Definition.
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable common disease of the respiratory system, characterized by persistent airflow limitation, often progressive in development, accompanied by chronic inflammation of the airways and lungs to harmful particles or gases. Surveys in China have shown that the overall prevalence of COPD is above 5%, with a prevalence of 8.2% in people over 40 years of age and a higher prevalence in people over 65 years of age.
Chronic airflow limitation in COPD is caused by a combination of small airway pathology (obstructive bronchitis) and destruction of the lung parenchyma (emphysema). Chronic bronchitis is defined as a chronic cough and sputum that lasts for 3 months per year for 2 consecutive years, with the exception of other causes of chronic cough and sputum. Emphysema is defined as permanent dilatation of the air spaces distal to the terminal fine bronchi with destruction of the alveolar wall without significant fibrosis.
Etiology.
1, Smoking: smoke produced including cigarettes, pipe tobacco, cigars and other types of tobacco.
2, Indoor pollution caused by the use of biofuels for heating and cooking: an important risk factor for COPD in women in poor areas of developing countries.
3, prolonged and high exposure to occupational dust and chemical fumes: including vapor fumes, irritating toxic fumes and smoke.
4, outdoor air pollution: aggravate the accumulation of respirable particles in the lungs, but its impact on the occurrence of COPD is small.
5, Individual factors: Hereditary antitrypsin alpha-1 deficiency is the most important genetic susceptibility risk factor. Finally, any cause that may affect embryonic and early childhood lung development, such as low birth weight infants, respiratory infections, etc., are also risk factors that can potentially lead to COPD.
Diagnosis
1. Clinical manifestations
The characteristic symptoms of COPD are cough, sputum and progressive dyspnea. Chronic cough and sputum can precede airflow limitation for many years. Conversely, significant airflow limitation can also occur without chronic cough and sputum.
Cough: Chronic cough is usually the first symptom of COPD development. Initially, the cough is intermittent and heavy in the morning, but later it becomes daily and often lasts all day, but the cough is not pronounced at night. In some cases, significant airflow limitation may occur even in the absence of a cough.
Coughing up sputum: A small amount of mucous sputum is coughed up after coughing, more in the morning in some patients, increased sputum in co-infections, or pus sputum is coughed up. Increased sputum can identify acute exacerbation of bacterial infection onset.
Dyspnea: Dyspnea is the basic symptom of COPD and is a major cause of disease-related loss of physical ability and anxiety. Typical COPD patients describe their symptoms as an exacerbation of the effects on breathing, dullness, air hunger, and wheezing.
Wheezing and chest tightness: “These are not specific symptoms of chronic obstructive pulmonary disease, especially in severe patients with significant wheezing, extensive inspiratory or expiratory phase rales on auscultation, and chest tightness that often occurs after exertion and is associated with respiratory effort and intercostal muscle contraction. The absence of croup on auscultation does not clinically exclude the diagnosis of slow-onset lung, nor does it establish the diagnosis of asthma due to the presence of the above symptoms.
Other symptoms: systemic symptoms such as weight loss, loss of appetite, peripheral muscle atrophy and dysfunction, mental depression and/or anxiety may occur during the clinical course of slow-onset lung, especially in patients with more severe degrees.
2., Ancillary tests
Pulmonary function measurement: Pulmonary function measurement is the best test for airflow limitation and requires measuring the volume of air exhaled at the fastest rate and with the greatest force to the residual air volume after maximum inspiration to the total lung volume (force spirometry FVC) the volume of air exhaled in the first second of the test (force expiratory volume in the first second FEV1) and calculating the ratio of these two measurements (FEV1/FVC). The reference values for spirometry were corrected for age, height, gender and race.
Imaging: Chest X-rays are important to establish the diagnosis of COPD, to understand lung changes and to diagnose other complications. For example, concomitant respiratory diseases (e.g., pulmonary fibrosis, bronchiectasis, pleural disease), skeletal muscle disorders, cardiovascular disease, associated with COPD can also include imaging changes in pulmonary emphysema, such as manifestations of diaphragmatic hypoplasia and increased lung volume. CT thin-section scans of the chest are not routinely performed as COPD examinations, but CT scans can help in the differential diagnosis of complications. In addition, when pulmonary decompression is required, because the distribution of emphysema is an important part of determining the indications for surgery, a CT scan of the chest is required at this time.
3. Diagnosis and differential diagnosis: COPD diagnosis should be considered in patients with the following characteristics: cough, sputum production, dyspnea, and a history of exposure to COPD risk factors, and the diagnosis of COPD needs to be considered clinically. pulmonary function tests are required to confirm the diagnosis. the presence of irreversible airflow limitation can be confirmed with FEV1/FVC force spirometry <0.7 after the use of bronchodilators Functional classification is based on FEV1 as a percentage of the expected value.
COPD is often combined with other diseases (comorbidities) that have an important impact on the prognosis of COPD.
1. cardiovascular disease (including ischemic heart disease, heart failure, atrial fibrillation and hypertension): the most common and important comorbidity of COPD.
2. Osteoporosis, anxiety/depression and cognitive dysfunction: are also common comorbidities of COPD. However, these comorbidities are often not diagnosed in a timely manner. The presence of these comorbidities can lead to a reduced quality of life and often suggests a poor prognosis.
3. Lung cancer: It is very common in COPD patients. Studies have confirmed that lung cancer is the most common cause of death in patients with mild COPD.
4, severe infections: especially respiratory infections, are common in COPD patients.
5. Metabolic syndrome and diabetes: The combination of diabetes can have an impact on the prognosis of patients. Gastroesophageal reflux disease (GERD) is a systemic comorbidity that can have an impact on pulmonary lesions.
6, bronchiectasis and interstitial lesions: the combination of bronchiectasis and interstitial lung lesions can lead to a prolonged course of COPD acute exacerbations and increased mortality.
Treatment principles
Smoking cessation is the most important factor influencing COPD disease progression:.
1. Pharmacological treatment of stable COPD
Bronchodilators: Bronchodilators are drugs used to improve lung function FEV1 or improve other lung function parameters.
β2 agonists.
β2 agonist receptor agonist’s mainly work by agonizing β2 receptors on bronchial smooth muscle to increase adenylate cyclase (cAMP) and play a role in counteracting bronchoconstriction. Short-acting β2 agonists are generally effective for 4-6 hours. Regular and as-needed use of short-acting β2 agonists can improve FEV1 and symptoms. If a patient is already treated with a long-acting bronchodilator, the application of high doses of short-acting β2 agonists for on-demand treatment is not recommended due to side effects. Short-acting β2 agonists mainly include salbutamol, terbutaline and other quantitative nebulized inhalers, which take effect within minutes and last for 4-5 hours, 100-200 μg (1-2 sprays) each time, and no more than 8-12 sprays in 24 hours; long-acting β2 agonists mainly include salmeterol and formoterol, which last for more than 12 hours and are inhaled twice a day.
Anticholinergic drugs.
For example, ipratropium bromide, oxytocin and tiotropium bromide, anticholinergic drugs have a blocking effect on muscarinic-like acetylcholine receptors, the existing short-acting anticholinergic drugs mainly agonize M2 and M3 receptors and can block the postganglionic vagal efferent branch, the long-acting anticholinergic drug tiotropium bromide selectively acts on M3 and M1 receptors. The duration of action of inhaled short-acting anticholinergic drugs generally lasts for more than 8 hours, while the effect of tiotropium bromide can last for more than 24 hours. Tiotropium bromide reduces acute exacerbations and associated hospitalizations, improves symptoms and health status, and may enhance the effectiveness of pulmonary rehabilitation therapy. Short-acting anticholinergics include ipratropium bromide (trade name Albuterol) quantitative nebulized inhaler, which has a slower onset of action than salbutamol, with efficacy lasting 6-8 hours, 40-80 μg per dose, 3-4 times daily; and long-acting anticholinergics include tiotropium bromide (Servial), which has a duration of action of more than 24 hours, 18 μg per inhaled dose, once daily.
Theophylline.
Theophylline is one of the most commonly used methylxanthines and is metabolized by cytochrome P450 mixed function oxidase. Its metabolic clearance decreases with age, and many factors and drugs regulate the metabolism of theophylline. Theophylline may alter inspiratory muscle function in patients. Short-acting and long-acting dosage forms are included. Short-acting dosage forms, such as aminophylline, are commonly used at doses of 100-200 mg per dose, three times daily; long-acting dosage forms, such as theophylline extended-release tablets, are commonly used at doses of 100-200 mg per dose, once every 12 hours. High-dose theophylline is not recommended for routine application because of its potential toxic side effects, and the elderly should be more cautious in using theophylline.
Glucocorticoids.
Inhaled glucocorticosteroids for COPD are currently unclear regarding issues such as the dose of the hormone, the response relationship, and the safety of long-term use. Whether glucocorticoids can suppress pulmonary and systemic inflammation in COPD patients is controversial, and there are only limited specific indications for glucocorticoids in the treatment of stable COPD. Oral glucocorticosteroids have numerous side effects.
Phosphodiesterase-4 inhibitors.
Phosphodiesterase-4 inhibitors work by inhibiting the inflammatory response through the degradation of intracellular cAMP. The phosphodiesterase-4 inhibitor roflumilast has been approved for use in some countries. Once-daily oral roflumilast has no direct bronchodilator effect, but has been shown to improve FEV1 in patients already treated with salmeterol or tiotropium .
Note: SAMA-short-acting anticholinergic, SABA-short-acting β2-agonist; LAMA-long-acting anticholinergic; LABA-long-acting β2-agonist; ICS-inhaled hormone; PDE-4-Phosphodiesterase-4
2.Treatment of acute exacerbation of chronic obstructive pulmonary disease
Acute exacerbation of COPD is defined as a short-term exacerbation of a patient’s respiratory symptoms beyond their daily fluctuating range, requiring a change in drug therapy. The most common cause of acute exacerbation in patients is respiratory tract infection (viral or bacterial infection).
(1) Oxygen therapy: Adjunctive oxygen therapy should adjust the oxygen supply concentration to improve hypoxemia, with a target value of 88%-92% blood oxygen concentration.
(2) Bronchodilator therapy: short-acting bronchodilators are preferred for acute exacerbations and can be combined with muscarinic receptor antagonists.
(3) Systemic glucocorticoids: Systemic glucocorticoids can shorten the recovery time of patients, improve their pulmonary function (FEV1) and hypoxemia (PaO2); and reduce the risk of early relapse, treatment failure, and prolonged hospital stay. The recommended dose is: prednisone or methylprednisolone 40mg/day for 5-7 days.
(4) Antibiotics: Anti-infective therapy is indicated in the following cases: increased dyspnea, increased sputum and increased pus sputum; sputum becoming purulent and accompanied by one other major symptom; severe acute exacerbations requiring mechanical ventilation.
Adjunctive therapy: may be used as appropriate to the patient’s condition. Including the maintenance of appropriate fluid balance (especially for diuretics); the use of anticoagulants; treatment of comorbidities; nutritional support, etc.
3.Oxygen therapy and ventilator support
Long-term oxygen therapy can improve the patient’s quality of life and increase the survival rate. The indications for long-term oxygen therapy are.
1.PaO2≤55mmHg or SaO2≤88% with or without hypercapnia in the last 3 weeks.
2. 55 mmHg ≤ PaO2 ≤ 60 mmHg or SaO2 ≤ 88% with evidence supporting hypercapnia, congestive heart failure as indicated by peripheral edema, or erythrocytosis (erythrocyte pressure product > 55%). Long-term oxygen therapy for >15 hours per day in patients with chronic obstructive pulmonary respiratory failure may improve survival and improve severe hypoxemia at rest. Oxygen therapy method: 3-5 liter home oxygen concentrator can be used to administer oxygen by nasal cannula with oxygen flow rate of 1.0-2.0L/min and oxygen duration >15h/d to achieve arterial partial pressure of oxygen (PaO2) >60mmHg and/or to raise oxygen saturation to above 90% in the patient’s resting state. Noninvasive ventilators can be a treatment option for COPD patients, especially for daytime hypercapnia, which can improve survival but affect quality of life.
4.Lung decompression
Pulmonary decongestion is the surgical removal of part of the lung to reduce emphysema, improve the efficiency of respiratory muscles and increase the elastic retraction force of the lung thus increasing the expiratory flow rate and reducing acute exacerbations. In emphysema patients with poor pulmonary rehabilitation exercises pulmonary decompression improves the survival rate of patients, in patients with good pulmonary rehabilitation, there is no significant difference in the survival rate between pulmonary rehabilitation and pulmonary decompression, in elderly people pulmonary decompression is more risky.
5.Rehabilitation therapy
The aim of pulmonary rehabilitation therapy is to reduce symptoms, improve quality of life, improve activity tolerance and increase physical and emotional involvement in daily activities. For COPD especially grade III-IV patients due to poor exercise capacity, relative social isolation, dangerous emotional state (especially depressed patients), muscle wasting and weight loss. Pulmonary rehabilitation should be actively pursued. Large clinical trials have shown an increase in peak exercise load, peak oxygen consumption, and endurance time after rehabilitation therapy. The rehabilitation program can be selected according to the actual situation. Rehabilitation therapy includes correct coughing, sputum expulsion methods and lip reduction breathing; muscle training includes whole body exercise and respiratory muscle exercise, such as walking, bicycling and abdominal breathing exercise; scientific nutritional support and strengthening health education are also important aspects of rehabilitation therapy.