Bronchial asthma due to physical stress is a variant of bronchial asthma, characterized by the obligatory development of asthma attacks 1-10 minutes after exercise. Asthma due to physical stress is especially often observed in children.
The type of physical activity matters. Most often, asthma attacks occur when running, playing soccer, basketball, mountain climbing, less often – with intermittent loads (weight lifting); swimming is well tolerated. The formation of an attack is more affected by the duration of the load than its intensity.
In connection with the rapid and complete reverse development of asthma attacks due to physical stress, it is believed that bronchial obstruction is caused by bronchospasm without the presence of inflammation, swelling, and mucus secretion. Bronchospasm is not associated with immunological mechanisms. In the pathogenesis of asthma attacks due to physical stress, various regulatory disorders are expected to be involved: a relative decrease in the functions of adrenergic B receptors due to the hyperreactivity of adrenergic a receptors in combination with the peculiarities of the release of catecholamines during exercise. The participation of adrenergic mechanisms is confirmed by the effectiveness of adrenergic drugs (3-stimulating in the prevention and relief of bronchospasm induced by physical stress, as well as by provoking bronchospasm with a-adrenoreceptor stimulants and the preventive effect of a-blocking adrenergic drugs in people who are sensitive to stress; isolation of mediators of immediate allergy, which is proved by the following facts: the presence of a refractory period after an attack (depletion of copper reserves is assumed tori under load); Protective effect Intalum and calcium antagonists preventing mast cell degranulation, and antihistamines; sensitization cells of patients to degranulation and release of mediators; hyperstimulation irritant vagal receptors due to rapid cooling of the upper respiratory tract and hyperventilation during the loading process Participation. of these mechanisms is confirmed by: a pronounced correlation between the sensitivity of the bronchi to vagotonic agents and to physical. stress; the preventive effect of atropine and lidocaine (pharyngeal ring anesthesia); increased sensitivity of the bronchi to anticholinergics in some patients; heat loss during breathing. It is assumed non-immunological stimulation of the release of mediators due to mechanical irritation (body shake during exercise), direct action of physical. factors, in particular cooling, on the peripheral respiratory tract, the effect of catecholamines and acetylcholine. In the genesis of bronchospasm on physical. metabolic acidosis and impaired fatty acid utilization also matter . The central and peripheral airways are involved in the pathological reaction to the load, however, obstruction of the large bronchi most often dominates.
Attacks of suffocation induced by physical. load, mainly observed in atopic asthma and are not observed in chronic bronchitis. They occur 1-2 minutes after the load is stopped and in mild cases they stop spontaneously after
5-10 minutes (increase in individuals within 30-60 minutes), in severe cases, the attack begins during the load and lasts more than 1 hour (without treatment ); bronchospasm progresses with alternating different loads with an interval of less than 1 hour. The initial condition of the patient is not critical: in sensitive individuals, an attack may appear during complete remission, while in resistant individuals it does not develop even with initial bronchial obstruction. The initial level of obstruction affects the severity of bronchospasm, which can be short-term and asymptomatic (subclinical form of bronchial asthma due to physical stress) in 25% of cases, especially in children, moderate bronchospasm is observed in 25-30% of patients, and severe bronchospasm in 15-25%.
Reaction to physical. the load is established using clinical observation and pulmonary function tests, studied before and after the standard load –
6-8 minutes of running on the treadmill (p-stimulating adrenergic drugs are canceled in 3-4 hours, intal is removed in 8-12). A decrease in FVC1 by more than 15% of the initial level indicates the development of bronchospasm. In the first 24 minutes, FVC increases, then decreases, reaching 40-50% of the initial value in individuals. In mild cases, two-, three-fold testing is necessary before a reaction is detected. Diagnostic value is the constant nature of the reaction – the mandatory occurrence of bronchospasm on the physical. voltage. Load tests are not performed for concomitant heart diseases.
Attacks of suffocation due to physical. loads can prevent aerosols of adrenergic drugs that stimulate p2-adrenergic receptors, intala, methylxanthines (the latter are prescribed 30 minutes before the load, intal – immediately before or at the same time as the load).
Glucocorticosteroid drugs are relatively ineffective. In certain cases, certain sports are allowed (swimming). Before sports, it is recommended
to prophylactically take theophylline and intal, the appointment of p-stimulating adrenergic drugs is prohibited. Recently, reports appeared about the effectiveness of calcium antagonists (nifedipine, 20 mg sublingually) and a-adrenergic receptors (prazosin, 2 mg, inhalation).