Search databaseBooksAll DatabasesAssemblyBiocollectionsBioProjectBioSampleBioSystemsBooksClinVarConserved DomainsdbGaPdbVarGeneGenomeGEO DataSetsGEO ProfilesGTRHomoloGeneIdentical Protein Web CatalogNucleotideOMIMPMCPopSetProteinProtein ClustersProtein Family ModelsPubChem BioAssayPubChem CompoundPubChem SubstancePubMedSNPSRAStructureTaxonomyToolKitToolKitAllToolKitBookgh Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

You are watching: Bronchial airway obstruction marked by paroxysmal dyspnea, wheezing, and cough

Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990.



A wheeze is a high-pitched, musical, adventitious lung sound produced by airflow through an abnormally narrowed or compressed airway(s). A wheeze is synonymous with a high-pitched or sibilant rhonchus.

Asthma is a heterogeneous syndrome characterized by variable, reversible airway obstruction and abnormally increased responsiveness (hyperreactivity) of the airways to various stimuli. The syndrome is characterized by wheezing, chest tightness, dyspnea, and/or cough, and results from widespread contraction of tracheobronchial smooth muscle (bronchoconstriction), hypersecretion of mucus, and mucosal edema, all of which narrow the caliber of the airways. The resulting airflow obstruction may be chronic or episodic, with respiratory symptoms resolving either spontaneously or as a result of therapy (bronchodilators or corticosteroids). A generally accepted definition of asthma does not yet exist because the syndrome has different causes, mechanisms, clinical features, and responses to therapy.


Wheezing is a subjective complaint that may be described in various ways. Some patients report noisy, difficult breathing (wheezy dyspnea), whereas others describe a whistling type of breathing or rattling secretions in the throat. The majority of asthmatic patients who report active wheezing generally have this finding documented by the examining physician. Nevertheless, wheezing is not always present during active asthma, and its absence should not exclude the diagnosis. Some patients with chronic asthma may become accustomed to wheezing and do not volunteer this information unless specifically asked. Most patients with asthma complain more frequently about chest tightness (in combination with shortness of breath or cough) than wheezing. Thus, any patient with chronic or episodic respiratory symptoms or who presents with a history of asthma or other chronic airway disease should be asked about wheezing.

The diagnosis of asthma is usually obvious from the patient"s history. It should be highly suspected from a description of episodic and variable respiratory symptoms (with or without wheezing) or recurrent chest colds and bronchitis (productive cough). A careful, thorough history is fundamental not only in arriving at an accurate diagnosis but also in determining the severity of an individual"s asthma and its appropriate therapy. The clinician should inquire about the following:

General (relating to the overall course of asthma in an individual):

Age of onset of asthma
Continuous or intermittent, with or without medications
Environmental survey (e.g., allergens, occupational or home exposures, smoking, air pollution)
Medications, past and present, for asthma, noting the name or type of drugs, dosages, frequency, side effects, and compliance
Related disability (e.g., time lost from work, school, or recreation)
Frequency of visits to a physician or emergency room for asthma
Frequency of hospitalizations, including any intubation and mechanical ventilation
Associated medical conditions, (e.g., nasal polyps, sinusitis, allergies, gastroesophageal reflux, infection, psychological stress, and disorders that may simulate asthma)
Personal and family history of asthma, atopy (allergic rhinitis, hay fever, eczema), positive skin tests for allergens, immunotherapy


Table 37.1

Contributing or Precipitating Factors in Asthma.

Specific (relating to acute episode in an individual):

Frequency, duration, intensity of attacks
Time of onset (e.g., morning or night, following exposure to a medication, food, or other substances)

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.

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.

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.

See more: Can You Tell Me Where I Am Mar, Somebody, Please Tell Me Who I Am

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.