Oxygenation

Pure Nursing and Its Dedication

  • Pure calling, dedication, excellence, compassion in nursing

  • Focus on infectious processes and alterations in oxygenation

  • Course: NSG 3280 Pathophysiology I

Alterations in Oxygenation: Asthma

Overview

  • Asthma defined as an obstructive lung disease characterized by:
      - Airway obstruction
      - Inflammation of the airway
      - Increased reactivity of the airway to various stimuli

  • Reference: Banasik, 2022

Etiology of Asthma

  • Most cases triggered by:
      - Allergens ——→ pollen, dust, smoke, strong fragrances, pet dander
      - Physical stimuli (exercise, cold air exposure)

  • Airway obstruction is generally reversible

  • Types of asthma:
      - Extrinsic (Allergic) Asthma: related to allergens (external), common in children

  • associated with the release of IgE ——→ attaches to allergen ——→ IgE w/ allergen attaches to mast cells ——→ histamine & leukotrienes release ——→ massive inflammation ——→ bronchoconstriction
      - Intrinsic (Nonallergic) Asthma: non-allergic type (can be cause by a respiratory infection)
        - Lacks a history of allergies
        - Typically develops in middle age
        - Less favorable prognosis with common severe attacks
        - Symptoms: extreme dyspnea, orthopnea, agitation
        - Treatments less effective

Pathogenesis of Asthma

  • Inflammatory process characterized by:
      - Release of inflammatory chemicals ——→ ex. histamines (can be reversed with antihistamines)
        - Leading to:
          - Epithelial denudation
          - Collagen deposition under the basement membrane
          - Mast cell activation
          - Mucosal edema
          - Increased viscid secretions
          - Smooth muscle contraction

Pathophysiologic Basis of Asthma and Drug Management

Role of the Nervous System

  • Parasympathetic stimulation via acetylcholine can trigger an asthma response

  • Various stimuli (antigenic vs. non-antigenic) can lead to mast cell degranulation

  • Blocked by mast cell stabilizers (corticosteroids, cromolyn, nedocromil)

Key Chemical Mediators

  • Histamine, leukotrienes, prostaglandins play critical roles in asthma pathology:
      - Blocked by:
        - Corticosteroids
        - Leukotriene inhibitors (e.g., zafirlukast)
        - Histamine receptor blockers (e.g., diphenhydramine)

  • Effects on target tissues include contraction of bronchial smooth muscle and mucus secretion, which can be inhibited by:
      - B2 agonists
      - Theophylline
      - Muscarinic antagonists

Allergic Asthma

Mechanism

  • Exposure to antigens leads to:
      - Initial response involving histamine release, leukotrienes, bradykinins, and eosinophilic chemotactic factors serotonin
      - Secondary response after 6-12 hours
        - Involves neutrophil chemotactic factors

Physical Results

  • Effects include:
      - Mucosal edema
      - Inflammatory exudate (mucous)
      - Hyperresponsiveness and increased microvascular permeability

  • Basal membrane——→ tensile strength and support, filter, histologic changes =permanent damage, thickening, epithelium replaced by goblet cells, metaplasia, Potential progression to chronic obstructive pulmonary disease (COPD)

  • Vagal Stimulation Possible ——→edema, mucous hypersecretion, bronchoconstriction

Diagnosis of Allergic Asthma

  • Various tests include:
      - Positive skin tests
      - Challenge tests
      - Clinical findings/ Progressive worsening

  • Asthma Diagnosis ——→ hx & physical findings, sputum, PEFR, pulmonary function tests, + reactions on skin testing

Clinical Manifestations of Asthma

  • Common symptoms:
      - Diffuse wheezing (expiration) ——→ due to narrowing of the bronchioles
      - Dyspnea
      - Chest tightness
      - Cough due to bronchospasms & increased mucous production

  • low O2, higher RR and HR

Special Types of Asthma

Exercise-Induced Asthma

Pathophysiology

  • Bronchospasm occurs shortly after exercise and resolves within 60 minutes

  • Mechanism involves osmolarity increase from heat and water loss leading to mediator release of basophils and tissue mast cells leading to smooth muscle contraction

  • common in children and adults

Clinical Manifestations

  • Difficulty breathing during or after physical exertion

  • Cough due to bronchial spasms

Occupational Asthma

Pathophysiology

  • Triggered by workplace exposure to allergens (fumes, formaldehyde, etc.)

  • Little or no IgE response

Diagnosis

  • Positive skin test reactions to allergens in work environment

  • History of worsening symptoms with continued exposure

Drug and Chemical-Induced Asthma

Etiology

  • Genetic predisposition (chromosomes 5/11/14) and exposure to food additives (tartrazine, MSG) and medications such as aspirin & NSAIDs (e.g., ibuprofen) can trigger asthma

  • Aspirin & NSAIDs =

Status Asthmaticus

Pathophysiology

  • A severe asthma attack not relieved by inhaled medications

  • Symptoms include——→ cough, wheezing, and signs of respiratory distress, hyperinflated chest, decreased breath sounds

  • Sputum examination ——→Charcot Leyden crystals, eosinophils, churchman spirals

Diagnosis

  • Key diagnostic indicators:
      - Blood gas analysis shows respiratory alkalosis (due to fast breathing), hypoxemia, elevated PaCO2
      - Chest radiography may show hyperinflation or pneumothorax

  • Labs ——→ CBC w/ Increased eosinophils

Clinical Manifestations

  • Symptoms include dyspnea, retractions, nasal flaring, loss of consciousness, or respiratory arrest, restlessness, agitation, confusion

Occupational Lung Diseases

Etiology

  • Caused by inhalation of toxic gases or particles (pneumoconiosis)
      - Examples include: asbestos, dust, cigarette smoke

Pathogenesis

  • Mucociliary mechanisms impaired by atmospheric pollutants (sulfur oxides, nitrogen oxides, & tobacco smoke) leading to loss of clearance and damage to alveolar walls resulting in restrictive lung disease

  • Ex. asbestos, dust, smoke (cigarette, factory, soot)

Diagnosis

  • Chest radiographs may show micronodular mottling, haziness, calcifications, and fibrosis (may or may not show these)

  • Pulmonary function tests (PFTs) indicate hypoxemia and hypercapnia ——→ decrease O2 in blood and increase CO2

Clinical Manifestations

  • Symptoms may initially be asymptomatic or minimal

  • Late symptoms include worsening dyspnea, productive cough, clubbing, and weakness/fatigue ——→ normally triggered by the pt being active

  • Education ——→ protective measures (mask), don’t smoke, know the symptoms to report/look for

  • Read pg 488

References

  • Banasik, J. L. (2022). Pathophysiology (7th ed.). Elsevier.