Exercise induced asthma

Occurs when the airways narrow as a result of exercise.

Also known as exercise-induced bronchoconstriction.

Exercise does not cause asthma, but is frequently an asthma trigger.

Patients present with shortness of breath, tachypnea, wheezing, decreased stamina, difficulty in recovering from exertion, paroxysmal coughing from an irritable airway.

Clinical findings include wheezing and prolonged expiratory phase, but may be normal.

Measurement of airflow, such as peak expiratory flow rates, may prove helpful in diagnosis.

The underlying pathogenesis for exercise induced asthma is poorly understood, but usually occurs after several minutes of vigorous activity.

With vigorous exercise the normal nasal breathing requires supplementation by mouth breathing, resulting inhalation of air that has not been warmed and humidified by the nasal passages.

Such mouth inhalation increases blood flow to the linings of the bronchial tree, causing edema and constriction of small airways then follows, obstructing airflow.

Smooth muscle that lines the airways become progressively more sensitive to changes that occur as a result of injury to the airways from dehydration.

Mediators that provoke the muscle spasm arise from mast cells.

Differential diagnosis includes: vocal cord dysfunction, cardiac arrhythmias, cardiomyopathies, and gastroesophageal reflux disease.

Spirometry at rest in exercise-induced bronchoconstriction is within normal limits.

Treadmill or ergometer-based testing in lung function are effective methods for diagnosing exercise-induced bronchoconstriction.

False negative results may result if the exercise stimulus is not intense enough.

Eucapnic voluntary hyperventilation challenge is recommended as the test to document exercise-induced asthma in Olympic athletes.

Pharmacological challenge tests, including the methacholine challenge test, have a lower sensitivity for detection of exercise-induced bronchoconstriction and exercise-induced asthma.

Pref2242ed management is avoidance of conditions predisposing to attacks.

Treatment include: a beta agonist taken about 20 minutes before exercise, inhaled anti-inflammatory mists such as corticosteroids or leukotriene antagonists, and mast cell stabilizers.

Comparing oral montelukast with inhaled salmeterol, both given two hours before exercise have similar benefit but montelukast lasts 24 hours.

Vitamin C decreases post-exercise decline in FEV1 by 48%.

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