Although we know that the onset of inflammation arises with activation of a multitude of cells and various mediators and is the underlying state responsible for asthma, we do not completely understand what sets off these inciting agents. Nevertheless, inflammation results in constriction of the small muscles of the airways due to hyperresponsiveness of the airways and swelling of the cells of the airway walls associated with increased mucus secretion in the airways.
This situation results in narrowing of the airways and hyperinflation of the lungs. The clinical manifestations of this narrowing are wheezing, coughing and/or dyspnea which are the hallmarks of asthma. Other findings include tightness of the chest, enlarged hyperinflated lungs with flat diaphragms, intercostal muscle retractions and use of accessory muscles of respiration.
The fundamental explanation for these findings can be presented based on the changes in the airway size and content. In a normal patient, the airway resistance (Ra) due to the movement of gas (air) through the airways of the lungs is characterized by
turbulent (disorganized, chaotic, and forming eddies) flow in the upper (larger major bronchi) airways
and laminar (orderly or streamlined) flow through the middle (mid-sized – segmental and subsegmental bronchi to the smaller bronchioles) and lower (smaller) airways.
Mathematically, airway resistance (Ra) is directly proportional to the driving pressure (P1 – P2) and inversely proportional to the flow rate (V with a dot over it) or
where P1 is the pressure exerted at the alveolus on expiration and P2 which is the pressure at the mouth or airway opening on expiration.
With the onset of asthma the Ra rises due to narrowing of the airways. In the above equation the driving pressure (P1 – P2) needs to be increased to maintain flow (V with a dot over it). Therefore, Ra must increase.
In asthma pathophysiology, in order to have an objective measurement of these changes as well as to properly classify asthma severity, the patient needs to have spirometry with measurement of the peak expiratory flow rate (PEFR), the FEV-1, and/or the FEV-1/FVC because a patient’s perception of airway narrowing or obstruction is highly variable and spirometry sometimes reveals obstruction much more severe than would have been estimated from the history and physical examination.