ABSTRACT

The most distinctive functional abnormality in asthma is increased airway resistance (Raw), especially in those airways located peripherically (‹ 2 mm diameter). Smooth muscle contraction, mucous hypersecretion and swelling of the airway wall due to inflammation and/or remodeling are major factors originating airway lumen diminution. However, two other factors also favoring airway closure in asthma are surfactant alterations produced by the inflammatory process and decrement of transpulmonary pressure (PL), also known as elastic recoil pressure. In normal conditions, at the end of a passive expiration there is equilibrium between the lung tendency to collapse and of the chest wall tendency to expansion. During an asthma exacerbation lungs loss elasticity, the already decreased PL is accentuated, making that equilibrium between lungs and chest wall is achieved at higher volumes (increment of functional residual capacity [FRC]), which implies that the patient breaths maybe the same tidal volume but with more inflated lungs. During a forceful expiration the premature airway closure originates air trapping (increased residual volume). If asthma exacerbation is severe enough, abnormal regional ventilation might be in disequilibrium with respect to blood perfusion and cause hypoxemia, and the enhanced respiratory work load might lead to respiratory muscle fatigue, hypoventilation and hypercapnia.

KEYWORDS

Asthma exacerbation, physiopathology, lung function, transpulmonary pressure, airway resistance, tidal volume, residual volume.

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