Patients with a history of chronic respiratory inflammation or asthma before surgery have bronchospasm induced by the stimulation of many factors such as mechanical or chemical anesthesia. All of them can be relieved by timely and appropriate treatment. Bronchospasm can occur with slight provocation in patients with release of biologically active substances, vagal excitation, and airway hyperreactivity. Manual control of breathing, combined with intravenous administration of dexamethasone, aminophylline, and ketamine, is reliable. Bronchospasm is manifested as spasmodic contraction of bronchial smooth muscle, narrowing of the airway, sudden increase in ventilation resistance, expiratory dyspnea, which causes severe hypoxia and carbon dioxide accumulation, and improper treatment can lead to death. 1, the causes of bronchospasm during general anesthesia As the bronchial smooth muscle is innervated by the vagus nerve and sympathetic nerves, stimulation of the vagus nerve can excite the M receptors on the mast cell membrane, increasing the activity of guanyl cyclase, promoting the conversion of guanosine triphosphate into guanosine cyclophosphate, accelerating the release of bioactive substances, causing bronchospasm. More importantly: the airway subepithelium is rich in vagal afferent fibers, especially in the bulge, once mechanical stimulation, it is easy to cause vagal excitation, so that the bronchial reactivity is excessively increased, causing bronchial smooth muscle contraction, and thus bronchospasm occurs. Many factors can induce bronchial smooth muscle contraction during general anesthesia, including vagal excitation, mechanical or chemical stimulation, histamine release, and direct drug action. Patients with airway hyperreactivity are more sensitive to these triggers. Patients with chronic inflammation of the respiratory tract or a history of asthma have increased vagal tone and bronchial smooth muscle is in a state of stress, and bronchospasm can occur with the slightest provocation; these patients are called airway hyperresponsive patients. Succinylcholine produces allergic-like reactions and releases histamine. The use of sodium thiopental and succinylcholine-induced bronchospasm may be related to these induction drugs, and bronchospasm mostly occurs before the start of inhalation anesthesia and after the end of inhalation anesthesia because of the use of inhalation anesthesia maintenance that allows bronchial smooth muscle to relax, thus causing contraction of bronchial smooth muscle by the cholinesterase inhibitor neostigmine, which excites cholinergic M receptors. Bronchospasm can be induced directly when surgical anesthetic operations stimulate the pharynx, trachea, and bronchi, especially under shallow general anesthesia. Neck surgery and anesthesia operations such as tracheal intubation, tracheal extubation, aspiration and other mechanical stimuli can also directly induce bronchospasm. 2, the treatment of bronchospasm during general anesthesia For patients with airway hyperreactivity, preoperative antibiotics, hormones and bronchodilators should be used routinely to control respiratory inflammation and improve ventilatory function, and respiratory function tests should be routinely performed. During the anesthesia and surgery of such patients, the airway stimulation should be minimized and drugs that can cause bronchospasm should be avoided. Once intraoperative airway resistance increases substantially for a short period of time and upper airway obstruction is excluded, both lungs should be auscultated, and bronchospasm can be diagnosed if both lungs are full of croup. After bronchospasm occurs, the cause should be immediately identified and treated symptomatically. For bronchospasm caused by anesthesia and surgical mechanical stimulation, the stimulating operation should be stopped immediately and comprehensive treatment, including medication and respiratory management, should be actively implemented. Aminophylline can prevent the acute attack of asthma and relieve the spasm of bronchial smooth muscle, but its toxicity/therapeutic index is low, and it cannot enhance the therapeutic effect of β2 agonist on patients with acute attack of bronchospasm, so the dose should not be increased blindly in clinical application to avoid toxic side effects. Hormonal drugs have the effect of reducing the edema of respiratory mucosa, anti-inflammatory, anti-allergic, and direct expansion of tracheal smooth muscle, etc. Inflammation of the respiratory tract will cause edema of the airway mucosa and reduction of the tube diameter. A slight contraction of smooth muscle in these patients can cause a significant increase in respiratory resistance, so most physicians use hormonal drugs as the first-line drugs for the prevention and treatment of bronchospasm. β2 agonists (epinephrine, isoprenaline, albuterol, terbutaline, etc.) are fast-acting and reliable. They excite the β2 receptors of bronchial smooth muscle and make the trachea diastolic, and also have a diastolic effect on the contracted bronchial smooth muscle, and at the same time have a contracting effect on the airway mucosal vessels, and can be administered by nebulized inhalation, subcutaneous injection or intravenous injection. Atropine can reduce the excitability of the vagus nerve, and has a dilating effect on the bronchial smooth muscle. Most of the anesthetic drugs can relax the bronchial smooth muscle, such as isoproterenol, ketamine, sodium oxybutyrate, desflurane, halothane, isoflurane, aflurane, lidocaine, valium, mydriatic acid, haloperidol, etc. In addition, some commonly used anesthetic drugs such as sodium nitroprusside, nitroglycerin, etc. can also relax the bronchial smooth muscle, among which ketamine and inhalation anesthetics have the strongest effect. Along with drug therapy, good respiratory management is essential. In conclusion, many factors can induce bronchospasm during general anesthesia surgery, and most of them occur in patients with high airway response. Good preoperative preparation for such patients is very important, and the selection of anesthetic drugs and anesthetic management should be strengthened to reduce the incidence of bronchospasm in anesthesia. In one patient in this group, a history of asthma was missed before anesthesia, and drugs that can cause bronchial smooth muscle contraction were used during anesthesia, leading to the occurrence of bronchospasm, and the lesson is profound.