COPD (Chronic Obstructive Pulmonary Disease)

Introduction

Chronic obstructive pulmonary disease (COPD) is a common and treatable disease characterized by progressive airflow limitation and tissue destruction. It is associated with structural changes in the lungs caused by chronic inflammation most commonly caused by long-term exposure to noxious particles or gases Cigarette smoke. Chronic inflammation leads to narrowing of the airways and reduced lung recoil. The disease often presents with coughing, dyspnea and sputum production. Symptoms can range from asymptomatic to respiratory failure. [1]

Epidemiology

COPD is mainly found in smokers and people over the age of 40. Prevalence increases with age and is currently the third most common cause of morbidity and mortality worldwide. The prevalence of COPD in 2015 was 174 million and approximately 3.2 million people died from COPD worldwide. However, the prevalence may be underestimated due to the underdiagnosis of COPD. [1]

Etiology

COPD is caused by long-term exposure to harmful particles or gases.

• Smoking is the most common cause of COPD worldwide.
• Other causes may include environmental and occupational exposure to secondhand smoke and alpha-1 antitrypsin deficiency (AATD) [1].

[2]

Injury Mechanism/Pathological Process

COPD is an inflammatory disease that affects the airways, lung parenchyma and pulmonary vasculature. [1] Emphysema describes a structural change in COPD in which the alveolar air sacs (the gas-exchange surfaces of the lungs) are disrupted, resulting in physiological dysfunction.

Image 2: Healthy Alveoli.

This process is thought to involve oxidative stress and protease-antiprotease imbalance. In emphysema, an irritant, such as smoking, causes an inflammatory response. Neutrophils and macrophages are recruited and release various inflammatory mediators. Oxidants and excess proteases lead to Destruction of the airbag. Protease-mediated destruction of elastin results in loss of elastic recoil and causes airway collapse during expiration.

• The inflammatory response and airway obstruction lead to a decrease in forced 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 due to airway collapse during exhalation.
• Inability to fully exhale can also lead to elevated carbon dioxide (CO2) levels.
• As the disease progresses, CO2 trapping results from decreased ventilation or increased physiological dead space.
• Acute exacerbations of COPD are common and usually occur due to triggers such as bacterial or viral pneumonia environmental stimuli. Increased inflammation and air trapping usually require treatment with corticosteroids and bronchodilators. [1]

Clinical Presentation

COPD usually presents in adulthood, and usually in winter. Patients typically complain of chronic and progressive dyspnea, cough, and sputum production. Patients may also experience wheezing and chest tightness. Although a history of smoking is present in most cases, there are many There is no such history. They should be asked about their occupational and environmental exposure to secondhand smoke, as well as their family history.

COPD is a complex interplay between asthma, chronic bronchitis, and emphysema.

Evaluation

COPD is usually evaluated in patients with associated symptoms and risk factors. The diagnosis was confirmed by spirometry. Other tests may include a 6-minute walk test laboratory test and radiographic imaging.

• Evaluation – A diagnosis of COPD should be considered in patients over the age of 35 who have risk factors (usually smoking) and present with dyspnea on exertion, chronic cough, frequent sputum production, winter “bronchitis,” or frequent wheezing.
• X-rays – Chest X-rays may show overexpansion (hyperinflation) of the lungs and help rule out other lung diseases.
• Lung function tests – essential in the diagnostic staging and monitoring of COPD. Spirometry was performed before and after bronchodilator inhalation. Inhaled bronchodilators may be short-acting beta2-agonists (SABAs), short-acting anticholinergics, or a combination of both. proportion A ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC) of less than 0.7 confirms the diagnosis of COPD. Patients with markedly reduced FEV1 and signs of dyspnea should have oxygenation assessed by pulse oximetry or arterial blood gas analysis.
• Blood tests – A blood sample taken from an artery can measure blood gas levels, which may indicate low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show high blood counts (reactive polycythemia) Hypoxemia.

[3][4]

Outcome Measures

There can be a different number of ways to measure the impact or change in someone’s COPD sample, such as lung function lung volume and exercise capacity. A cross-sectional study recommends cardiopulmonary exercise testing (CPET) as an effective tool for assessing functional capacity and capacity Prognosis in patients with heart failure and COPD [5].

Other outcome measures include:

The beep test; shuttle walk test; dynamometer; Borg RPE; 6-minute walk test are commonly used to assess a patient’s submaximal functional capacity. The test is performed indoors on a flat and straight surface. The length of the hallway is typically 100 feet, the test measures the distance Patient walks 6 minutes[1]; grip strength; 30 seconds from sit to stand

According to a longitudinal study [6], changes in frailty status in COPD patients were associated with important clinical outcomes in terms of: mobility; physical activity; grip strength and quadriceps strength. It was found that five sit-to-stand and weighting were independent Predictors of improvement in frailty status.

Management / Interventions

The main goals of treatment are to control symptoms, improve quality of life, and reduce exacerbations and mortality. Non-drug approaches include smoking cessation and pulmonary rehabilitation.

Annual influenza vaccination is recommended for all COPD patients.

Drug classes commonly used in COPD include:

• Bronchodilators (beta2-agonist antimuscarinic methylxanthines)
• Inhaled corticosteroids (ICS) and systemic glucocorticoids
• Phosphodiesterase-4 (PDE4) inhibitors,
• Antibiotics.

Exercise

[7]

Exercise prescription is a key component of a pulmonary rehabilitation program as part of a nonpharmacologic approach to managing COPD. There is substantial evidence that pulmonary rehabilitation is beneficial for patients with COPD [8] Patients with chronic obstructive pulmonary disease [9]

Referring to a nutritionist, it may also be beneficial to combine protein supplements with exercise.

The muscles required for arm movement are also involved in the movement of the chest wall during respiration, so the need to breathe often impairs an individual’s ability to perform daily activities, so exercise prescriptions involving arm movement need to be carefully formulated Regulation. [10]

Promote Effective Inhaled Therapy

For patients with stable COPD who experience dyspnea or exacerbations despite short-acting bronchodilators as needed, offer the following maintenance therapy:

• If forced expiratory volume in one second (FEV1) ≥ 50% predicted: long-acting beta2-agonist (LABA) or long-acting muscarinic antagonist (LAMA)
• If FEV1

LAMA and LABA ICS were given to COPD patients who, despite taking LABA ICS, had difficulty breathing or became ill regardless of their FEV1.

Provide Pulmonary Rehabilitation

Pulmonary rehabilitation (PR) should be offered to all appropriate COPD patients, including those recently hospitalized for an exacerbation. A Randomized Study Shows Positive Effects of Functional Electrical Stimulation in Patients with Severe Chronic Obstructive Pulmonary Disease Pulmonary disease hospitalized for acute exacerbations [11]. A study showed that patients with COPD and pulmonary hypertension had lower exercise capacity and quality of life [12]. Another randomized controlled trial examining the effects of virtual training (VR) and exercise Studies on the rehabilitation training of COPD patients have shown that pulmonary rehabilitation programs supplemented with VR training have a positive effect on improving the physical fitness of COPD patients [13]. PR has been shown to be useful in patients with moderate to severe COPD [14]. a quasi A multicenter randomized controlled trial will determine whether an 8-week PR program (exercise training will include: ground or treadmill walking lower body stationary cycling upper and lower body strengthening exercises) is equivalent to a 12-week PR program in COPD patients [15].

Utilise a Multidisciplinary Team

COPD care should be provided by a multidisciplinary team.

Palliative Setting

• In patients with end-stage COPD unresponsive to other medications, opioids should be used, as appropriate, to relieve dyspnea
• Use of benzodiazepines, tricyclic antidepressants, primary sedatives, and oxygen for dyspnea
• Provide access to multidisciplinary palliative care teams and hospices

Resources

• Clinical Guidelines for COPD
• KNGF guidelines for physical therapy for patients with chronic obstructive pulmonary disease
• Mesothelioma Resources for Patients