Pathophysiology Description

Normal Physiology

• Main function of the lungs = supply adequate oxygen to the blood and remove carbon dioxide from the blood
  • Air enters the body through the nose and mouth and travels done the trachea, into the smaller airways (bronchi and bronchioles), reaching the alveoli, balloon-like sacs at the end of the bronchioles.
  • The alveoli are surrounded by thin capillaries that allow for the exchange of gases between the pulmonary system and the blood.
  • Upon inhalation, the lungs fill with oxygen-enriched air providing oxygenation for the blood. Upon exhalation, carbon dioxide is removed from the lungs which has been removed from the blood through alveolar-capillary exchange.
• Adequate gas exchange occurs in the lungs when air passages are unobstructed and the Ventilation / Perfusion Ratio (V/Q) is 0.8:
  • 4 liters of air enter the respiratory tract while 5 liters of blood diffuse through the capillaries every minute (McCance & Huether, 2019)

[Mads, Lause & Mogensen, Mads. (2019)]

Childhood Asthma is a disorder caused by chronic inflammation of the bronchial mucosa.  It is the most prevalent chronic pediatric disease, and ½ of the total asthma cases are developed and diagnosed during childhood.  Asthma is caused by a complex interaction between environment and genetic susceptibility and presents more severely in younger children due to smaller airway diameters (McCance & Huether, 2019).

Pathophysiology

• Episodic attacks caused by an IgE mediated Type I hypersensitivity immune over-response that results in reversible bronchial hyperresponsiveness, bronchoconstriction, mucosal edema, increased mucous production and airway obstruction that leads to ventilation-perfusion (V/Q) mismatch, hypoxemia and expiratory airway obstruction.
• Early Asthmatic Response – acute bronchoconstriction that peaks at 30 minutes and lasts from 1-3 hours
  • Bronchial mucosa comes in contact with an antigen which activates dendritic cells in lung tissue and alveoli that present the antigen to T helper cells (CD4+ T cells) and release various inflammatory cytokines
    • IL-4 activates eosinophils and B lymphocytes
    • IL-5 causes activation and proliferation of eosinophils what can result in direct tissue injury, bronchial hyperresponsiveness, epithelial damage and formation of scarring of the airway
    • IL-8 activates neutrophils that invoke a hyper reactive immune response
    • IL-9 promotes mast cell proliferation
    • IL-13 results in decreased mucociliary function and causes bronchoconstriction and airway remodeling
    • IL-25 Increases occurrence of airway remodeling
  • Inflammatory mediators activate inflammatory cells and cause vasodilation, edema, bronchospasms, mucous secretion and increased capillary permeability (McCance & Huether, 2019)
• Late Asthmatic Response – begins 4-8 hours after early response and is characterized by airway hyperresponsiveness
  • Recruitment of lymphocytes, eosinophils, basophils and neutrophils through chemotaxis causes a release of inflammatory mediators resulting in bronchospasms, excess mucous secretion and edema
  • Prolonged smooth muscle contraction leads to scar tissue and collagen matrix formation which can lead to airway scarring
  • Accumulation of mucous and debris caused by impaired mucociliary function form plugs in the airways that result in airway remodeling
  • Mucous plugs cause air trapping and hyperinflation distal to the obstruction that can result in hypoxemia and increased work of breathing (McCance & Huether, 2019)

[ Simple Bio, 2019]

• Asymptomatic between episodes
• Nonproductive cough
• Dyspnea
• Tachycardia
• Tachypnea
• Prolonged expiration
• Wheezing upon expiration

Diagnostic Tools / Tests

• Rule out other disorders / diseases that present similarly to asthma
• Lung function test (spirometry)
• Exhaled nitric oxide test
• Thorough medical history including family member history
• Allergy testing (Asthma Diagnosis, 2019)

[Pulmonary Function Testing, 2019]