COPD (Chronic Obstructive Pulmonary Disease): Difference between revisions

Introduction[edit|edit source]

Chronic obstructive pulmonary disease (COPD)^[1]is a common and treatable disease characterized by progressive airflow limitation and tissue destruction. It is associated with structurallungchanges due to chronicinflammationfrom prolonged exposure to noxious particles or gases most commonly cigarette smoke. Chronic inflammation causes airway narrowing and decreased lung recoil. The disease often presents with symptoms of cough,dyspnea, and sputum production. Symptoms can range from being asymptomatic torespiratory failure.^[2]

Epidemiology[edit|edit source]

COPD is primarily present insmokersand those greater than age 40. Prevalence increases with age and it is currently the third most common cause of morbidity and mortality worldwide. In 2015, the prevalence of COPD was 174 million and there were approximately 3.2 million deaths due to COPD worldwide. However, the prevalence is likely to be underestimated due to the under-diagnosis of COPD.^[2]

Etiology[edit|edit source]

COPD is caused by prolonged exposure to harmful particles or gases.

• Cigarette smoking is the most common cause of COPD worldwide.^[1]
• Other causes may include second-hand smoke, environmental and occupational exposures, and alpha-1 antitrypsin deficiency (AATD)^[2].

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Mechanism of Injury / Pathological Process[edit|edit source]

COPD is an inflammatory condition involving the airways,lungparenchyma, and pulmonary vasculature.^[2]Emphysemadescribes one of the structural changes seen in COPD where there is destruction of thealveolarair sacs (gas-exchanging surfaces of the lungs) leading to obstructive physiology.

Image 2: Healthy Alveoli.

The process is thought to involveoxidative stressand protease-antiprotease imbalances. In emphysema, an irritant (e.g., smoking) causes aninflammatoryresponse. Neutrophils and macrophages are recruited and release multiple inflammatory mediators. Oxidants and excess proteases lead to the destruction of the air sacs. The protease-mediated destruction of elastin leads to a loss of elastic recoil and results in airway collapse during exhalation.

• The inflammatory response and obstruction of the airways cause a decrease in theforced expiratory volume(FEV1) and tissue destruction leads to airflow limitation and impaired gas exchange.
• Hyperinflation of the lungs is often seen on imaging studies and occurs due to air trapping from airway collapse during exhalation.
• The inability to fully exhale also causes elevations in carbon dioxide (CO2) levels.
• With disease progression the reduction inventilationor increase inphysiologic dead space导致二氧化碳潴留。
• Acute exacerbations of COPD are common and usually occur due to a trigger (e.g.,bacterialorviralpneumonia, environmental irritants). There is an increase in inflammation and air trapping often requiringcorticosteroidand bronchodilator treatment.^[2]

Clinical Presentation[edit|edit source]

COPD will typically present in adulthood and often during the winter months. Patients usually present with complaints of chronic and progressivedyspnea, cough, and sputum production. Patients may also have wheezing and chest tightness. While a smoking history is present in most cases, there are many without such history. They should be questioned on exposure to second-hand smoke, occupational andenvironmentalexposures, and family history.

COPD is a complex interaction betweenasthma,chronic bronchitis, andemphysema.

Evaluation[edit|edit source]

COPD is often evaluated in patients with relevant symptoms and risk factors. The diagnosis is confirmed byspirometry. Other tests may include a6-minute walk test, laboratory testing, andradiographic imaging.

• Assessment - A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and who present with exertional breathlessness, chronic cough, regular sputum production, frequent winter ‘bronchitis’ or wheeze.
• X-Ray - An x-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases.
• Pulmonary function tests- Essential in the diagnosis, staging, and monitoring of COPD.Spirometryis performed before and after administering an inhaled bronchodilator. Inhaled bronchodilators may be a short-acting beta2-agonist (SABA), short-acting anticholinergic, or a combination of both. A ratio of the forced expiratory volume in one second to forced vital capacity (FEV1/FVC) less than 0.7 confirms the diagnosis of COPD. Patients with significantly reduced FEV1 and signs of dyspnea should be evaluated for oxygenation with pulseoximetryorarterial blood gasanalysis.
• Blood tests- A blood sample taken from an artery can be tested forblood gas levelswhich may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a highbloodcount (reactive polycythemia), a reaction to long-term hypoxemia.

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Outcome Measures[edit|edit source]

There can be a different number of ways of measuring the impact or change of someone's COPD, examples being lung function,lung volumesandexercisecapacity. A cross-sectional study recommendscardiopulmonary exercise testing(CPET) as an efficient tool in assessing functional capacity and prognosis in Heart Failure and COPD patients^[6].

Otheroutcome measuresinclude:

Bleep Test; Shuttle Walk Test; Ergometry;BORG RPE;6-minute walk testis commonly performed to assess the submaximal functional capacity of a patient. This test is performed indoors on a flat and straight surface. The length of the hallway is usually 100 feet and the test measures the distance the patient walks over a period of 6 minutes^[2];Grip Strength;30 second Sit to stand

According to a longitudinal study^[7], changes infrailtystatus of COPD patients were associated with significant clinical outcomes related to: dyspnea; mobility;physical activity; handgrip andquadriceps的力量。发现5次sit-to-stand and exacerbations were independent predictors of the improvement in frailty status.

Management / Interventions[edit|edit source]

The primary goals of treatment are to control symptoms, improve thequality of life, and reduce exacerbations and mortality. The non-pharmacological approach includessmoking cessationandpulmonary rehabilitation.

Annualinfluenzavaccinationis recommended in all patients with COPD.

The classes of commonly used medications in COPD include:

• Bronchodilators (beta2-agonists, antimuscarinics, methylxanthines),
• Inhaledcorticosteroids(ICS) and systemic glucocorticoids,
• Phosphodiesterase-4 (PDE4) inhibitors,
• Antibiotics.

Exercise[edit|edit source]

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Exercise prescription is a key component of pulmonary rehabilitation programmes, which are part of the non-pharmacological approach to managing COPD. There is a high level of evidence for the benefits of pulmonary rehabilitation for people with COPD^[9]Strengthand endurance exercise are endorsed for people with COPD.^[10]

Use ofprotein supplements, in combination with exercise, could also be beneficial, refer to dietician.

Muscles that are required for arm exercise are also involved in the movement of the chest wall during respiration and thus the need to breathe often compromises the individual’s ability to undertake daily activities, therefore exercise prescription involving arm exercise needs to be carefully prescribed.^[11]

Promote Effective Inhaled Therapy[edit|edit source]

In people with stable COPD who remain breathless or have exacerbations despite use of short-acting bronchodilators as required, offer the following as maintenance therapy:

• if forced expiratory volume in 1 second (FEV1)≥50% predicted: either long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist (LAMA)
• if FEV1<50% predicted: either LABA with an inhaled corticosteroid (ICS) in a combination inhaler, or LAMA

Offer LAMA in addition to LABA + ICS to people with COPD who remain breathless or have exacerbations despite taking LABA + ICS, irrespective of their FEV1.

Provide Pulmonary Rehabilitation[edit|edit source]

Pulmonary rehabilitation应该让availa (PR)ble to all appropriate people with COPD including those who have had a recent hospitalisation for an acute exacerbation. A randomised study suggests positive outcomes with functional electrostimulation in patients with severe chronic obstructive pulmonary disease hospitalized for acute exacerbation^[12]. A study suggests that patients affected with COPD and pulmonary hypertension experience a lower exercise capacity and quality of life^[13]. Another randomized controlled trial examining the effects of virtual training (VR) and exercise training on the rehabilitation of patients with COPD suggests that pulmonary rehabilitation program supplemented with VR training has positive outcomes in improving physical fitness in patients with COPD^[14]. Studies suggest PR was useful in patients with moderate to severe COPD^[15]. A prospective, multisite, randomised controlled trial will determine whether an 8-week PR programme (exercise training will comprise: overground or treadmill walking, lower limb stationary cycling, lower and upper limb strengthening exercises) is equivalent to a 12-week PR programme in people with COPD^[16].

Utilise a Multidisciplinary Team[edit|edit source]

COPD care should be delivered by a multidisciplinary team.

Palliative Setting[edit|edit source]

• Opioidsshould be used when appropriate for the palliation of breathlessness in people with end-stage COPD unresponsive to other medical therapy
• Use benzodiazepines, tricyclic antidepressants, major tranquillisers and oxygen to treat breathlessness
• Provide access to multidisciplinary palliative care teams and hospices

Resources[edit|edit source]

• Clinical Guidelines for COPD

• KNGF guidelinesfor physical therapy in patients with chronic obstructive pulmonary disease
• Mesothelioma Resources for Patients

Videos[edit|edit source]

[17]

[18]

References[edit|edit source]