Bronchospasm is a continuous constriction of the bronchi, causing narrowing of the bronchial lumen and impairment of pulmonary ventilation. The impairment of inspiration leads to hypoxia, and the impairment of expiration makes alveolar residual air increasingly available and gas exchange increasingly difficult, leading to an acute asthma attack. The basic cause of bronchospasm in asthma is chronic non-specific inflammation of the bronchi. This inflammation aggravates bronchial hyperresponsiveness, so that bronchospasm can be caused when the asthmatic patient inhales or is exposed to specific allergens again, or when the bronchi are subjected to non-specific stimuli (e.g. cold air, chemically irritating gases). Etiology of bronchospasm 1. Airway hyperresponsiveness: Patients with respiratory diseases such as bronchial asthma or chronic inflammation make the airways more sensitive to various stimulus responses than normal people. This is related to the enhancement of excitatory nerve and receptor activity, and the weakening of inhibitory nerve and receptor activity. There are also inflammatory cell sensitization, airway epithelial damage and changes in airway surface liquid gram molecular osmotic concentration, etc., which are not negligible triggering factors. 2.Neural reflexes related to anesthesia surgery: such as pull reflex, pain reflex, and even cough reflex and pulmonary distension reflex can be triggering factors for airway contraction. Local stimuli such as tracheal intubation: Local stimuli such as tracheal intubation are the most common cause of airway spasm during induction of anesthesia. Since the airway is rich in vagal afferent fibers under the epithelium, especially at the rongeur site. Direct stimulation of the rongeur by deep tracheal intubation or tracheal intubation and aspiration under shallow anesthesia can also cause reflex bronchospasm. It is generally believed that in addition to the central reflex via the vagus nerve, there are also axial reflexes and released neuromediators such as substance P, neurokinin A and calcitonin gene-related peptide receptors, and tryptamine receptors involved. 4, applied anesthetics, muscle relaxants or other drugs that have excitatory vagus nerve and increase airway secretions prompting histamine release. For example, patients with bronchial asthma should avoid the application of drugs with excitatory vagus nerve such as sodium thiopental, sodium 7-hydroxybutyrate, or muscle relaxants that promote the release of histamine. Bronchospasm in the early postoperative period is not due to asthma, but is commonly caused by partial obstruction or irritation of the trachea due to displacement or obstruction of the endotracheal tube. It should be noted that bronchospasm may be the only symptom in the early stages of acute pulmonary edema and may appear much earlier than rales or foamy sputum.