| disease | Obstructive Pulmonary Emphysema |
| alias | Obstructive Pulmonary Emphysema |
Obstructive pulmonary emphysema refers to the expansion of the distal part of the terminal bronchioles (including respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli) accompanied by the destruction of the alveolar walls. Over the past few decades, the incidence of obstructive pulmonary emphysema has significantly increased due to factors such as air pollution, smoking, and chronic lung infections, which induce chronic bronchitis and further evolve into this disease. According to a nationwide survey of over 60 million people in China, the prevalence of chronic bronchitis is 3.9%, and it reaches 15% or more among those aged 50 and above. The prevalence of obstructive pulmonary emphysema varies across the country, with the lowest being 0.6% and the highest being 4.3%. This disease is a chronic, progressive condition with a long course, affecting health and labor capacity, and causing significant losses to social production and the economy. For example, in the United States, the economic losses due to medical expenses and absenteeism caused by obstructive pulmonary emphysema amount to tens of billions of dollars annually.
bubble_chart Etiology
The causes of obstructive lung qi tumor disease are extremely complex, summarized as follows.
(1) Smoking: Cigarettes contain various harmful components such as tar, nicotine, and carbon monoxide. Smokers have increased levels of fucose and neuraminic acid in their mucus glands, which can inhibit the activity of bronchial membrane cilia, reflexively cause bronchial spasms, and weaken the function of alveolar phagocytes. Smokers are far more likely to develop lung qi tumors or chronic bronchitis and die from respiratory failure or lung heart disease than non-smokers.
(2) Air pollution: Autopsy materials prove that under similar climatic and economic conditions, the incidence of lung qi tumors is higher in areas with severe air pollution than in less polluted areas.(3) Infection: Respiratory viral and bacterial infections are somewhat related to the occurrence of lung qi tumors. Repeated infections can cause congestion and edema of the bronchial membrane, glandular hyperplasia and hypertrophy, hyperactive secretion function, thickening and narrowing of the tube wall, leading to airway obstruction. The increase in protease activity during lung infections may also be related to the formation of lung qi tumors.
(4) Protease-antiprotease imbalance: Some proteolytic enzymes in the body have a digestive effect on lung tissue, while antiproteases inhibit various proteases such as elastase. The balance between proteases and antiproteases is an important factor in maintaining the normal structure of lung tissue and preventing its destruction. Proteases that digest lung tissue come from two sources: exogenous from pathogens such as bacteria and fungi, and endogenous from neutrophils and alveolar macrophages. Smoking increases the activity of elastase and inactivates antiproteases.
α1 Antitrypsin is a glycoprotein synthesized by the liver that can inhibit the activity of various serine proteases. α1 Antitrypsin is controlled by a pair of autosomal recessive genes, with normal humans being of the M type, i.e., PiMM. If lysine replaces glutamic acid, it becomes the Z type. Foreign data reports that PiZZ homozygotes account for about 1/4000 in the population, and PiMZ heterozygotes account for about 3-5%. PiZZ homozygotes have severely reduced α1
antitrypsin activity in their serum and are prone to hepatitis and lung qi tumors. Lung qi tumors caused by α1 antitrypsin deficiency have the following characteristics: earlier onset age, no smoking history; shorter course, obvious shortness of breath; serum protein electrophoresis shows reduced α1 globulin, and decreased serum α1 antitrypsin activity. Pathologically, it is mostly panlobular lung qi tumors. Other types such as PiSS and various heterozygotes PiMZ and PiSZ do not have an increased incidence of lung qi tumors. α1 Antitrypsin deficiency is more common in Caucasians and rare in China.The pathogenesis of obstructive lung qi swelling is not yet fully understood. It is generally believed to be related to bronchial obstruction and the imbalance between proteases and antiproteases. Smoking, infections, and air pollution can cause inflammation of the bronchioles, leading to narrowing or blockage of the lumen. During inhalation, the bronchiolar lumen expands, allowing air to enter the alveoli; during exhalation, the lumen narrows, causing air stagnation, and the pressure within the alveoli continuously increases, leading to overexpansion or rupture of the alveoli. The loss of radial traction around the bronchioles causes them to contract, further narrowing the lumen. Thickening of the pulmonary vascular membrane, reduced blood supply to the alveolar walls, and weakened alveolar elasticity contribute to the rupture of overexpanded alveoli. In cases of infection, the activity of proteases in the body increases, and the activity of the antiprotease system in normal individuals also increases accordingly to protect lung tissue from damage. Individuals with α1
antitrypsin deficiency have a reduced ability to inhibit proteases, making them more susceptible to lung qi swelling. Smoking also adversely affects the balance between proteases and antiproteases.bubble_chart Pathological Changes
(1) Gross and Microscopic Changes in the Lungs The volume of the lungs increases, potentially reaching twice the normal size. The lungs appear ischemic, with a grayish-white or pale appearance, and may have bullae of varying sizes on the surface. The elasticity of the lungs is reduced, and they do not collapse after thoracotomy, remaining in an expanded state. Microscopically, the distal air spaces of the terminal bronchioles are dilated, the septa are narrowed, and the elastic fibers are thinned or broken. The alveolar pores are enlarged, and the alveolar walls are destroyed. Based on the location of emphysema, it can be divided into the following three types:
Panlobular emphysema This type can affect the entire lung, presenting diffusely, but is more commonly seen in the anterior and lower parts of the lung. Alpha-1 antitrypsin deficiency is associated with this type. The lesions involve the entire pulmonary lobule, including the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli, all of which are dilated. The emphysematous cavities are relatively small.
Centrilobular emphysema This type is more common in the upper parts of the lung. The air spaces are located in the center of the secondary lobules, specifically in the respiratory bronchioles, while the surrounding lung tissue remains normal. Smoking and dust inhalation result in the highest concentration around the respiratory bronchioles, making this area the most significantly affected.
It is also possible for both pathological changes described above to coexist in the same lung, known as mixed emphysema.
(2) Changes in the Bronchioles The walls of the bronchioles show congestion, edema, and inflammatory cell infiltration. The cilia are shed and sparse, and the mucous glands and goblet cells are hyperplastic and hypertrophic. The Reid index, which is the ratio of gland thickness to bronchial wall thickness, is normally 0.3 but can be as high as 0.6 in chronic bronchitis. Secretions are retained within the lumen. The cartilage in the bronchiolar walls undergoes degeneration or destruction, and elasticity is reduced.
(3) Changes in Pulmonary Vessels and the Heart The small pulmonary vessels accompanying the bronchioles exhibit inflammatory changes, with edema, degeneration, and necrosis of the smooth muscle in the media, leading to narrowing or complete occlusion of the lumen. Due to alveolar rupture and inflammatory erosion, the number and cross-sectional area of pulmonary capillaries are reduced. Autopsy data confirm that approximately 40% of patients with obstructive emphysema develop right ventricular hypertrophy.
bubble_chart Clinical Manifestations
The onset of this disease is insidious. In cases where chronic bronchitis is the cause of the disease, there is a history of many years of cough and sputum production. Smokers often experience coughing and expectoration of mucus sputum after getting up in the morning. During concurrent respiratory infections, the sputum becomes mucopurulent. The symptoms of cough and sputum production usually worsen in winter and gradually alleviate when the weather warms up the following year. In severe cases, cough and sputum production persist throughout the year without the seasonal pattern of being worse in winter and better in summer. Patients with lung qi distension often experience shortness of breath, which initially occurs after activities such as climbing stairs or walking briskly, and later progresses to experiencing shortness of breath even when walking on flat ground. If shortness of breath occurs during speaking, dressing, washing the face, or even at rest, it indicates that the lung qi distension is quite severe. Additionally, there are systemic symptoms such as fatigue, poor appetite, and weight loss. Acute stages of attack complicated by respiratory failure or right heart failure may present with corresponding symptoms. Headache in patients with lung qi distension may indicate CO2 retention, and further arterial blood gas analysis should be performed. Hypoxemia may present with cyanosis and can also lead to secondary polycythemia.
In the early stages of the disease, signs are often unremarkable. In severe cases of lung qi distension, the anteroposterior diameter of the chest increases, giving it a barrel-shaped appearance, and the intercostal spaces are full. Percussion reveals increased resonance of the chest, the area of cardiac dullness is reduced or absent, and the liver dullness is lowered. Breath sounds and vocal resonance are diminished, expiration is prolonged, and sometimes dry and wet rales can be heard at the lung bases. Heart sounds are distant.
Due to hyperinflation of the lungs and increased residual volume, X-ray examination shows increased lung transparency. However, this X-ray sign is not sensitive in the early stages. In grade III lung qi distension, the chest is full, the ribs become flattened, and the intercostal spaces widen. Lateral X-rays show an increased anteroposterior diameter of the chest and an excessively wide retrosternal space. The diaphragm is displaced downward, and the diaphragmatic dome becomes flattened. The transparency of both lungs is increased, and the vascular markings in the outer lung fields are fine and sparse. The heart shadow is vertically elongated. Fluoroscopy shows reduced mobility of the chest and diaphragm. Some cases may present with increased lung markings, with less obvious increase in lung transparency, widened pulmonary arteries at the hilum, and often an enlarged heart.
The clinical manifestations of obstructive lung qi distension can be divided into two types (Table 1), although many patients do not fit the typical presentation of either type.
Table 1 Two types of obstructive lung qi distension
| Bronchitic type (BB type) | Emphysematous type (PP type) | |
| Clinical features | Obesity, bloated appearance, cyanosis, jugular vein distension, lower limb edema, history of cough, sputum production, recurrent respiratory infections, edema, and right heart failure | Weight loss, shortness of breath, absence of cyanosis, minimal sputum, no lower limb edema or history of right heart failure |
| Hypertrophy of bronchial mucous glands | Significant | Not significant |
| Degree of lung qi distension | Not severe | Severe |
| Ventilatory function (FEV1 MMEF, MBC, etc.) | Reduced | Reduced |
| Total lung capacity | Grade I increased | Significantly increased |
| Gas distribution | Uneven | Even |
| Diffusion capacity | Normal | Reduce |
| PaO2(mmHg) | <70 | <70 |
| PaCO2(mmHg) | >45 | >45 |
| Hematocrit | >60 | >55 |
| Chest X-ray findings | Lung qi swelling is not significant, lung fields are normal or congested, heart is enlarged | Lung qi swelling is significant, peripheral pulmonary vessels are slender, heart is normal or elongated and vertical |
[Note]FEV1: Forced expiratory volume in one second
MMEF: Maximum mid-expiratory flow
MBC: Maximum breathing capacity
PaO2: Stirred pulse oxygen partial pressure
PaCO2: Stirred pulse carbon dioxide partial pressure
1. Bronchitis type, also known as the blue bloated type (BB type), has more severe bronchial lesions, swollen mucous membranes, hyperplasia of mucous glands, and mild lung qi swelling lesions. Patients often have a long history of smoking and chronic cough and sputum production. Physical examination reveals obesity, cyanosis, jugular vein distension, lower limb edema, and rales heard at the base of both lungs. Chest X-ray shows lung congestion, thickened lung markings, and no significant signs of lung qi swelling. Pulmonary function tests show significant impairment of ventilation function, uneven gas distribution, increased functional residual capacity and total lung capacity, normal diffusion function, decreased stirred pulse oxygen partial pressure, increased carbon dioxide partial pressure, increased hematocrit, and a tendency to develop respiratory failure and/or right heart failure.
2. Lung qi swelling type, also known as the non-cyanotic wheezing type (PP type), has more severe lung qi swelling but less severe bronchial lesions. It is more common in the elderly, with a thin constitution, obvious dyspnea, and no cyanosis. Patients often adopt a special posture, such as high shoulders, arms resting on the bed, puffed cheeks and pursed lips during exhalation. Chest X-ray shows increased transparency of both lungs. Although ventilation function is also impaired, it is not as severe as in the bronchitis type, gas distribution is uniform, the ratio of residual volume to total lung capacity is increased, alveolar ventilation is normal or even hyperventilated, so the stirred pulse oxygen partial pressure is not significantly decreased, and the carbon dioxide partial pressure is normal or decreased.
The diagnosis of obstructive lung disease, especially early diagnosis, is relatively difficult and should be made based on a combination of medical history, signs, chest X-ray, and pulmonary function tests. A diagnosis can be confirmed if there is a history of progressively worsening dyspnea, pulmonary function tests showing increased residual volume and residual volume/total lung capacity, decreased forced expiratory volume in one second/forced vital capacity, reduced maximum ventilation, uneven gas distribution, and decreased diffusion capacity; and if there is no significant improvement in pulmonary function after bronchodilator treatment.
bubble_chart Treatment Measures
Obstructive lung qi tumors are mainly secondary to chronic bronchitis. There are numerous disease causes that lead to chronic bronchitis. Chemical factories should properly handle harmful gases, and factories that produce dust should improve their operational methods, such as adopting wet operations, sealing dust sources, enhancing ventilation, and personal protection. These should be strictly enforced by the labor department. Quitting smoking is a practical method for individuals, and the health department should vigorously promote the harms of smoking. After quitting smoking, cough and phlegm are reduced, and the rate of decline in forced expiratory volume in the first second slows down compared to before quitting.
Lung qi tumor patients are prone to respiratory infections in winter and should use antibacterial drugs, phlegm-expelling formulas, and bronchodilators as appropriate. The treatment of concurrent respiratory failure and right heart failure can be referred to in relevant chapters.
Patients with obstructive lung qi tumors should continue treatment during the stage of remission to alleviate symptoms, prevent acute attacks, reduce the number of outpatient and emergency visits and hospitalizations, maintain lung function, and improve quality of life. Medical staff should provide necessary education and guidance to family members and patients, and insist on outpatient or home follow-up. The specific content of treatment during the stage of remission is as follows.
(1) Improving the general condition of patients: Lung qi tumor patients often experience worsening symptoms and further decline in lung function due to respiratory infections. Therefore, it is crucial to enhance the body's resistance and prevent common colds and lower respiratory tract infections. Measures such as cold resistance training, intramuscular injection of nucleic acid or BCG polysaccharide nucleic acid can be taken.
Patients with obstructive lung qi tumors have increased respiratory load and function, and higher energy consumption. However, dietary intake may not increase correspondingly or may even decrease due to shortness of breath, hypoxia, right heart failure, or medication use, often leading to malnutrition. Malnutrition not only impairs lung and respiratory muscle function but also weakens the body's immune mechanisms. Therefore, attention should be paid to nutrient intake to improve nutritional status.
Whole-body exercises such as walking, cycling, treadmill, radio gymnastics, and Tai Chi not only increase muscle activity but also exercise respiratory and circulatory functions.
(2) Breathing training: Guide patients to perform deep and slow abdominal breathing and pursed-lip breathing.
Lung qi tumor patients often exhibit shallow and rapid breathing with poor respiratory efficiency. Guiding patients to perform deep and slow abdominal breathing can reduce respiratory resistance, increase tidal volume, decrease dead space ventilation ratio, improve gas distribution, and correct ventilation/perfusion mismatch.
Lung qi tumor patients have reduced alveolar elastic recoil, increased small airway resistance, and a shift of the equal pressure point towards the peripheral small airways, causing premature closure of small airways during exhalation and gas trapping in the lungs, worsening ventilation/perfusion mismatch. Pursed-lip breathing increases the resistance of the airway's outer segment, shifting the equal pressure point towards the central large airways, preventing premature airway closure.
(3) Respiratory muscle training: Lung qi tumor patients are adversely affected by factors such as lung hyperinflation, malnutrition, and hypoxia, which impact respiratory muscles. In cases of lung infections, the respiratory load further increases, potentially leading to respiratory muscle fatigue, a contributing factor to respiratory failure. Training through resistance breathing or isocapnic hyperventilation can improve respiratory muscle function.
(4) Home Oxygen Therapy For patients whose arterial oxygen partial pressure remains below 7.33 kPa (55 mmHg) after anti-infection, dispelling phlegm, and bronchodilator treatment during the remission stage, home oxygen therapy should be administered. For patients with secondary polycythemia or refractory right heart failure due to lung qi distension, the indications for oxygen therapy can be appropriately relaxed. Oxygen therapy can improve symptoms, enhance work efficiency, increase activity intensity, and expand the range of activities. Adhering to 15 hours of oxygen inhalation per day yields better results than intermittent oxygen therapy. To prevent the inhibitory effect of high-concentration oxygen on ventilation, low-flow oxygen therapy should be used. Oxygen delivery devices have also been improved. Conventional compressed gas cylinders are bulky and heavy, making them inconvenient for home use. Oxygen concentrators can concentrate oxygen from the air, offering convenience. Liquid oxygen storage devices preserve oxygen in a liquid state at ultra-low temperatures, making them compact, lightweight, and portable, which are their advantages. Synchronized oxygen delivery devices are triggered by the patient's inhalation to supply oxygen and do not supply oxygen during exhalation, conserving oxygen. In recent years, there have been reports abroad of using trans-cricothyroid membrane indwelling catheters for oxygen delivery.
(5) Others The development of non-invasive mechanical ventilation provides conditions for home mechanical ventilation for patients with obstructive lung qi swelling. It is generally connected through a nasal mask or oronasal mask or ventilator, and negative pressure ventilation can also be applied. Intermittent home mechanical ventilation can allow respiratory muscles to rest, relieve respiratory muscle fatigue, and improve respiratory muscle function.
Almitrine bismesylate (Vectarion) not only stimulates respiration and improves ventilation but also improves ventilation/perfusion mismatch and increases arterial oxygen partial pressure, and can be used for the treatment of obstructive lung qi swelling in the remission stage.
In recent years, lung transplantation has been performed abroad for the treatment of advanced-stage lung qi swelling patients. Single lung transplantation is relatively simple, with lower complications and mortality rates.
(1) Spontaneous Pneumothorax: Spontaneous pneumothorax complicating obstructive lung qi swelling is not uncommon, mostly caused by the rupture of subpleural bullae, leading to air leakage into the pleural cavity. If the patient's basic lung function is poor and the pneumothorax is tension-type, even a small amount of gas can lead to severe clinical manifestations, necessitating active rescue without negligence. Patients with lung qi swelling often have higher lung field translucency and the presence of bullae, making the signs less typical and posing certain difficulties in diagnosing localized pneumothorax.
(2) Respiratory Failure: Obstructive lung qi swelling often severely impairs respiratory function. Under certain triggers such as respiratory infections, dry and retained secretions, inappropriate oxygen therapy, excessive use of venous agents, and surgical operations, the impairment of ventilation and gas exchange functions can further worsen, potentially inducing respiratory failure.
(3) Chronic Pulmonary Heart Disease and Right Heart Failure: Hypoxemia, carbon dioxide retention, and destruction of alveolar capillary beds can all lead to pulmonary hypertension. During the compensatory phase of heart function, there may be no signs of right heart failure. When respiratory diseases further worsen and blood gas deteriorates, pulmonary pressure significantly increases, heart load intensifies, and factors such as myocardial hypoxia and metabolic disorders can induce right heart failure.
(4) Gastric Ulcer: Autopsy confirms that about 18-30% of patients with obstructive lung qi swelling also suffer from gastric ulcers. The pathological mechanism is not yet fully understood.
(5) Sleep Respiratory Disorders: Normal people may experience a slight decrease in ventilation during sleep, while patients with obstructive lung qi swelling have a more pronounced decrease. Especially when the patient's awake state blood oxygen partial pressure is already as low as about 8.00kPa (60mmHg), a further decrease during sleep is even more dangerous. The patient's sleep quality decreases, and arrhythmias and pulmonary hypertension may occur.
Attention should be paid to the differential diagnosis of pulmonary subcutaneous nodules, lung tumors, and occupational lung diseases. In addition, chronic bronchitis, bronchial asthma, and obstructive lung qi swelling all belong to chronic obstructive pulmonary diseases, and both chronic bronchitis and bronchial asthma can be complicated by obstructive lung qi swelling. However, the three are both related and distinct, and should not be equated. Before the complication of lung qi swelling, the lesions of chronic bronchitis are mainly limited to the bronchi, and there may be obstructive ventilation disorders, but the degree is mild, and the diffusion function is generally normal. The bronchial asthma attack stage is characterized by obstructive ventilation disorders and lung hyperinflation, and the gas distribution can be severely uneven. However, the above changes are largely reversible, and the response to inhaled bronchodilators is good. The diffusion dysfunction is also not obvious. Moreover, the airway reactivity of bronchial asthma is significantly increased, and the diurnal fluctuation of lung function is also large, which is its characteristic.
The key points for differentiating chronic bronchitis, bronchial asthma, and obstructive lung qi swelling are listed in Table 2.
Table 2 Key Points for Differentiating Obstructive Pulmonary Diseases
| Chronic Bronchitis | Bronchial Asthma | Obstructive Lung Qi Swelling | ||
| Family History | None | Often present | None | |
| Age of Onset | Middle or old age | Childhood or youth | Middle or old age | |
| Smoking History | Often present | Rare | Often present | |
| Nature of Sputum | Mucous or purulent, containing neutrophils | Mucous foam, containing eosinophils | Mucous | |
| Peripheral Blood Eosinophils | Not increased | Often >300/mm 3 | Not increased | |
| X-ray Signs | Normal or increased lung markings in the lower lungs | During attacks, lung hyperinflation, increased transparency, normal in remission stage | Hyperinflation, increased transparency, both diaphragms lowered, often accompanied by bullae | |
| Lung Function Tests | Closing Volume | Slightly increased | Slightly increased | Significantly increased or undetectable |
| Maximum Expiratory Flow-Volume Curve | Slightly reduced | Normal or slightly reduced | Significantly reduced, sometimes with notches in the expiratory curve | |
| Maximum Ventilation Volume | Normal or slightly reduced | Reduced during attacks | Reduce | |
| Vital Capacity | Normal | Normal or slightly reduced | Slightly reduced or severely reduced | |
| Residual Volume | Normal | Increased during episodes | Increased | |
| Residual Volume/Total Lung Capacity × 100 | Normal | Increased during episodes | Increased | |
| Total Lung Capacity | Normal | Increased during episodes | Increased | |
| Gas Mixing Index | Slightly increased | Increased during episodes | Increased | |
| Carbon Monoxide Diffusing Capacity | Normal | Normal or slightly reduced | Significantly reduced | |
| Isoproterenol Test | Slightly improved | Significantly improved (Maximum Ventilation Volume increased by more than 20%) | No improvement | |
