travel by air without further assessment.[1][191] Supplemental oxygen is recommended for patients with SaO₂ 92% to 95% at sea level and SaO₂ <84% after a 6-minute walk test, and for patients with SaO₂ <92% at sea level.[191] Hypoxia-altitude simulation testing should be performed for other patients.[191] For patients who have COPD and obstructive sleep apnea, ventilatory support with continuous positive airway pressure (CPAP) can improve survival and reduce hospital admissions.[1][192] Noninvasive ventilation (NIV) is occasionally used in patients with very severe but stable COPD, although the optimal timing for initiation and best selection criteria for candidates is unclear.[1][193][194] A Cochrane review found that chronic NIV delivered via a facial mask improved survival and conferred short-term health-related quality of life benefit in stable COPD. Chronic NIV also improved duration of hospital admission-free survival in patients with persistent hypercapnia following an exacerbation.[194] Another study reported a significant decrease in exacerbation frequency with NIV versus control therapy, although no improvements were observed in mortality, PaO₂, PaCO₂, or pH.[195] Guidelines from the American Thoracic Society suggest the use of nocturnal NIV in addition to usual care for patients with chronic stable hypercapnic COPD.[196] The European Respiratory Society and Canadian Thoracic Society have issued similar guidance.[197][198] SurgerySurgical
interventions (bullectomy, lung volume reduction
surgery,[199][200] [ Criteria for referral for lung transplantation include:[205]
[ BODE Index for COPD Survival Prediction ] Lung transplantation has been shown to improve quality of life and functional capacity.[200] However, lung transplantation does not appear to confer a survival benefit.[206] Palliative carePalliative therapies to improve symptoms of dyspnea, offer nutritional support, address anxiety and depression, and reduce fatigue may benefit patients with COPD who experience these despite optimal medical therapy.[1] End-of-life care and hospice admission should be considered for patients with very advanced disease. Patient and family should be well educated about the process, and it is suggested that discussions should be held early in the course of the disease before acute respiratory failure develops.[207] Opioid analgesics, fans, neuromuscular electrical stimulation, and chest wall vibration can relieve dyspnea.[1] One study has suggested that low doses of an opioid analgesic and a benzodiazepine are safe and are not associated with increased hospital admissions or mortality.[208] Another study found that regular, low-dose, oral sustained-release morphine for 4 weeks improved disease-specific health status in patients with COPD and refractory breathlessness.[209] One Cochrane review concluded that there is no evidence for or against benzodiazepines for the relief of breathlessness in people with advanced cancer and COPD.[210] Acupuncture and acupressure may also improve breathlessness and quality of life in patients with advanced COPD.[211] What is the best exercise for COPD patients?Best exercises for COPD. walking.. jogging.. jumping rope.. bicycling.. skating.. low-impact aerobics.. swimming.. resistance training (with hand weights or bands). What are pulmonary exercises?Belly Breathing. Lie comfortably on your back or sit straight and supported on a chair.. Place one hand on your chest, and one hand on your belly.. Breathe in slowly through your nose. Your belly should push out, while your chest stays flat.. Breathe in for a count of 2, and breathe out for a count of 4.. What are the 4 types in pulmonary rehabilitation that improves airway clearance?Comprehensive pulmonary rehabilitation programs generally have the following 4 major components:. Exercise training.. Education.. Psychosocial/behavioral intervention.. Outcome assessment.. |