bubble_chart Overview

Emphysema is classified into chronic obstructive emphysema, senile emphysema, compensatory emphysema, and interstitial emphysema. The chronic obstructive emphysema described in this chapter is the most common clinically.

Chronic obstructive emphysema (chronic obstructive emphysema, emphysema) refers to the overinflation, persistent expansion, and structural destruction of the distal air spaces of the terminal bronchioles, along with reduced elastic recoil of the lung tissue and increased lung volume, all occurring on the basis of small airway obstruction.

Chronic obstructive emphysema is distinctly different from senile emphysema caused by physiological degenerative changes in aging lung tissue, as it involves structural damage to the lung tissue. Additionally, it is also markedly different from compensatory emphysema, which results from physiological compensation when healthy lung tissue overexpands due to the loss of respiratory function in part of the lung tissue, such as after atelectasis or lobectomy for disease. Chronic obstructive emphysema is the most common type of emphysema in the broad sense.

bubble_chart Etiology

The occurrence of emphysema is closely related to a combination of factors such as smoking, air pollution, and infections. The vast majority of chronic obstructive emphysema develops from chronic bronchitis, followed by conditions like bronchial asthma and bronchiectasis, which can also lead to emphysema. Approximately 2% of cases are associated with a deficiency of alpha-1 antitrypsin (α1AT). This enzyme, produced and secreted by the liver, inhibits the activity of various proteases. A deficiency in α1AT increases the activity of proteases such as trypsin, plasmin, and elastase, leading to damage in lung tissue.

bubble_chart Pathogenesis

Chronic bronchitis, bronchial asthma, pulmonary fibrosis, and other conditions can all cause lung qi swelling, with chronic bronchitis being the most common. Taking chronic bronchitis as an example, let’s analyze the pathological mechanism of lung qi swelling:

(1) Gas retention in the lungs, with centrilobular or panlobular hyperinflation and persistent distension. Mechanism of occurrence:

1. Congestion of the mucous membrane, edema, increased secretions, smooth muscle spasms, and other inflammatory changes narrow the bronchial lumen. Additionally, destruction of elastic fibers and collapse of small bronchioles further obstruct ventilation, creating a valve-like effect that allows less gas to be exhaled and more to be inhaled.
2. During exhalation, the physiological narrowing of the bronchial lumen, combined with the aforementioned valve-like effect, results in even less gas being exhaled than inhaled. Consequently, the alveoli become hyperinflated and persistently distended, leading to gas retention and increased pressure.

(2) Reduced alveolar elasticity and destruction of tissue structure

1. Due to excessive alveolar distension and increased pressure, alveolar capillaries are compressed and occluded. Alternatively, the elevated pressure may cause alveolar rupture, forming larger air spaces. As a result, alveolar capillaries are damaged, their numbers significantly reduced, leading to a lack of alveolar nutrition and decreased elasticity.
2. In chronic bronchitis, the accompanying small stirred pulse also becomes inflamed, causing vascular narrowing and obstruction, which reduces alveolar blood supply and nutrition. This further contributes to decreased alveolar elasticity and structural damage.
3. Some patients exhibit a deficiency of anti-trypsin, leading to destruction of lung tissue and reduced lung elasticity.

In summary, hyperinflation and persistent distension of the alveoli, structural damage, diminished elastic recoil, and increased lung volume collectively result in the formation of lung qi swelling.

bubble_chart Pathological Changes

During lung qi swelling, the lung volume increases. Due to reduced blood supply, the lung surface appears grayish-white, elasticity decreases, the lung tissue softens, and bullae of varying sizes can be seen on the surface. Microscopically, the following can be observed: alveolar expansion, fusion of alveoli forming larger air spaces, narrowing of alveolar septa, compression and occlusion of capillaries, and a reduction in their number. Based on the location of pathological changes, obstructive lung qi swelling can be classified into:

1. Centrilobular lung qi swelling, where inflammation affects the terminal bronchioles and first-order respiratory bronchioles, narrowing their lumens, causing second-order respiratory bronchioles to form hyperinflated and significantly expanded air spaces, while alveolar ducts, alveolar sacs, and alveoli are rarely involved.
2. Panlobular lung qi swelling, where inflammation affects the terminal bronchioles, narrowing their lumens, leading to hyperinflation and cystic dilation of the entire distal lobule.

bubble_chart Clinical Manifestations

The clinical manifestations vary depending on the type and severity of the primary disease and lung qi swelling. In addition to the symptoms of the primary disease, such as chronic bronchitis, asthma, and other signs, the following manifestations may also occur:

1. Symptoms are not obvious in the early stages. As the condition progresses, gradually worsening dyspnea may occur. Initially, shortness of breath often appears during labor, uphill walking, or climbing stairs. Later, it may also be felt during activities on flat ground, and in severe cases, shortness of breath may occur even at rest. Persistent dyspnea is an important symptom of lung qi swelling. In patients with lung qi swelling, infection can severely impair ventilation and gas exchange functions, leading to hypoxemia and hypercapnia.
2. Signs upon inspection may include barrel chest, widened intercostal spaces, weakened respiratory movements, decreased tactile fremitus, hyperresonance on percussion, lowered lower lung borders, and weakened breath sounds on auscultation. If respiratory failure occurs, in addition to more severe dyspnea, clinical manifestations related to hypoxemia and hypercapnia may appear successively, such as cyanosis, confusion, unconsciousness, etc. If the condition progresses to chronic cor pulmonale, systolic apical pulsations may be observed below the xiphoid process in the upper abdomen, where the heart sounds are more pronounced than at the apex, indicating signs of right heart enlargement.

bubble_chart Auxiliary Examination

1. X-ray examination reveals increased radiolucency in the lung fields. The diaphragm is lowered, with a flattened dome, and the movements of the diaphragm and thorax are weakened.
2. Pulmonary function tests show abnormalities in ventilation once chronic obstructive pulmonary emphysema occurs, such as: (1) Decreased maximum voluntary ventilation (MVV). (2) Forced expiratory volume in one second (FEV1.0)/forced vital capacity <60%. (3) Increased residual volume (RV), with RV/total lung capacity >40%, which is highly significant for the diagnosis of pulmonary emphysema.
3. Blood gas analysis indicates that respiratory dysfunction directly affects arterial oxygen partial pressure (PaO₂), leading to its decrease, and arterial carbon dioxide partial pressure (PaCO₂), causing its increase. In decompensated respiratory acidosis, the pH value drops.

bubble_chart Diagnosis

Typical lung qi swelling can be diagnosed based on:

1. the presence of a primary disease (mainly chronic bronchitis);
2. progressively worsening dyspnea;
3. lung qi swelling signs.

Diagnosis is not difficult. Based on clinical manifestations, combined with disease etiology and pathology, chronic obstructive lung qi swelling is clinically classified into two types: (1) emphysematous lung qi swelling (also known as Type A, PP type, pink puffer type), and (2) bronchitic lung qi swelling (also known as Type B, BB type, blue bloater type). The differentiation between the two types is shown in Table 2-3-1. Type B exhibits significant hypoxemia and earlier onset of pulmonary stirred pulse hypertension and right heart failure, indicating that Type B is more prone to developing lung heart disease and has a poorer prognosis compared to Type A. However, in clinical practice, many patients are difficult to classify.

bubble_chart Treatment Measures

General Treatment

1. Strengthening Diaphragmatic Movement (i.e., enhancing abdominal breathing exercises): During inhalation, the abdomen expands, and during exhalation, the abdomen contracts. Perform this for 10–15 minutes each time, 2–3 times or more daily. This can increase the range of diaphragmatic movement, enhance alveolar ventilation, and improve respiratory function.
2. Pursed-Lip Breathing: Exhale with pursed lips, resembling blowing a whistle, slowly exhaling. The ratio of inhalation to exhalation should be 1:2 or 1:3 to maximize the expulsion of air from the lungs, benefiting ventilation. Slow exhalation with pursed lips reduces the pressure of expiratory airflow in the airways gradually, preventing premature closure of small airways and avoiding excessive gas retention in the lungs.

Controlling Respiratory Infections

Select effective antibiotics. Initially, penicillin 800,000 units or a combination with streptomycin 0.5g can be administered intramuscularly twice daily. Based on bacterial culture sensitivity tests or clinical condition, antibiotics such as ampicillin, cephalosporin, compound formula SMZ, norfloxacin, etc., may be chosen to control respiratory inflammation. This is crucial for both Type A and B lung qi swelling, especially Type B, as it helps alleviate symptoms, control the progression of lung qi swelling, and prevent further decline in respiratory function.

Symptomatic Treatment

1. Phlegm-Expelling Formula: Options include bromhexine, ammonium chloride, etc. If phlegm remains thick and difficult to expel, acetylcysteine or carbocisteine may be used to thin the phlegm for easier expulsion. Steam inhalation can also be employed to moisten the respiratory tract and dilute phlegm.

2. Bronchodilators: These dilate the bronchi and clear the airways. Commonly used are aminophylline 0.1g three times daily, diprophylline 0.2–0.3g three times daily, salbutamol 2–4mg three times daily, or aerosol inhalation of 0.1–0.2mg per dose. Other options include terbutaline or its aerosol form, fenoterol, etc.
3. Oxygen Therapy: For those with hypoxia, low-flow continuous oxygen therapy is recommended. This helps alleviate hypoxic pulmonary vasoconstriction, reduce cardiac load, improve constitution, and enhance exercise tolerance. It also prevents or delays the onset of lung-heart disease.

bubble_chart Prevention

Prevention and treatment of primary diseases such as chronic bronchitis are important measures to prevent lung qi swelling.

bubble_chart Complications

Spontaneous pneumothorax is caused by the rupture of pulmonary bullae due to severe coughing or sudden excessive exertion. At this point, dyspnea suddenly worsens, accompanied by significant chest pain, cyanosis, weakened or absent breath sounds, tympanic percussion notes, and diagnosis can be confirmed by X-ray examination.