Initial attack causes infiltration of eosinophils and neutrophils which release EVEN MORE inflammatory mediators (cytokines, histamines, leukotrienes, Prostaglandins); occurs in 50% of asthma pts.
-Parasympathetic NS (autonomic) increased release of acetylcholine (due to allergens) causing increased smooth muscle contraction and mucous secretions leading to bronconstriction.
-chronic inflammation may lbead to structual bronchial wall changes (remodeling), smooth muscle hypertrophy, and angiogenesis (new blood vessels)
-decreased perfusion and ventillation and increased alveolar gas pressure
-> hypoxemic early on with decreased pa CO2 iand increaed pH (respiratory alkalosis) causing lungs to work harder so that CO2 normalizes when patient tires AND THEN INCREASESTO PRODUCE RESPIRATORY ACIDOSIS (MEANING RESP FAILURE)
Self-sustaining cycle of inflammation
Corticosteroids required to treat this phase THIS IS WHEN YOU NEED IT to stop inflammation process.
- =>Chronic inflammation that isn't controlled, can lead toStructural changes known as remodeling (scar tissues, less compliance-doesn't expand as much as the lungs should)
- -Pulmonary fibrosis: scar tissues in the lungs, and lungs don't expan, not a lot they can do about it.
Progressive limitation of airflow obstruction mimics COPD