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Bronchoconstriction during anesthesia occurs in patients with preexisting conditions such as reactive airway disease, but it also occurs from noxious stimulation of tracheal and laryngeal structures that activate vagal afferent nerves and from histamine-releasing drugs. Bronchoconstriction is more pronounced in smokers, or lightly anesthetized patients.

If a patient wheezes on expiration with auscultation prior to surgery, it is necessary to postpone surgery until the patient returns to normal condition. With chronic wheezing, such as chronic obstructive pulmonary disease (COPD), the patient must be optimized before elective surgery. Wheezing in patients with COPD results from gas flow obstruction due to smooth muscle contraction, secretions, and mucosal edema. Bronchodilators reverse the bronchospastic component of obstructive disease.


Sympathomimetic drugs are either mixed beta-1 and beta-2 adrenergic receptor agonists or selective beta-2 receptor agonists. These drugs increase the formation of cyclic adenosine monophosphate (cAMP) by activating adenylate cyclase. Adenylate cyclase converts ATP to cAMP, which is responsible for bronchodilation. Conversely, cyclic guanosine monophosphate (cGMP) causes bronchoconstriction. The balance between these two molecules relaxes or constricts bronchial smooth muscle cells.

The mixed sympathomimetic agents are epinephrine, isoproterenol, and isoetharine. Their beta-1 adrenergic effects stimulate cardiac muscle and therefore must be used cautiously in patients with cardiac conditions. The physiologic effects of beta-1 receptor stimulation include increased heart rate, contractility, and myocardial oxygen consumption. These agents produce tachyphylaxis with chronic usage. Epinephrine can be given intravenously, subcutaneously, or via endotracheal tube. The subcutaneous dose is 0.3–0.5 mg for bronchospasm, with peak effect seen in 5–25 minutes. Isoproterenol is effective via inhalation or intravenous routes.

Selective beta-2 receptor agonists avoid cardiac stimulation. These drugs include albuterol, terbutaline, and metaproterenol, which can be administered by aerosol or metered dose inhaler. These agents promote bronchodilation if wheezing is present. Albuterol reduces airway resistance for 4–6 hours with minimal cardiac effects. Terbutaline is given subcutaneously 0.25 mg, although some beta-1 effect occurs. Metaproteronol is given via inhaler and lasts 1–4 hours.


Phosphodiesterase inhibitors inhibit cAMP breakdown by suppressing the action of phosphodiesterase in the cytoplasm. Increased cAMP levels lead to increased bronchial smooth muscle relaxation. Methylxanthines (aminophylline, theophylline) are the most common phosphodiesterase inhibitors, although the entire class is rarely prescribed due to a narrow therapeutic window. Aminophylline is given intravenously or orally. It stimulates the diaphragm, improving contractility at the expense of diaphragmatic fatigue. Aminophylline also induces catecholamine release and blocks histamine release. It may cause ventricular dysrhythmias. Smokers exhibit induced metabolism, while heart failure, liver disease, and COPD patients risk toxicity due to reduced drug metabolism.

Theophylline reduces obstruction in asthmatics in a dose-dependent manner. It also decreases pulmonary vascular resistance, with a therapeutic range of 10–20 μg/mL. It stimulates cardiac receptors, increasing cardiac output. Side effects include nausea and vomiting, seizures (>40 μg/mL), tachycardia, and dysrhythmias.


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