Intraoperative wheezing: Etiology and treatment

Published on 07/02/2015 by admin

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Last modified 07/02/2015

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Intraoperative wheezing: Etiology and treatment

Mary M. Rajala, MS, MD

Wheezing or rhonchi, lung sounds detected by auscultation, are produced when gas flows through a narrowed or obstructed upper or lower airway. The lung sounds are caused by turbulence or resistance to flow. The obstruction can be extrinsic to the airway, intrinsic (within the airway wall), or within the lumen (Box 154-1). For a patient who is intubated and ventilated, an increase in peak airway pressure, a decrease in tidal volume, or a decrease in the slope of the expiratory CO2 curve may indicate airway narrowing or increased airway resistance. Persistent and severe airway obstruction may be followed by O2 desaturation, hypercapnia, and hypotension secondary to increased intrathoracic pressure. Most (80%) of the resistance to flow in airways occurs in the large central airways, leaving 20% of airway resistance from the peripheral bronchioles. Thus, large changes in the caliber of small airways may result in small changes in resistance, making the small airways a clinically silent area. In the American Society of Anesthesiologists closed claims analysis, respiratory events that lead to death or permanent brain damage, 56 (11%) were associated with bronchospasm.

Reversible and irreversible airway disease

Wheezing may indicate the presence of obstructive lung disease—asthma, chronic obstructive pulmonary disease, chronic bronchitis, or cystic fibrosis. Asthma, a reactive airway disease, is manifest by reversible airway obstruction. Resting bronchial tone is regulated primarily by the parasympathetic nervous system via vagal nerve fibers and muscarinic acetylcholine receptors, of which 3 types exist, M1 and M3, which enhance the parasympathetic effects, and M2, which is inhibitory. Numerous factors—including exercise, cold air, allergens, respiratory infections, emotional factors, β-adrenergic blockade, and the use of a prostaglandin inhibitor, such as aspirin—may override the baseline bronchial tone, provoking an attack in patients with bronchospastic disease. Cross-sensitivity between aspirin and other nonsteroidal antiinflammatory drugs is common and needs to be considered as a cause for bronchospasm, especially in patients with the triad of asthma, nasal polyps, and aspirin-induced asthma. The immunologic component to asthma is well recognized and includes immunoglobulin-E antibody fixed to mast cells and basophils, which release immune mediators in response to challenge with specific antigens. In adults, irritant reflexes are a more important cause, whereas, in children, allergy is an important component in reactive airway disease. The immune mediators include serotonin, eicosanoids, prostaglandins (PGD2, PGF2), thromboxane A2 and leukotrienes (LTC4, LTD4, LTE4), kinin, and perhaps histamine (H1