Asthma

　　1. Genetic Factors:The relationship between asthma and heredity has attracted increasing attention. According to family data, early research mostly considered asthma to be a monogenic genetic disease, with some scholars believing it to be an autosomal dominant genetic disease, while others believe it to be an autosomal recessive genetic disease. Currently, it is considered to be a polygenic genetic disease with a heritability of about 70% to 80%. Polygenic genetic diseases are caused by the combined action of multiple pathogenic genes located on different chromosomes, with no obvious dominant or recessive distinction among these genes, each having a weak influence on the phenotype, but with an additive effect. The onset of the disease is greatly influenced by environmental factors. Therefore, bronchial asthma is composed of several pathogenic genes with minor effects but cumulative effects, forming its genetic factors. The risk of disease caused by the genetic basis of an individual is called susceptibility. The possibility of an individual being susceptible to asthma, determined by the combined action of genetic and environmental factors, is called predisposition. The size of heritability can measure the role of genetic factors in the onset of the disease. The higher the heritability, the greater the role of genetic factors in the onset of the disease. Many survey data show that the prevalence rate of asthma in relatives of patients is higher than that in the general population, and the closer the kinship, the higher the prevalence rate. In a family, the more people who have the disease, the higher the prevalence rate among their relatives; the more severe the patient's condition, the higher the prevalence rate among their relatives. Wang Min gang and others investigated the prevalence rate of asthma in the first and second-degree relatives of asthma children and compared it with the control group. The prevalence rate of asthma in the first-degree relatives of the asthma group was 8.2%, and the prevalence rate in the second-degree relatives was 2.9%, with the prevalence rate of asthma in the former significantly higher than that in the latter. The prevalence rates of asthma in the first and second-degree relatives in the control group were 0.9% and 0.4%, respectively, which were lower than the prevalence rates of asthma in the first and second-degree relatives of the asthma group.

　　An important feature of asthma is the presence of airway hyperreactivity. Studies on humans and animals show that some genetic factors control the reaction of the airway to environmental stimuli. Zhang Xiaodong and others used the tissue inhalation method to measure the airway reactivity of the parents of 40 asthma children and 34 normal children. Most of the parents of asthma children have varying degrees of increased airway reactivity, with an average PC20 of 11.6 mg/ml, while the PC20 of the parents of normal children is all greater than 32 mg/ml, indicating that there is a basis for airway hyperreactivity in the families of asthma patients. Therefore, the inheritance of airway hyperreactivity plays an important role in the inheritance of asthma.

　　Currently, the related genes of asthma are not fully identified, but there are studies showing that there may be asthma-specific genes, IgE regulatory genes, and specific immune response genes. The autosomal 11q12q13 region contains asthma genes that control the reactivity of IgE; recent research results on the genetics of total serum IgE in foreign countries suggest that the genes regulating total IgE are located on the fifth pair of chromosomes; the specific immune response is not controlled by IgE regulatory genes, but by immune response genes. Immune response genes have a high recognition ability of antigenic molecules, and experiments in mice have confirmed that immune response genes are located in the MHC region on chromosome 17. Studies have shown that there are also immune response genes in the HLA region on chromosome 6 in humans, which control the immune response to a specific antigen. Therefore, in the pathogenesis of asthma, the interaction between IgE regulatory genes and immune response genes plays a role. In addition, the different sensitivity states of cell receptors in the nervous and respiratory systems, as well as the congenital lack of certain enzymes, may also be influenced by genetic factors. In summary, the relationship between asthma and genetics needs to be further studied and explored in order to benefit early diagnosis, early prevention, and treatment.

　　Second, triggering factors:The formation and recurrent exacerbation of asthma are often the result of the combined effects of many complex factors.

　　1. Inhaled substances: Inhaled substances are divided into specific and non-specific types.The former includes dust mites, pollen, fungi, animal dander, etc.; non-specific inhaled substances include sulfuric acid, sulfur dioxide, ammonia, etc. Specific inhaled substances for occupational asthma include toluene diisocyanate, phthalic anhydride, ethylenediamine, penicillin, protease, amylase, silk, animal dander or excrement, etc. In addition, there are also non-specific substances such as formaldehyde and formic acid.

　　2. Infection: The formation and exacerbation of asthma are related to recurrent respiratory tract infections.In asthma patients, there may be specific IgE to bacteria, viruses, mycoplasma, and other antigens, and if inhaled, they can trigger asthma. After viral infection, it can directly damage the respiratory epithelium, leading to increased reactivity of the respiratory tract. Some scholars believe that interferon and IL-1 produced by viral infection increase the release of histamine by basophils. In the neonatal period, many children with respiratory symptoms, especially respiratory syncytial virus infection, are also observed. Asthma caused by parasites such as ascaris and hookworm is still seen in rural areas.

　　3. Food:The phenomenon of asthma exacerbation induced by diet is often seen in asthma patients, especially in infants and young children who are prone to food allergies, but this decreases gradually with age. The most common allergenic foods are fish, shrimp and crabs, eggs, milk, and so on.

　　4. Climate change:Asthma exacerbation can be induced by changes in temperature, humidity, air pressure, and (or) ions in the air, so it is more common in cold seasons or during climate changes in autumn and winter.

　　5. Mental factors:Emotional excitement, tension, anger, and other factors in patients can trigger asthma exacerbation, which is generally believed to be caused by reflexes or overventilation via the cerebral cortex and vagus nerve.

　　6. Exercise:Approximately 70% to 80% of patients with asthma exacerbation are induced by strenuous exercise, known as exercise-induced asthma or exercise asthma. Typical cases show the most significant bronchospasm within 1 to 10 minutes after stopping exercise, with many patients recovering spontaneously within 30 to 60 minutes. There is an approximate 1-hour refractory period after exercise, during which 40% to 50% of patients will not experience bronchospasm if they exercise again. Clinical manifestations include cough, chest tightness, shortness of breath, wheezing, and the auscultation may reveal wheezing sounds. Some patients may not show typical asthma symptoms after exercise, but pulmonary function tests before and after exercise can reveal bronchospasm. This disease is more common in adolescents. If sodium cromoglycate, ketotifen, or aminophylline are administered beforehand, the attack can be alleviated or prevented. Relevant studies suggest that due to overventilation after strenuous exercise, the moisture and heat in the airway mucosa are lost, leading to a temporary increase in molar concentration of respiratory epithelium, which causes bronchial smooth muscle contraction.

　　7, Asthma and medication:Some medications can trigger asthma attacks, such as propranolol, which can cause asthma by blocking β2-adrenergic receptors. Approximately 2.3% to 20% of asthma patients may develop asthma due to the use of aspirin and related drugs, known as aspirin-induced asthma. Patients with nasal polyps and low tolerance to aspirin are also referred to as the aspirin triad. The clinical characteristics include: asthma attacks can be triggered by aspirin, with symptoms usually appearing within 2 hours after taking the drug, and occasionally up to 2 to 4 hours later. Patients may have cross-reactivity with other antipyretic and analgesic drugs and non-steroidal anti-inflammatory drugs; most asthma attacks in children occur before the age of 2, but most patients are middle-aged, with the majority being between 30 and 40 years old; women are more affected than men, with a ratio of about 2:3; attacks are not seasonal, and the condition is severe and persistent, with most patients being dependent on corticosteroids; more than half of the patients have nasal polyps, often accompanied by perennial allergic rhinitis and/or sinusitis, and sometimes asthma symptoms may worsen or be triggered after nasal polyp surgery; common inhalant allergen skin tests often show negative reactions; total serum IgE levels are usually normal; there are few patients with allergic diseases in the family. The pathogenesis of the disease has not been fully elucidated; some believe that the bronchial cyclooxygenase of patients may be susceptible to inhibition by aspirin and related drugs due to the influence of a contagious medium (possibly a virus), making it easy for cyclooxygenase to be inhibited by aspirin and related drugs, i.e., intolerance to aspirin. Therefore, when patients take aspirin and related drugs, it affects the metabolism of arachidonic acid, inhibits the synthesis of prostaglandins, causing an imbalance between PGE2/PGF2α, leading to an increase in leukotriene production, resulting in strong and persistent contraction of bronchial smooth muscle.

　　8, Menstruation, pregnancy, and asthma:Many female asthma patients experience exacerbation of asthma symptoms 3 to 4 days before the menstrual period, which may be related to the sudden drop in progesterone levels before menstruation. If some patients have a monthly exacerbation but not much menstrual bleeding, they can be injected with progesterone at the appropriate time, which may sometimes prevent severe premenstrual asthma. The influence of pregnancy on asthma is not regular; some patients may experience improvement, while others may worsen, but most patients do not show significant changes. The main effects of pregnancy on asthma are mechanical and related to changes in hormones associated with asthma. In the late stages of pregnancy, as the uterus grows, the diaphragm moves up, resulting in varying degrees of decrease in residual volume, expiratory reserve volume, and functional residual capacity, as well as an increase in ventilation and oxygen consumption. If asthma is properly managed, it will not have adverse effects on pregnancy and childbirth.

　　3. Hypersensitivity:The onset of bronchial asthma is related to hypersensitivity, which is recognized as the main type I hypersensitivity. Most patients have atopic constitution and often have other allergic diseases. After the allergen enters the body and stimulates the organism, high-titer specific IgE can be synthesized and combined with high-affinity Fcε receptors (FcεR1) on the surface of mast cells and basophils; it can also bind to low-affinity Fcε receptors (FcεR2) on the surface of certain B cells, macrophages, monocytes, eosinophils, NK cells, and platelets. However, the affinity of FcεR2 for IgE is about 10 to 100 times lower than that of FcεR1. If the allergen enters the body again, it can cross-link with the IgE bound to FcεR, synthesize and release a variety of active mediators, causing bronchial smooth muscle contraction, increased mucus secretion, increased vascular permeability, and infiltration of inflammatory cells. Moreover, inflammatory cells can release a variety of mediators under the action of the mediators, exacerbating airway inflammation. According to the time from allergen inhalation to the onset of asthma, it can be divided into immediate asthmatic reaction (IAR), delayed asthmatic reaction (LAR), and biphasic asthmatic reaction (DAR). IAR almost occurs immediately upon inhalation of the allergen, reaching its peak within 15 to 30 minutes, and gradually returning to normal within 2 hours. LAR starts late, occurring about 6 hours later, with a long duration, lasting for several days. Some severe asthma patients have a close relationship with delayed reactions, with severe clinical symptoms and significant and persistent lung function damage, often requiring recovery after treatment with inhaled corticosteroids and other drugs. In recent years, the clinical importance of LAR has attracted great attention. The mechanism of LAR is more complex, not only related to the degranulation of mast cells mediated by IgE, but mainly caused by airway inflammation, possibly involving the redelivery of mast cells and the release of delayed mediators such as leukotrienes (LT), prostaglandins (PG), and thromboxanes (TX). Studies have shown that the degranulation reaction of mast cells is not unique to the immune mechanism, and non-immunological stimuli such as exercise, cold air, and sulfur dioxide inhalation can also activate mast cells and release particles. It is now believed that asthma is a chronic inflammatory disease involving the interaction of various inflammatory cells, with many mediators and cytokines participating. LAR is the result of airway inflammatory response, with mast cells as the primary effector cells, and eosinophils, neutrophils, monocytes, lymphocytes, and platelets as the secondary effector systems. These cells can also release a large amount of inflammatory mediators, activate the target organs of the airways, causing bronchial smooth muscle spasm, microvascular leakage, mucosal edema, and hypersecretion of mucus, leading to the excitation of neurogenic reflexes. The airway reactivity of patients is significantly increased. Clinically, the use of general bronchodilators alone is not easy to alleviate, while the use of inhaled corticosteroids and sodium cromoglycate can prevent the occurrence of LAR.

　　Controversy has been proposed regarding the relationship between bronchial asthma and type III hypersensitivity. The traditional view holds that exogenous asthma belongs to type I hypersensitivity, manifesting as IAR; while endogenous asthma belongs to type III hypersensitivity (Arthus phenomenon), manifesting as LAR. However, research results indicate that the majority of LAR are secondary to IAR, and LAR has a significant dependence on IAR. Therefore, not all LAR are type III hypersensitivity.

　　Four, airway inflammation:Airway inflammation has been an important progress in the research field of the pathogenesis of asthma in recent years. The airway inflammation in asthmatic patients with bronchial asthma is a chronic non-specific airway inflammation involving a variety of cells, especially mast cells, eosinophils, and T lymphocytes, and the interaction of more than 50 inflammatory mediators and more than 25 cytokines. Airway inflammation is an important determinant of reversible airway obstruction and non-specific bronchial hyperreactivity in asthmatic patients. The airway inflammation response process in asthma has three stages, namely, IgE activation and FcεR initiation, release of inflammatory mediators and cytokines, and expression of adhesion molecules promoting leukocyte transmembrane migration. When allergens enter the body, B cells recognize antigens and become activated, and their activation pathways include: T and B cells recognize different epitopes of antigens and express activation separately; B cells phagocytize, process antigens, and bind to major histocompatibility complex (MHCⅡ), which is recognized by Th and releases IL-4, IL-5 to further promote B cell activation. The activated B cells produce corresponding specific IgE antibodies, which then cross-link with mast cells, eosinophils, and other cells, and under the action of allergens, produce and release inflammatory mediators. It is known that mast cells, eosinophils, neutrophils, epithelial cells, macrophages, and endothelial cells all have the ability to produce inflammatory mediators, which can be divided into three categories according to the order of their production: rapidly released mediators (such as histamine), secondary produced mediators (PG, LT, PAF, etc.), and granule-derived mediators (such as heparin). Mast cells are the main primary effector cells in airway inflammation. After activation, mast cells can release histamine, eosinophil chemotactic factor (ECF-A), neutrophil chemotactic factor (NCF-A), LT, and other mediators. Alveolar macrophages may also play an important role in initiating asthma inflammation, and after activation, they can release TX, PG, and platelet activating factor (PAF) and other mediators. ECF-A induces chemotaxis of eosinophils and induces the release of major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), eosinophil neurotoxin (EDN), PAF, LTC4, etc., MBP and EPO can cause the shedding of airway epithelial cells, exposing sensory nerve endings, causing airway hyperreactivity. MBP and EPO can also activate mast cells to release mediators. NCF-A can induce chemotaxis of neutrophils and release LT, PAF, PGS, oxygen free radicals, and lysosomal enzymes, aggravating the inflammatory response. LTC4 and LTD4 are strong bronchoconstrictors and promote increased mucus secretion and increased vascular permeability. LTB4 can induce chemotaxis, aggregation, and secretion of mediators by neutrophils and eosinophils. PGD2, PGF2, PGF2α, PGI2, and TX are all powerful bronchoconstrictors. PAF can constrict bronchi and induce chemotaxis and activation of inflammatory cells such as eosinophils, induce increased microvascular exudation, and is one of the important asthma inflammatory mediators. In recent years, it has been found that endothelin (ET5) produced in airway epithelial cells and vascular endothelial cells is an important mediator that causes airway constriction and reconstruction.ET1 is the strongest bronchial smooth muscle contraction agent known so far, its contraction strength is 100 times that of LTD4 and neuropeptides, 1000 times that of acetylcholine, and ET also has the effects of promoting the secretion of submucosal glands and promoting the proliferation of smooth muscle and fibroblasts. The pro-inflammatory cytokine TNFα can stimulate the secretion of ET1 by airway smooth muscle cells, which not only intensifies the contraction of smooth muscle but also increases the contractile reactivity of airway smooth muscle and can lead to airway reconstruction caused by abnormal proliferation of airway cells, which may become an important cause of chronic refractory asthma. Adhesion molecules (adhesion molecules, AMs) are a class of glycoproteins that can mediate cell-cell adhesion. A large number of research data have confirmed that adhesion molecules play an important role in the pathogenesis of asthma. In airway inflammatory reactions, adhesion molecules mediate the adhesion and transendothelial migration of leukocytes and endothelial cells to the inflammatory site.

　　In summary, the inflammatory response of actual asthma is involved by various inflammatory cells, inflammatory mediators, and cytokines, and the relationship is very complex, which needs to be further discussed.

　　V. Airway hyperreactivity:Airway reactivity refers to the contraction response of the airway to various chemical, physical, or pharmacological stimuli. Airway hyperreactivity (AHR) refers to an excessive airway contraction response to non-allergenic stimuli that normally do not cause or only cause mild response. AHR is one of the important characteristics of actual asthma. AHR often has a familial tendency, affected by genetic factors, but the role of exogenous factors is more important. It is widely believed that airway inflammation is one of the most important mechanisms leading to airway hyperreactivity. When the airway is exposed to allergens or other stimuli, AHR occurs due to the participation of various inflammatory cells, inflammatory mediators, and cytokines, as well as damage to the airway epithelium and intracellular nerves. It is believed that the autocrine and paracrine of endothelin in airway stromal cells, as well as the interaction between cytokines, especially TNFα, and endothelin, play an important role in the formation of AHR. In addition, AHR is related to hypoactivity of β-adrenergic receptors, increased cholinergic neuronal excitability, and defective inhibitory function of non-adrenergic non-cholinergic (NANC) neurons. The stimulation of physical and chemical factors such as viral respiratory tract infection, SO2, cold air, dry air, hypotonic and hypertonic solutions can all increase airway reactivity. The degree of airway hyperreactivity is closely related to airway inflammation, but the two are not identical. It is currently recognized that AHR is a common pathophysiological feature of bronchial asthma patients, however, not all patients with BHR have bronchial asthma, such as those with long-term smoking, exposure to ozone, viral upper respiratory tract infection, chronic obstructive pulmonary disease (COPD), allergic rhinitis, bronchiectasis, tropical pulmonary eosinophilia, and allergic alveolitis may also have BHR, so the clinical significance of BHR should be understood comprehensively.

　　Six, Nerve factors:The innervation of the bronchus is very complex, in addition to the cholinergic nerves and adrenergic nerves known before, there is also a non-adrenergic non-cholinergic (NANC) nervous system. Bronchial asthma is related to hypoactivity of β-adrenergic receptors and increased vagal nerve tone, and there may be an increased responsiveness of α-adrenergic nerves. The NANC inhibitory nervous system is the main nervous system for producing bronchial smooth muscle relaxation, and its neurotransmitters have not been fully elucidated, possibly vasoactive intestinal peptide (VIP) and/or methionine, while the contraction of bronchial smooth muscle may be related to the dysfunction of this system. The NANC excitatory nervous system is an unmyelinated sensory nervous system, and its neurotransmitter is substance P, which exists in the C-type传入fibers of the vagus nerve chemosensitivity of the airway. When the airway epithelium is damaged and the C fiber sensory nerve endings are exposed, stimulated by inflammatory mediators, it causes local axon reflexes, retrograde conduction along the lateral column of the传入nerve, and the release of sensory neuropeptides such as substance P, neurokinin, and calcitonin gene-related peptide, resulting in bronchial smooth muscle contraction, increased vascular permeability, and increased mucus secretion. Recent research has shown that nitric oxide (NO) is the main neurotransmitter of human NANC, and endogenous NO has a dual effect on the airway; on the one hand, it can relax the airway smooth muscle and kill pathogenic microorganisms, playing an important role in the regulation of airway smooth muscle tension and pulmonary immune defense; on the other hand, the excessive production of NO locally can aggravate the damage to the airway tissue and induce AHR, the effect of which may vary due to the concentration of local tissue and the target site, and regulating the generation of NO in the airway may be beneficial to the treatment of asthma.

　　The basic pathological changes of the airway include infiltration of mast cells, pulmonary macrophages, eosinophils, lymphocytes, and neutrophils. The mucosal tissue of the airway is edematous, the permeability of microvessels increases, bronchial secretions accumulate, bronchial smooth muscle spasms, ciliated epithelium is stripped off, the basement membrane is exposed, goblet cells proliferate, and an increase in bronchial secretions, etc., which is called chronic desquamative eosinophilic bronchitis. These changes can vary with the degree of airway inflammation. If asthma attacks are long-term and recurrent, it can enter the stage of irreversible airway narrowing, mainly manifested as hypertrophy of the muscular layer of bronchial smooth muscle, fibrosis under the airway epithelial cells, and the disappearance of the supporting role of the surrounding lung tissue in the airway.

　　In the early stage of the disease, due to the reversibility of the pathology, there are rarely any organic changes anatomically. With the progression of the disease, pathological changes become more evident. Macroscopically, lung expansion and emphysema are more prominent, the lungs are soft, loose, and elastic, and the bronchi and bronchioles contain thick sputum and mucus plugs. The bronchial wall thickens, the mucosa becomes congested and swollen, forming folds, and local mucous plug obstruction can be found in atelectasis.

　　I. Sudden death:Sudden death is the most serious complication of bronchial asthma, as it often has no obvious warning symptoms and death often occurs before rescue can be carried out. The important causes of asthma sudden death can be summarized as:

　　1. Specific hypersensitivity reaction:Due to the hyperreactive state of the airways, specific or non-specific stimuli, especially during airway reactivity testing, can cause severe laryngeal and tracheal edema and widespread bronchospasm, leading to tracheal obstruction and asphyxiation or triggering severe arrhythmias or sudden cardiac arrest and death.

　　2. Atelectasis:They can be caused by widespread sputum plug obstruction of the bronchi or the side effects of isoproterenol. The latter is due to the intermediate metabolite of the drug, 3-methoxyisoproterenol, which not only cannot activate beta receptors but also can act as a beta-blocker, causing bronchospasm and airway obstruction.

　　3. Lethal arrhythmias:It can be caused by severe hypoxia, water and electrolyte imbalance, and acid-base imbalance, or by improper use of drugs, such as digoxin in the presence of heart failure, beta-agonists during bronchodilation, aminophylline, etc. If aminophylline is administered intravenously, a blood concentration of >30mg/L can induce rapid arrhythmias.

　　4. Sudden onset of bronchial asthma:Death often occurs before medication can be administered, and the mechanism is unclear.

　　5. Incorrect use of anesthetics or improper use of sedatives:Anesthetics can cause respiratory depression or even sudden stoppage, and some sedatives also have a significant inhibitory effect on the respiratory center, such as barbiturates and chlorpromazine. In case of sudden death, artificial airways should be established immediately, artificial ventilation should be performed, and corresponding and effective treatments should be given to vital organs such as the heart and brain at the same time or subsequently.

　　II. Lower respiratory tract and lung infections:According to statistics, about half of asthma cases are induced by upper respiratory tract viral infections. As a result, the immune function of the respiratory tract is interfered with, making it prone to secondary lower respiratory tract and lung infections. Therefore, it is necessary to strive to improve the immune function of asthma patients, keep the airways unobstructed, clear secretions from the airways, maintain a clean ward, prevent colds, and reduce infections; once infection symptoms appear, appropriate antibiotics should be selected based on bacteria and drug sensitivity for treatment.

　　Third, water and electrolyte and acid-base imbalance:Due to asthma attacks, hypoxia, insufficient intake of food and water, dehydration, and dysfunction of the heart, liver, especially the respiratory and renal functions, water and electrolyte imbalances and acid-base imbalances often occur, which are important factors affecting the efficacy and prognosis of asthma. It is necessary to strive to maintain water and electrolyte and acid-base balance, monitor electrolytes even daily, and perform arterial blood gas analysis in time to detect abnormalities and treat them in a timely manner.

　　Fourth, pneumothorax and mediastinal emphysema:Due to gas retention in the alveoli during asthma attacks, the alveoli contain too much air, resulting in a significant increase in intrapulmonary pressure. Chronic asthma with concurrent emphysema can lead to rupture of bullae, forming spontaneous pneumothorax. When mechanical ventilation is used, excessive peak pressure in the airway and alveoli can easily cause alveolar rupture, leading to barotrauma, pneumothorax, and even mediastinal emphysema.

　　Fifth, respiratory failure:Common causes of asthma-induced respiratory failure include insufficient ventilation during severe asthma attacks, infection, improper treatment and medication, concurrent pneumothorax, atelectasis, and pulmonary edema. Once respiratory failure occurs, due to severe hypoxia, carbon dioxide retention, and acidosis, asthma treatment becomes more difficult. It is necessary to eliminate and reduce the causes, prevent their occurrence; and rescue according to respiratory failure after they occur.

　　Sixth, multiple organ dysfunction and multiple organ failure:Due to severe hypoxia, severe infection, acid-base imbalance, gastrointestinal bleeding, and the toxic and side effects of drugs, severe asthma often leads to multiple organ dysfunction and even failure. To prevent and correct the above causes, actively improve the function of all important organs.

　　 Real asthma refers to asthma caused by the prevalence of evil qi. Real asthma is characterized by sputum as the main symptom, often induced by external wind-cold or dry evil. It has an acute onset, a short course, rapid breathing, and strong breath.

　　1, Wind-cold blocking the lung syndrome

　　Asthma and cough with reversed breath, rapid breathing, chest oppression, excessive thin and frothy sputum, white and sticky in color, often with headache, aversion to cold, or fever, no thirst, no sweating, thin white and slippery tongue coating, floating and tight pulse.

　　Summary of the pathogenesis: Wind-cold ascending to the exterior, internalizing into the lung, evil qi is solid, and lung qi is not ventilated.

　　Treatment method: Ventilate the lung and disperse cold.

　　Representative formula: Mahuang Tang combined with Huagai San with modifications. Mahuang Tang ventilates the lung and relieves asthma, disperses cold and relieves the exterior, used for cough and asthma with body pain and fever; Huagai San ventilates the lung and resolves phlegm, used for asthma and cough with chest oppression and phlegm qi obstruction. Compared with the former, it has stronger power to relieve the exterior and disperse cold, while the latter has a more significant effect on descending the qi and resolving phlegm.

　　Commonly used drugs: Mahuang and Zisu (Perilla frutescens) to warm the lung and disperse cold; Banxia, Juhong (Citrus reticulata), Xingren, Susi, Ziyuan, and Baiqian (Platycodon grandiflorus) to resolve phlegm and benefit the qi.

　　If the exterior syndrome is marked, with no sweating and aversion to cold and heat, headache and body pain, add Guizhi with Mahuang to relieve the exterior and disperse cold; for severe cold phlegm, white and thin sputum, in large quantity, with froth, add Xixin (Asarum sieboldii) and Shengjiang (Zingiber officinale) to warm the lung and resolve phlegm; if cough and asthma are severe, with chest fullness and reversed qi, add Shegan, Qianhu, Houpu (Magnolia officinalis), and Ziyuan (Anemone flaccida) to ventilate the lung, descend the qi, and resolve phlegm; if there is retained cold drink in the lung, and triggered by external cold, Xiao Qinglong Tang can be used to relieve exterior and warm the interior.

　　2, Exterior cold and lung heat syndrome

　　Asthma and cough with reversed breath, chest distension or pain, rough breathing, flaring nose, coughing not smooth, thick and sticky sputum, accompanied by aversion to cold, fever, oppression, body pain, sweating or not, thirst, thin white or yellowish tongue coating, red tongue edges, floating and rapid or slippery pulse.

　　Summary of the pathogenesis: Cold evil binds the exterior, heat is retained in the lung, and lung qi rises upwards.

　　Treatment method: Relieve the exterior and clear the interior, resolve phlegm and relieve asthma.

　　Representative formula: Mahuang Shigao Tang with modifications. This formula has the effects of ventilating the lung, draining heat, descending the qi, and relieving asthma, which is suitable for exterior syndrome with interior heat, cough and asthma with upward breath, eye swelling and exophthalmos, aversion to cold and fever, floating and large pulse.

　　Commonly used drugs: Mahuang (Ephedra sinica) to ventilate the lung and relieve the exterior; Huangqin, Sangbaipi, and Shigao to clear interior heat; Susi (Perilla frutescens), Xingren (Armeniaca sinica), Banxia (Pinellia ternata), and Kudouhua (Anemone coronaria) to descend the qi and resolve phlegm.

　　For severe exterior cold, add Guizhi (Cinnamomum cassia) to relieve the exterior and disperse cold; for severe phlegm heat, yellow and sticky phlegm in large quantity, add Guolou (Trichosanthes kirilowii) and Bamaye to clear phlegm heat; for phlegm rattle and surging breath, add Tinglài Zi and Shegan to drain the lung and resolve phlegm.

　　3, Phlegm heat retaining in the lung syndrome

　　Asthma and cough with surging breath, chest distension or pain, excessive phlegm with sticky yellow color, or mixed with blood, accompanied by chest oppression, fever, sweating, thirst for cold drinks, red face, dry throat, reddish urine, constipation, red tongue, thin yellow or greasy tongue coating, slippery and rapid pulse.

　　Summary of the pathogenesis: Pathogenic heat is retained in the lung, vaporizing fluid into phlegm, phlegm heat blocks, and the lung loses its purity and order.

　　Treatment method: Clear heat and resolve phlegm, ventilate the lung and relieve asthma.

　　Representative formula: Sangbaipi decoction with modifications. This formula has the function of clearing heat, purging the lung, and resolving phlegm, which is suitable for asthma, chest oppression, and yellowish and turbid sputum.

　　Commonly used drugs: Sangbaipi (Broussonetia papyrifera) and Huangqin (Scutellaria baicalensis) to clear lung heat; Zhimu (Anemarrhena asphodeloides), Bamaye (Fritillaria thunbergii), Shegan (Euphorbia thunbergii), Guoloupi (Trichosanthes kirilowii), Qianhu (Peucedanum praeruptorum), and Dilong (Pheretima) to clear phlegm heat and stabilize asthma.

　　If there is a high fever, add Shigao (Gypsum fibrosum) to clear the heat; if there is severe asthma with excessive phlegm, sticky and yellow in color, add Tinglài Zi (Descurainia Sophia), Haigeke (Merulin), Yuxingcao (Houttuynia cordata), Dongguazi (Benincasa hispida), and Yiren (Coix seed) to clear heat, drain the lung, resolve phlegm, and drain turbidity; if the qi of the bowels is not passing, phlegm surges and constipation occurs, add Guolouren (Trichosanthes sphaerocarpa) or Dahuang (Morphine) or Fenghua Xiaoyao San (Sulphur) to clear the bowels, clear the lung, and relieve obstruction.

　　4, Phlegm turbidity obstructing the lung syndrome

　　Shortness of breath with chest fullness and oppression, severe cases may present with chest fullness and back breathing, cough, excessive phlegm with sticky, white color, difficult to cough up, accompanied by nausea, decreased appetite, sticky mouth without thirst, white greasy tongue coating, slippery or soft pulse.

　　Pathogenesis summary: Deficiency of middle-yang, accumulation of dampness producing phlegm, phlegm turbidity obstructing the lung, and lung not descending.

　　Treatment method: Remove phlegm, reverse the adverse flow, and relieve asthma.

　　Representative formula: Erchen Decoction combined with Sannizi Yangqin Decoction with modifications. Erchen Decoction dries dampness and resolves phlegm, regulates qi and harmonizes the middle-jiao, used for cough with abundant phlegm, thick phlegm, chest oppression and epigastric fullness, with greasy tongue coating; Sannizi Yangqin Decoction lowers qi and resolves phlegm, used for phlegm turbidity obstructing the lung, cough with reverse flow and abundant phlegm, chest fullness and shortness of breath, with slippery and greasy tongue coating. Both formulas are used to treat phlegm and dampness, the former focuses on the spleen and stomach, suitable for those with abundant phlegm and epigastric fullness; the latter focuses on the lung, more suitable for those with abundant phlegm and shortness of breath.

　　Commonly used drugs: Fashen, Chenpi, Fuling to resolve phlegm; Suizi, Baijiezi, Laihuazi to resolve phlegm and lower qi to relieve asthma; Xingren, Ziai, Xuanfuhua to clear the lung and resolve phlegm and reverse the adverse flow.

　　With heavy phlegm and turbidity, thick and greasy tongue coating, add Cangzhu, Pohuopu to dry dampness and regulate qi to help resolve phlegm and relieve asthma; for spleen deficiency, decreased appetite, fatigue, loose stools, add Dangshen and Baizhu to invigorate the spleen and benefit the qi; for phlegm transforming from cold, white and thin, aversion to cold, add Ganjiang and Xixin; for phlegm turbidity transforming into heat, treat according to the syndrome of phlegm and heat.

　　5. Lung Qi Depression Syndrome

　　It often occurs in response to emotional stimulation, with sudden shortness of breath, coarse breathing, chest stuffiness, chest pain, as if there is something stuck in the throat, but the sound of phlegm in the throat is not prominent, or there is no phlegm sound. In daily life, there is often a lot of worry and depression, insomnia, palpitations. Thin tongue coating, wiry pulse.

　　Pathogenesis summary: Liver depression and qi reversal, ascending to attack the lung, causing lung qi not to descend.

　　Treatment method: Open depression, lower qi, and relieve asthma.

　　Representative formula: Wumoyin Decoction with modifications. This formula promotes qi, opens depression, and reverses the adverse flow, suitable for chest oppression and shortness of breath due to liver qi stagnation.

　　Commonly used drugs: Chenxiang, Muxiang, Chuanghua, Zhike to promote qi and relieve depression; Suizi, Jingjiecao, Dazhishi, Xingren to reverse the adverse flow and relieve asthma.

　　In cases of liver depression and qi stagnation, add Chaihu, Yujin, and Qingpi to regulate liver qi; for those with palpitations and insomnia, add Baihe, Hehuanpi, Suanzaoren, and Yuanzhi to calm the mind and nourish the heart; for those with qi stagnation and abdominal distension, constipation, add Dahuang to lower qi and unblock the bowels, which is the essence of Liumoyu Decoction.

　　In the treatment of this condition, it is advisable to encourage the patient to maintain a cheerful mood and cooperate with treatment.

　　With marked excess syndrome, phlegm and turbidity obstruct the lung, causing frequent coughing with phlegm, urgent and stuffy chest, greasy tongue coating, indicating 'upper excess and lower deficiency'. Treatment should be to resolve phlegm and reverse the adverse flow, warm the kidney and absorb the qi, and can use Suizi Jiangqi Decoction with additions of Zishiying and Chenxiang.

　　Dyspnea due to kidney deficiency, often accompanied by blood stasis, such as dark, blackish complexion, lips, nails, and tongue, with visible blue veins under the tongue, can be treated with additions of peach kernel, safflower, and Chuanxiong to promote blood circulation and remove blood stasis.

　　The diagnosis of real asthma, in addition to clinical manifestations, is characterized by an acute onset, a short course, rapid breathing, and strong breath.

　　Firstly, it is advisable to

　　1. For those with real asthma and heat symptoms, it is recommended to have a light diet, eat more fresh fruits like pears, oranges, loquats, and vegetables like radishes, adzuki beans, luffa, and walnuts. Honey and sesame seeds can be taken to promote bowel movements and alleviate asthma symptoms.

　　2. For those with asthmatic weakness, it is advisable to consume nourishing and invigorating foods, such as chicken, fish, jellyfish, ducks, bird's nest, etc.

　　Secondly, avoid

　　1. Avoid smoking, drinking, and other spicy and stimulating substances.

　　2. Avoid seafood and greasy foods, such as shrimps (especially deep-fried shrimps and drunken shrimps), crabs, mandarin fish, yellow croaker, hairtail, flounder, fatty meat, eggs, etc.

　　3. Avoid foods that can cause an allergic reaction, such as Chinese cabbage, rapeseed greens, cucumbers, rice porridge, and sake, and seasonings should not be too salty or too sweet. Keep the temperature moderate.

　　4. Avoid foods that produce gas, such as beans, sweet potatoes, potatoes, sodas, etc., as they can cause bloating, pressure on the chest and upper abdomen, and exacerbate asthma.

　　5. Avoid eating cold fruits and vegetables, as they can trigger asthma.

　　1, Wind-cold blocking the lung syndrome

　　Asthma and cough with reversed breath, rapid breathing, chest oppression, excessive thin and frothy sputum, white and sticky in color, often with headache, aversion to cold, or fever, no thirst, no sweating, thin white and slippery tongue coating, floating and tight pulse.

　　Summary of the pathogenesis: Wind-cold ascending to the exterior, internalizing into the lung, evil qi is solid, and lung qi is not ventilated.

　　Treatment method: Ventilate the lung and disperse cold.

　　Representative formula: Mahuang Tang combined with Huagai San with modifications. Mahuang Tang ventilates the lung and relieves asthma, disperses cold and relieves the exterior, used for cough and asthma with body pain and fever; Huagai San ventilates the lung and resolves phlegm, used for asthma and cough with chest oppression and phlegm qi obstruction. Compared with the former, it has stronger power to relieve the exterior and disperse cold, while the latter has a more significant effect on descending the qi and resolving phlegm.

　　Commonly used drugs: Mahuang and Zisu (Perilla frutescens) to warm the lung and disperse cold; Banxia, Juhong (Citrus reticulata), Xingren, Susi, Ziyuan, and Baiqian (Platycodon grandiflorus) to resolve phlegm and benefit the qi.

　　If the exterior syndrome is marked, with no sweating and aversion to cold and heat, headache and body pain, add Guizhi with Mahuang to relieve the exterior and disperse cold; for severe cold phlegm, white and thin sputum, in large quantity, with froth, add Xixin (Asarum sieboldii) and Shengjiang (Zingiber officinale) to warm the lung and resolve phlegm; if cough and asthma are severe, with chest fullness and reversed qi, add Shegan, Qianhu, Houpu (Magnolia officinalis), and Ziyuan (Anemone flaccida) to ventilate the lung, descend the qi, and resolve phlegm; if there is retained cold drink in the lung, and triggered by external cold, Xiao Qinglong Tang can be used to relieve exterior and warm the interior.

　　2, Exterior cold and lung heat syndrome

　　Asthma and cough with reversed breath, chest distension or pain, rough breathing, flaring nose, coughing not smooth, thick and sticky sputum, accompanied by aversion to cold, fever, oppression, body pain, sweating or not, thirst, thin white or yellowish tongue coating, red tongue edges, floating and rapid or slippery pulse.

　　Summary of the pathogenesis: Cold evil binds the exterior, heat is retained in the lung, and lung qi rises upwards.

　　Treatment method: Relieve the exterior and clear the interior, resolve phlegm and relieve asthma.

　　Representative formula: Mahuang Shigao Tang with modifications. This formula has the effects of ventilating the lung, draining heat, descending the qi, and relieving asthma, which is suitable for exterior syndrome with interior heat, cough and asthma with upward breath, eye swelling and exophthalmos, aversion to cold and fever, floating and large pulse.

　　Commonly used drugs: Mahuang (Ephedra sinica) to ventilate the lung and relieve the exterior; Huangqin, Sangbaipi, and Shigao to clear interior heat; Susi (Perilla frutescens), Xingren (Armeniaca sinica), Banxia (Pinellia ternata), and Kudouhua (Anemone coronaria) to descend the qi and resolve phlegm.

　　For severe exterior cold, add Guizhi (Cinnamomum cassia) to relieve the exterior and disperse cold; for severe phlegm heat, yellow and sticky phlegm in large quantity, add Guolou (Trichosanthes kirilowii) and Bamaye to clear phlegm heat; for phlegm rattle and surging breath, add Tinglài Zi and Shegan to drain the lung and resolve phlegm.

　　3, Phlegm heat retaining in the lung syndrome

　　Asthma and cough with surging breath, chest distension or pain, excessive phlegm with sticky yellow color, or mixed with blood, accompanied by chest oppression, fever, sweating, thirst for cold drinks, red face, dry throat, reddish urine, constipation, red tongue, thin yellow or greasy tongue coating, slippery and rapid pulse.

　　Summary of the pathogenesis: Pathogenic heat is retained in the lung, vaporizing fluid into phlegm, phlegm heat blocks, and the lung loses its purity and order.

　　Treatment method: Clear heat and resolve phlegm, ventilate the lung and relieve asthma.

　　Representative formula: Sangbaipi decoction with modifications. This formula has the function of clearing heat, purging the lung, and resolving phlegm, which is suitable for asthma, chest oppression, and yellowish and turbid sputum.

　　Commonly used drugs: Sangbaipi (Broussonetia papyrifera) and Huangqin (Scutellaria baicalensis) to clear lung heat; Zhimu (Anemarrhena asphodeloides), Bamaye (Fritillaria thunbergii), Shegan (Euphorbia thunbergii), Guoloupi (Trichosanthes kirilowii), Qianhu (Peucedanum praeruptorum), and Dilong (Pheretima) to clear phlegm heat and stabilize asthma.

　　If there is a high fever, add Shigao (Gypsum fibrosum) to clear the heat; if there is severe asthma with excessive phlegm, sticky and yellow in color, add Tinglài Zi (Descurainia Sophia), Haigeke (Merulin), Yuxingcao (Houttuynia cordata), Dongguazi (Benincasa hispida), and Yiren (Coix seed) to clear heat, drain the lung, resolve phlegm, and drain turbidity; if the qi of the bowels is not passing, phlegm surges and constipation occurs, add Guolouren (Trichosanthes sphaerocarpa) or Dahuang (Morphine) or Fenghua Xiaoyao San (Sulphur) to clear the bowels, clear the lung, and relieve obstruction.

　　4, Phlegm turbidity obstructing the lung syndrome

　　Shortness of breath with chest fullness and oppression, severe cases may present with chest fullness and back breathing, cough, excessive phlegm with sticky, white color, difficult to cough up, accompanied by nausea, decreased appetite, sticky mouth without thirst, white greasy tongue coating, slippery or soft pulse.

　　Pathogenesis summary: Deficiency of middle-yang, accumulation of dampness producing phlegm, phlegm turbidity obstructing the lung, and lung not descending.

　　Treatment method: Remove phlegm, reverse the adverse flow, and relieve asthma.

　　Representative formula: Erchen Decoction combined with Sannizi Yangqin Decoction with modifications. Erchen Decoction dries dampness and resolves phlegm, regulates qi and harmonizes the middle-jiao, used for cough with abundant phlegm, thick phlegm, chest oppression and epigastric fullness, with greasy tongue coating; Sannizi Yangqin Decoction lowers qi and resolves phlegm, used for phlegm turbidity obstructing the lung, cough with reverse flow and abundant phlegm, chest fullness and shortness of breath, with slippery and greasy tongue coating. Both formulas are used to treat phlegm and dampness, the former focuses on the spleen and stomach, suitable for those with abundant phlegm and epigastric fullness; the latter focuses on the lung, more suitable for those with abundant phlegm and shortness of breath.

　　Commonly used drugs: Fashen, Chenpi, Fuling to resolve phlegm; Suizi, Baijiezi, Laihuazi to resolve phlegm and lower qi to relieve asthma; Xingren, Ziai, Xuanfuhua to clear the lung and resolve phlegm and reverse the adverse flow.

　　With heavy phlegm and turbidity, thick and greasy tongue coating, add Cangzhu, Pohuopu to dry dampness and regulate qi to help resolve phlegm and relieve asthma; for spleen deficiency, decreased appetite, fatigue, loose stools, add Dangshen and Baizhu to invigorate the spleen and benefit the qi; for phlegm transforming from cold, white and thin, aversion to cold, add Ganjiang and Xixin; for phlegm turbidity transforming into heat, treat according to the syndrome of phlegm and heat.

　　5. Lung Qi Depression Syndrome

　　It often occurs in response to emotional stimulation, with sudden shortness of breath, coarse breathing, chest stuffiness, chest pain, as if there is something stuck in the throat, but the sound of phlegm in the throat is not prominent, or there is no phlegm sound. In daily life, there is often a lot of worry and depression, insomnia, palpitations. Thin tongue coating, wiry pulse.

　　Pathogenesis summary: Liver depression and qi reversal, ascending to attack the lung, causing lung qi not to descend.

　　Treatment method: Open depression, lower qi, and relieve asthma.

　　Representative formula: Wumoyin Decoction with modifications. This formula promotes qi, opens depression, and reverses the adverse flow, suitable for chest oppression and shortness of breath due to liver qi stagnation.

　　Commonly used drugs: Chenxiang, Muxiang, Chuanghua, Zhike to promote qi and relieve depression; Suizi, Jingjiecao, Dazhishi, Xingren to reverse the adverse flow and relieve asthma.

　　In cases of liver depression and qi stagnation, add Chaihu, Yujin, and Qingpi to regulate liver qi; for those with palpitations and insomnia, add Baihe, Hehuanpi, Suanzaoren, and Yuanzhi to calm the mind and nourish the heart; for those with qi stagnation and abdominal distension, constipation, add Dahuang to lower qi and unblock the bowels, which is the essence of Liumoyu Decoction.

　　In the treatment of this condition, it is advisable to encourage the patient to maintain a cheerful mood and cooperate with treatment.

　　With marked excess syndrome, phlegm and turbidity obstruct the lung, causing frequent coughing with phlegm, urgent and stuffy chest, greasy tongue coating, indicating 'upper excess and lower deficiency'. Treatment should be to resolve phlegm and reverse the adverse flow, warm the kidney and absorb the qi, and can use Suizi Jiangqi Decoction with additions of Zishiying and Chenxiang.

　　Dyspnea due to kidney deficiency, often accompanied by blood stasis, such as dark, blackish complexion, lips, nails, and tongue, with visible blue veins under the tongue, can be treated with additions of peach kernel, safflower, and Chuanxiong to promote blood circulation and remove blood stasis.