Inflammation contributes to heightened airway activity
Multiple mechanisms contribute to airway inflammation involving a number of different pathways
Asthma is unlikely to be caused by either a single cell or single inflammatory mediator, rather it appears that asthma results in complex interactions between inflammatory cells, mediators, and the cells and tissues present in the airway
Recognition of the importance of inflammation has made the used of anti-inflammatory agent such as steroids, a key component of asthma therapy
Bronchospasm and obstruction are also important components of asthma
Mechanisms responsible for the obstructed symptoms include respiratory response stimuli, airway edema and accumulation of secretions of mucous
Spasm of the bronchi and bronchioles, and airway remodeling which causes permanent cellular changes
Airflow is determined by the size of the airway lumen, degree of the bronchial wall edema, mucous production, smooth muscle contraction and muscle hypertrophy
Bronchial constriction is a normal reaction to the foreign stimuli but in childhood asthma it is abnormally severe producing impaired respiratory function
The smooth muscles arranged the spinal bundle around the airway causing narrowing and shortening of the airway which significantly increases airway resistance to airflow
The respiratory difficulty is more pronounced due to expiratory phase of respiration
Increase resistance in the airway causes forced expiration through the narrowed lumen, the volume of air trapped in the lungs increases as airways are functionally closed at the point between the alveoli and the lobar bronchi
The trapping of gas forces the individual to breath at higher and higher volumes, causing fatigue, decreased respiratory effectiveness, and increased oxygen consumption
The inspiration occurring at higher lung volumes hyperinflates the alveoli and reduces the effectiveness of the cough
As the severity of the obstruction increases, there is reduced alveoli ventilation with carbon dioxide retention, hypoxemia respiratory acidosis and eventually respiratory failure