Pathophysiology of Acute Asthma Exacerbation

Pathophysiology of Acute Asthma Exacerbation Essay Assignment Paper

sthma’s onset in acute situations is precipitated by exposure to an allergen or trigger (Hammer, and McPhee, 2014). The trigger then stimulates a type I immune reaction mediated by T helper two lymphocytes cells (Th2) (Huether, and McCance, 2017). Antigen exposure causes the Th2 cells release cytokines. Then activates mast cells, dendritic cells, plasma cells presenting IgE antigens, and eosinophils (Huether, and McCance, 2017). The activation of the immune response cells causes an inflamed, narrowed airway, impaired mucociliary function, and vascular congestion resulting in bronchospasm increased mucus production and other intermittent asthma symptoms (Huether, and McCance, 2017). In an acute asthma exacerbation compromised inhalation and exhalation cause an increased work of breathing because of air trapping, distal hyperinflation of alveoli, and decreased perfusion (Huether, and McCance, 2017). Furthermore, airway constriction and inflammation cause ventilation-perfusion changes leading to hypoxemia, decrease in tidal volumes, increasing carbon dioxide retention resulting in respiratory alkalosis and respiratory failure (Huether, and McCance, 2017).

Acute asthma exacerbations are intermittent and due to a trigger, such as allergens (dust, pollens), air irritants (air pollution, smoke), chemicals, exercise, and stress (American Lung Association, n.d.). Acute asthma is best controlled with the use of a short-acting beta agonists such as albuterol (Mayo Clinic, 2016).NURS 6501 WeeK 6 Asthma Assignment

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