Asthma is a common disorder affecting 5–7% of the population. Its primary characteristic is airway (bronchiolar) inflammation and hyperreactivity in response to a variety of stimuli. Clinically, asthma is manifested by episodic attacks of dyspnea, cough, and wheezing. Airway obstruction, which is generally reversible, is the result of bronchial smooth muscle constriction, edema, and increased secretions.
Some patients also develop bronchospasm following ingestion of aspirin, nonsteroidal antiinflammatory agents, sulfiting agents, or tartrazine and other dyes. Exercise, emotional excitement, and viral infections also precipitate bronchospasm in many patients. Asthma is classified as acute or chronic. Chronic asthma is further classified as intermittent (mild) and mild, moderate, and severe persistent disease.
The pathophysiology of asthma involves the local release of various chemical mediators in the airway and, possibly, overactivity of the parasympathetic nervous system.
In classic allergic asthma, antigen binding to immunoglobulin E (IgE) on the surface of mast cells causes degranulation. Bronchoconstriction is the result of the subsequent release of histamine; bradykinin; leukotrienes C, D, and E; platelet-activating factor; prostaglandins (PG) PGE2, PGF2
Vagal afferents in the bronchi are sensitive to histamine and multiple noxious stimuli, including cold air, inhaled irritants, and instrumentation (eg, tracheal intubation). Reflex vagal activation results in bronchoconstriction, which is mediated by an increase in intracellular cyclic guanosine monophosphate (cGMP).
During an asthma attack, bronchoconstriction, mucosal edema, and secretions increase resistance to gas flow at all levels of the lower airways.
expiratory flow rates are initially decreased throughout an FVC procedure, but during resolution of the attack the expiratory flow rate is reduced only at low lung volumes. TLC, residual volume (RV), and FRC are all increased. In acutely ill patients, RV and FRC are often increased by more than 400% and 100%, respectively. The number of alveolar units with low ratios increases, resulting in hypoxemia. A normal or high PaCO2 indicates that the patient can no longer maintain the work of breathing and is often a sign of impending respiratory failure. A pulsus paradoxus and electrocardiographic signs of right ventricular strain (ST-segment changes, right-axis deviation, and right bundle branch block) are also indicative of severe airway obstruction.
Drugs used to treat asthma include
Sympathomimetic agents (Table 23–2) are the most useful and the most commonly used. They produce bronchodilation via
Methylxanthines traditionally are thought to produce bronchodilation by inhibiting phosphodiesterase, the enzyme responsible for the breakdown of cAMP. Their pulmonary effects appear much more complex and include catecholamine release, blockade of histamine release, and diaphragmatic stimulation.
Glucocorticoids are used for both acute treatment and maintenance therapy of patients with asthma because of their antiinflammatory and membrane-stabilizing effects.
Anticholinergic agents produce bronchodilation through their antimuscarinic action and may block reflex bronchoconstriction.
The emphasis in evaluating patients with asthma should be on determining the recent course of the disease
The clinical history is of critical importance. No or minimal dyspnea, wheezing, or cough is optimal. Complete resolution of recent exacerbations should be confirmed by chest auscultation. Patients with frequent or chronic bronchospasm should be placed on an optimal bronchodilating regimen, including
PFT sshould be used to confirm clinical impressions. FEV1, FEV1/FVC, and peak expiratory flow rate .
Asthmatic patients with active bronchospasm presenting for emergency surgery should be treated aggressively whenever possible. Supplemental oxygen, aerosolized
Some degree of preoperative sedation is desirable in asthmatic patients presenting for elective surgery—particularly in patients whose disease has an emotional component. In general, benzodiazepines are the most satisfactory agents for premedication.
The use of an H2-blocking agent (such as cimetidine, ranitidine, or famotidine) is theoretically detrimental, since H2-receptor activation normally produces bronchodilation; in the event of histamine release, unopposed H1 activation with H2 blockade may accentuate bronchoconstriction.
Bronchodilators should be continued up to the time of surgery.
Patients who have been receiving long-term glucocorticoid therapy should be given supplemental doses to compensate for adrenal suppression. Hydrocortisone (50–100 mg preoperatively and 100 mg every 8 h for 1–3 postoperative days, depending on the degree of surgical stress) is most commonly used.
The most critical time for asthmatic patients undergoing anesthesia is during instrumentation of the airway. General anesthesia by mask or regional anesthesia will circumvent this problem, but some clinicians believe that high spinal or epidural anesthesia may aggravate bronchoconstriction by blocking sympathetic tone to the lower airways (T1–T4) and allowing unopposed parasympathetic activity.
Thiopental is most commonly used for adults but occasionally can induce bronchospasm as a result of exaggerated histamine release.
Propofol and etomidate are suitable alternatives and, in fact, are preferred by some clinicians.
Ketamine, the only intravenous agent with bronchodilating properties, is a good choice for patients who are also hemodynamically unstable. Ketamine should probably not be used in patients with high theophylline levels, as the combined actions of the two drugs can precipitate seizure activity.
Reflex bronchospasm can be blunted before intubation by an additional dose of thiopental (1–2 mg/kg), ventilating the patient with a 2–3 minimum alveolar concentration (MAC) of a volatile agent for 5 min, or administering intravenous or intratracheal lidocaine (1–2 mg/kg). Note that intratracheal lidocaine itself can initiate bronchospasm if an inadequate induction dose of thiopental is used. A large dose of an anticholinergic (atropine, 2 mg, or glycopyrrolate, 1 mg) can also block reflex bronchospasm but causes excessive tachycardia.
Volatile anesthetics are most often used for maintenance of anesthesia to take advantage of their potent bronchodilating properties.
Ventilation should be controlled with warmed humidified gases whenever possible. minimizing the tidal volume ( 10 mL/kg) with prolongation of the expiratory time may allow more uniform distribution of gas flow to both lungs and may help avoid air trapping.
Intraoperative bronchospasm is usually manifested as wheezing, increasing peak inflation pressures (plateau pressure should remain unchanged), decreasing exhaled tidal volumes, or a slowly rising waveform on the capnograph. It should be treated by increasing the concentration of the volatile agent. If the bronchospasm does not resolve after deepening the anesthetic, less common causes should be considered before administering more specific drugs. Obstruction of the tracheal tube from kinking, secretions, or an overinflated balloon; bronchial intubation; active expiratory efforts (straining); pulmonary edema or embolism; and pneumothorax can all simulate bronchospasm
Bronchospasm should be treated with a
At the completion of surgery, the patient should ideally be free of wheezing. Reversal of nondepolarizing neuromuscular blocking agents with anticholinesterase agents does not precipitate bronchoconstriction if preceded by the appropriate dose of an anticholinergic .
Deep extubation (before airway reflexes return) prevents bronchospasm on emergence. Lidocaine as a bolus (1.5–2 mg/kg) or a continuous infusion (1–2 mg/min) may help obtund airway reflexes during emergence.
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