Chronic obstructive pulmonary disease (COPD) is a preventable and treatable common disease characterized by persistent airflow limitation. Airflow limitation progresses progressively and is accompanied by an increase in the chronic inflammatory response of the airways and lungs to harmful particles or gases. Acute exacerbations and comorbidities affect the overall severity of the disease in patients. COPD is currently the 4th leading cause of death worldwide. The risk factors for COPD include both individual susceptibility factors and environmental factors, which interact with each other.
Pathogenic factors.
Environmental factors
1, smoking: smoking is an important factor in the development of COPD. Smokers have a higher rate of abnormal lung function and a faster annual rate of decline in FEV1, and more smokers die of COPD than non-smokers. Passive smoking may also contribute to respiratory symptoms and the development of COPD. Smoking in pregnant women may affect the growth of fetal lungs and development in the womb, and have an effect on fetal immune system function.
2, occupational dust and chemical substances: When occupational dust and chemical substances (smoke, allergens, industrial exhaust and indoor air pollution, etc.) are too concentrated or exposed for too long, they can lead to COPD that is not related to smoking. Exposure to certain specific substances, irritants, organic dust and allergens can increase airway reactivity.
3, air pollution: chemical gases such as chlorine, nitrogen oxide, sulfur dioxide, etc., have an irritating and cytotoxic effect on the bronchial mucosa. When airborne soot or sulfur dioxide increases significantly, acute COPD attacks increase significantly. Other dusts such as silica, coal dust, cotton dust and cane dust also stimulate the bronchial mucosa, which impairs the airway clearance function and creates conditions for bacterial invasion. The large amount of fumes from cooking and soot from biofuels are associated with the onset of COPD, and indoor air pollution from biofuels may have a synergistic effect with smoking.
4, Infection: Respiratory infections are another important factor in the onset and exacerbation of COPD. Viruses also play a role in the onset and progression of COPD. Severe lower respiratory tract infections in childhood are associated with reduced lung function and the onset of respiratory symptoms in adulthood.
5. Socioeconomic status: The onset of COPD is associated with the socioeconomic status of the patient. This may be intrinsically linked to differences in the degree of indoor and outdoor air pollution, nutritional status or other and socioeconomic status.
Pathophysiology
The pathophysiological changes characteristic of COPD are based on the pulmonary pathology of COPD, including mucus hypersecretion, ciliary dysfunction, airflow limitation, lung hyperinflation, abnormal gas exchange, pulmonary hypertension and pulmonary heart disease, as well as systemic adverse effects. Mucus hypersecretion and ciliary dysfunction lead to chronic cough and sputum, which can precede other symptoms and pathophysiologic abnormalities. As COPD progresses, peripheral airway obstruction, lung parenchymal destruction and abnormalities in the pulmonary vasculature reduce the gas exchange capacity of the lungs, producing hypoxemia and later hypercapnia. Long-term chronic hypoxia can lead to extensive pulmonary vasoconstriction and pulmonary hypertension, often accompanied by intimal hyperplasia, fibrosis and occlusion of certain vessels, resulting in structural reorganization of the pulmonary circulation. pulmonary hypertension that occurs in the late stages of COPD is an important cardiovascular complication of the disease and leads to chronic pulmonary heart disease and right heart failure, suggesting a poor prognosis.
Laboratory tests and other monitoring indicators
1.Pulmonary function test: Pulmonary function test is an objective indicator to determine airflow limitation, which has good repeatability and is important for the diagnosis of COPD, severity evaluation, disease progression, prognosis and treatment response. Those with FEV1/FVC% <70% after inhalation of bronchodilator can be identified as not fully reversible airflow limitation. Peak expiratory flow rate (PEF) and maximum expiratory flow-volume curve (MEFV) can also be used as reference indicators of airflow limitation, but the correlation between PEF and FEV1 is not strong enough in COPD, and PEF may underestimate the degree of airflow obstruction. The increase in TLC is not as great as the increase in RV, so the RV/TLC is increased. The ratio of DLCO to alveolar ventilation (VA) (DLCO/VA) is more sensitive than that of DLCO alone. Deep inspiratory volume (IC) is the sum of tidal volume and compensatory inspiratory volume. IC/TLC is an indicator of lung hyperinflation, which has significance in reflecting the degree of dyspnea in COPD and even the survival rate of COPD.
2, chest X-ray examination: X-ray examination is important to identify pulmonary complications and differentiate from other diseases (such as pulmonary interstitial fibrosis, pulmonary tuberculosis, etc.) There may be no obvious changes in the early X-ray chest X-ray of COPD, and later there are non-characteristic changes such as increased lung texture and disorder; the main X-ray signs are lung hyperinflation: lung volume increases, anterior and posterior diameter of the chest cavity grows, the rib cage becomes flat, the lung field translucency increases, the diaphragm In case of pulmonary hypertension and pulmonary heart disease, in addition to the x-ray signs of right heart enlargement, there may also be conical bulging of the pulmonary artery, enlargement of the hilar vascular shadow and widening of the right lower pulmonary artery.
3.CT examination of the chest: CT examination is generally not used as a routine examination. However, CT examination is useful in differential diagnosis. High-resolution CT (HRCT) has high sensitivity and specificity in identifying lobar-centered or whole lobar emphysema and determining the size and number of pulmonary blisters, and is valuable in predicting the effect of pulmonary blister resection or surgical reduction surgery, etc.
4, blood gas examination: when FEV1 < 40% of the expected value or COPD patients with respiratory failure or right heart failure should do blood gas examination. Blood gas abnormalities are first manifested as mild or moderate hypoxemia. As the disease progresses, hypoxemia gradually worsens and even respiratory failure occurs with hypercapnia.
5, other laboratory tests: PaO2 < 55 mmHg, hemoglobin and erythrocytes can be increased, and erythrocyte pressure product > 55% can be diagnosed as erythrocytosis. In case of co-infection, a large number of neutrophils can be seen in sputum smear, and various pathogenic bacteria can be detected in sputum culture, commonly Streptococcus pneumoniae, Haemophilus influenzae, Katamora, Klebsiella pneumoniae, etc.
Differential diagnosis of COPD should be differentiated from bronchial asthma, bronchiectasis, congestive heart failure, tuberculosis, etc.
Differential diagnosis of chronic obstructive pulmonary disease
COPD can be divided into acute exacerbation phase and stable phase. acute exacerbation phase of COPD refers to the patient who has a continuous deterioration beyond the daily condition and needs to change the regular medication of the underlying COPD. The stable stage refers to patients with stable or mild symptoms such as cough, sputum and shortness of breath.
Treatment of acute exacerbation
(a) Pharmacological treatment: The pharmacological treatment for acute exacerbation includes three major categories: bronchodilators, systemic glucocorticoids and antibiotics. Single inhalation of short-acting β2 agonists, or a combination of short-acting β2 agonists and short-acting anticholinergics, are usually the preferred bronchodilators in acute exacerbations. These drugs can improve symptoms and FEV1, and there is no difference between using MDI and nebulized inhalation, although the latter may be more appropriate for more severe patients. It is uncertain whether long-acting bronchodilators combined with inhaled glucocorticoids are more effective in acute exacerbations. Theophylline is only indicated in patients with poor results with short-acting bronchodilators, and adverse effects are more common. Systemic glucocorticoids and antibiotics can shorten the recovery time, improve pulmonary function (FEV1) and arterial partial oxygen pressure (PaO2), and reduce the risk of early recurrence, treatment failure and hospitalization time. Oral prednisone 30-40 mg/d for 10-14 d is recommended, and nebulized inhalation budesonide is also an option. Antimicrobial drugs are recommended when AECOPD has three symptoms, namely dyspnea, increased sputum, and purulent sputum, or when only two symptoms are present and one of them is purulent sputum, including patients who are critically ill and require mechanical ventilation. The type of antimicrobial drug should be selected according to the local bacterial resistance. The recommended course of treatment is 5-7 d.
(b) Oxygen therapy: It is an important treatment for acute exacerbation of hospitalization, adjusting and maintaining oxygen saturation 88%-92% according to the patient’s blood oxygen status.
(C) mechanical ventilation
1, non-invasive ventilation: can improve carbon dioxide retention, reduce the respiratory rate and dyspnea, shorten the hospital stay, reduce death and intubation. Indications: At least one of the following conditions is met:
Respiratory acidosis ( arterial blood pH ≤ 7 . 35 and/or PaCO2 > 45 mm Hg)
Severe dyspnea combined with clinical symptoms, suggesting respiratory muscle fatigue
Increased respiratory effort; e.g., application of assisted respiratory muscles, paradoxical thoracoabdominal movements; or contraction of the intercostal muscles
2. Invasive ventilation: It can reduce the respiratory rate, improve PaO2, PaCO2 and pH, reduce mortality, and reduce the risk of treatment failure. The indications for invasive ventilation are as follows.
Intolerance to NIV or failure of NIV treatment (or inappropriate for NIV)
Respiratory or cardiac arrest
Apnea with loss of consciousness
Impaired mental status, severe psychiatric disorders requiring sedative control
Massive aspiration
Prolonged failure to expel airway secretions
Heart rate < 50 beats/min with loss of consciousness
Severe hemodynamic instability, unresponsive to fluid therapy and vasoactive drugs;
Severe ventricular arrhythmias;
Life-threatening hypoxemia, intolerant of NIV
Intolerance of NIV or failure of NIV therapy (or inappropriate for NIV)[3]
Disease prevention
The main focus is to avoid risk factors for the development of the disease. Avoid or prevent inhalation of dust, smoke, and noxious gases, especially smoking cessation. Smoking is the most important risk factor for COPD, and smoking cessation is the measure that has so far proven to be effective in delaying progressive decline in lung function. Regular lung function monitoring should be performed for people at high risk of COPD in order to detect COPD early and intervene in a timely manner.