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Bronchospasm is a reversible reflex constriction of the smooth muscle lining the bronchioles. It usually occurs as a result of worsening of underlying airway reactivity. Transient increases in airway resistance lead to an obstruction of both expiratory and inspiratory airflow. The inability to ventilate a patient despite the presence of a properly positioned endotracheal tube is life-threatening. In the perioperative course, this serious event typically occurs during induction of anesthesia, but may present during maintenance and emergence. Immediate diagnosis and management are critical to prevent hypoxemia, brain damage, and death.

The overall incidence of bronchospasm during general anesthesia is approximately 0.2%. However, the incidence of bronchospasm is highest (about 6%) in asthmatic patients receiving general endotracheal anesthesia. Regardless, life-threatening bronchospasm can still occur in healthy patients without any underlying pulmonary pathology. In fact, of the cases of bronchospasm in settled malpractice claims reported by the ASA Closed Claims study, only half of patients had any history of reactive airway disease (whether asthma or chronic pulmonary disease [COPD]).


Perioperative bronchospasm is a reflex that is mediated by the vagus nerve. A noxious stimulus, such as endotracheal intubation, activates afferent sensory fibers in the vagus nerve that stimulate neurons within the nucleus of the solitary tract. These neurons then stimulate efferent fibers through the vagus nerve to bronchiolar smooth muscle. Released acetylcholine neurotransmitters then bind to the M3 muscarinic receptor, resulting in an increase in cyclic guanosine monophosphate and inducing bronchiolar smooth muscle contraction. Other mediators that may participate in this reflex include histamine, tachykinins, vasoactive intestinal peptide, and calcitonin gene-related peptide.


Bronchospasm may occur in isolation or as one of several manifestations of a more serious underlying perioperative problem. Most causes of perioperative bronchospasm involve a nonallergic mechanism. The most common precipitating factor is airway irritation in patients known to be at higher risk of bronchial hyperreactivity, such as those with poorly controlled reactive airway disease (asthma and COPD), an upper respiratory tract infection, and history of smoking. In these at-risk patients, there are pharmacological causes of bronchospasm: desflurane, β-blockers, NSAIDs, cholinesterase inhibitors (neostigmine), and histamine-releasing drugs (atracurium, mivacurium, sodium thiopental, morphine). The bronchospasm reflex also highly depends on the depth of anesthesia. Therefore, surgical stimulation or mechanical manipulation of the airway (especially endotracheal intubation), in conjunction with an inadequate depth of anesthesia, significantly increases the chance of bronchospasm.

Bronchospasm that occurs after induction in a patient without risk factors for airway hyperreactivity may be the result of pulmonary aspiration of gastric contents. Aspiration may involve active vomiting or passive regurgitation. In addition to the classic signs of bronchospasm (bilateral expiratory wheezing, increased peak inspiratory pressures), the patient who aspirated typically develops hypoxemia. Aspiration can occur in a patient receiving general anesthesia with a face mask, laryngeal mask, and endotracheal tube.

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