Basic Science
Wheezing may result from localized or diffuse airway narrowing or obstruction from the level of the larynx to the small bronchi. The airway narrowing may be caused by bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor, foreign body, or tenacious secretions. Wheezes are believed to be generated by oscillations or vibrations of nearly closed airway walls. Air passing through a narrowed portion of an airway at high velocity produces decreased gas pressure and flow in the constricted region (according to Bernoulli’s principle). The internal airway pressure ultimately begins to increase and barely reopens the airway lumen. The alternation of the airway(s) between nearly closed and nearly open produces a “fluttering” of the airway walls and a musical, “continuous” sound. The flow rate and mechanical properties of the adjacent tissues that are set into oscillation determine the intensity, pitch, composition (monophonic or polyphonic notes), duration (long or short), and timing (inspiratory or expiratory, early or late) of this dynamic symptom and sign. Wheezes are heard more commonly during expiration because the airways normally narrow during this phase of respiration. Wheezing during expiration alone is generally indicative of milder obstruction than if present during both inspiration and expiration, which suggests more severe airway narrowing. However, most asthmatic patients are unable accurately to correlate their wheezing (or other respiratory symptoms) to the severity of airway obstruction as measured objectively by pulmonary function tests.
In contrast, the absence of wheezing in an asthmatic may indicate either improvement of the bronchoconstriction or severe, widespread airflow obstruction. The latter suggests that the airflow rates are too low to generate wheezes or the viscous mucus is obstructing large regions of the peripheral airways. Increasing exhaustion and a “silent chest” are ominous signs of respiratory muscle fatigue and failure, leading to status asthmaticus.
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In asthma, the markedly increased airway resistance (airflow obstruction) contributes to the characteristic physiologic and clinical changes observed during active or symptomatic periods. The airway obstruction is diffuse and nonuniform in distribution, resulting in ventilation-perfusion inequalities and hypoxemia. Airways tend to close early during expiration, and hyperinflation results. Although breathing at high lung volumes tends to maintain open airways, this response demands increased muscular work of breathing to provide adequate ventilation, which is increased secondary to stimulation of airway receptors and hypoxia. Most asthmatics complain of greater difficulty during inspiration than expiration, due to the uncomfortable work of breathing necessary to ventilate hyperinflated, abnormally stiff, or noncompliant lungs.
Several hypotheses have been proposed to explain the pathogenesis of bronchoconstriction and other airway abnormalities in asthma. None completely accounts for all the clinical forms of asthma. The proposed mechanisms probably overlap and interrelate even in the same individual.
The immediate, type I immunologic reaction occurs primarily in “allergic” asthma and involves biochemical reactions between an antigen and a specific antibody (immunoglobulin E, IgE) bound to sensitized airway mast cells and basophils. This immunologic reaction results in the release of potent biochemical mediators that contract bronchial smooth muscle, increase vascular permeability and mucus secretion, and attract inflammatory cells.
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Preformed histamine, neutrophil and eosinophil chemotactic factors, and platelet-activating factors are released. In addition, membrane-associated oxidative metabolism of arachidonic acid generates prostaglandins (PGF2α and PGD2) and leukotrienes (LTC4, D4, E4), which are potent bronchoconstrictors. Type III (arthus) immunologic reactions have also been implicated in some cases of asthma and in the related allergic bronchopulmonary aspergillosis.
A neurogenic or reflex mechanism is observed in “nonallergic” asthma provoked by nonspecific stimuli (e.g., exercise, infection, air pollution) that apparently do not initiate type I immunologic responses. This nonimmunologic hypothesis stresses the importance of the parasympathetic nervous system (vagus nerve) in regulating airway caliber. Chemical or mechanical inflammation stimulates cholinergic irritant receptors in the airway mucosa to hyperreact, leading to vagally mediated reflex bronchoconstriction. This reflex is produced by either direct mediator release or secondary stimulation of irritant receptors by smooth muscle constriction.
A partial beta-adrenergic blockade or deficiency has also been proposed to explain some types of “nonallergic” asthma (e.g., propranolol-induced asthma) because bronchial smooth muscle tone appears to be modulated by beta-adrenergic receptors and alterations in the metabolism of intracellular cyclic nucleotides. Beta-adrenergic stimulation increases cyclic 3,5-adenosine monophosphate (AMP) and decreases cyclic 3,5-guanosine monophosphate (GMP), resulting in smooth muscle relaxation (bronchodilation). Beta-adrenergic inhibition produces opposite effects, resulting in bronchoconstriction. Therefore, asthmatics may have relative beta-adrenergic hyporesponsiveness and an imbalance between adrenergic and cholinergic regulation that favor the latter, resulting in greater than normal mediator generation and unopposed bronchoconstriction.
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