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Alterations of Pulmonary Function part 1 notes

Review of Pulmonary Structures

  • Pulmonary Structures:

Restrictive Disorders

  • Definition: Decreased compliance of lung tissue.
  • Increased effort is required to expand the lungs during inspiration.
  • Decreased vital capacity and total lung capacity.
  • Increased lung stiffness.
  • Shallow, rapid breathing.
  • Alveolar hypoventilation.
  • The lung, pleural space, and chest cavity are involved.
  • Chest Wall Restriction - Causes:
    • Deformities - Kyphoscoliosis.
    • Trauma.
    • Obesity.
    • Immobilization.
    • Pain (surgical, medical conditions).
    • Neuromuscular alterations.
    • Flail Chest - severe trauma.
      • A portion of the rib cage is separated from the rest of the chest wall.
      • The injured area cannot contribute to lung expansion.

Pneumothorax

  • Spontaneous:
    • Primary.
    • Secondary - disease, atmospheric changes.
  • Open - communicating: Pressure in the pleural space = atmospheric pressure.
    • The usual negative intrapleural pressure is a stimulus for breathing.
    • The lung is unable to inflate.
  • Tension: Alveolar air enters the pleura but cannot escape the body.
    • Pneumothorax is serious and can be life-threatening due to a dramatic shift in circulation through the heart and great vessels, resulting in a significant decrease in cardiac output.

Pleural Effusion

  • Definition: Fluid in the pleural space.
    • Migration through pulmonary capillaries.
  • Types:
    • Transudative – watery.
    • Exudative – high concentrations of WBC and plasma proteins.
    • Empyema – pus.
    • Blood.
  • Clinical Manifestations
    • Lung expansion is inhibited by fluid mass.
    • Impaired ventilation leads to hypoxemia.

Pneumoconiosis

  • Definition: Inhalation of non-biodegradable substances (coal, silica, asbestos, talc, textiles, metals).
  • Chronic inflammation in lung tissues.
  • Scarring of the alveolar-capillary membrane.
  • Loss of alveolar surface area.
  • Formation of fibrotic nodules and tissue.
  • Decreased lung elasticity.
  • Effect: Progressive lung destruction.
  • Clinical Manifestations: Progressive worsening of dyspnea, CO_2 retention, and hypoxemia.

Obstructive Disorders

  • Definition: Narrowing of airways that is worse with expiration.
    • The work of breathing is increased to push air out of the lungs/alveoli.
    • Lung compliance increases, and lungs can be stretched with greater ease.
    • Increased use of accessory muscles for breathing.
    • Air is trapped in the lungs, resulting in hypoventilation and hypercapnia.
  • Disorders:
    • Asthma.
    • Chronic Bronchitis.
    • Emphysema.
  • Symptoms: Dyspnea.
  • Signs: Wheezing, abnormal pulmonary function test - Decreased forced expiratory volume in 1 second (FEV1).

Asthma

  • Characterized as a form of obstructive pulmonary disease.
  • Chronic inflammation within hyper-responsive bronchioles leads to airway obstruction that is worse during expiration.
  • Alveolar destruction occurs due to alveolar hyperventilation and air trapping.
  • Airflow limitation with asthma is considered reversible, while with other forms of obstruction pulmonary disease such as emphysema and chronic bronchitis, it is not reversible.
  • Etiology - Genes and Environment
    • Asthma is widely accepted to occur in families.
    • More than 120 genes have been identified that play a role in the onset and course.
    • Specific gene activity may contribute to asthma phenotypes with common forms:
      • Allergic - Type I hypersensitivity reaction is most common
      • Non - allergic
      • Adult-onset
      • Asthma with persistent airflow limitation
      • Asthma with obesity
    • Categorizing individuals guides treatment toward specific pathophysiology.
    • Environmental factors that influence gene activity and asthma include:
      • Allergens, urban living, air pollution, tobacco smoke, recurrent viral respiratory infections, obesity, medications with acetaminophen, and gastroesophageal reflux disease
  • Pathophysiology
    • Asthma results from innate and adaptive immune responses to an antigen (allergen) within the airway.
    • Chronic inflammation leads to ongoing biological and structural changes within the airway and lungs.
    • Acute asthma episodes involve an early asthmatic response and a late asthmatic response.

Pathophysiology – Early asthmatic response

  • The early asthmatic response is immediate with maximum effect at about 30 minutes and resolution in about 1-3 hours.
  • Dendritic cells (antigen-presenting macrophages) “present” antigen to CD4 T cells.
  • These CD4 cells differentiate into Th2 cells that release several specific cytokines in response to the antigen.
  • Activation of cytokines and inflammatory cells lead to:
    • Bronchoconstriction
    • Vasodilation
    • Increased capillary permeability
    • Edema
    • Thick mucus
    • These factors combine to narrow airways and limit airflow.

Pathophysiology – Late asthmatic response

  • 4-8 hours after initial event produces more airway hyper-responsiveness.
  • More bronchospasm, airway edema, & airflow limitation.
  • Leukotriene release leads to ongoing smooth muscle contraction in the airway.
  • CO_2 retention increases and with decreased blood pH, the result is respiratory acidosis.
  • Respiratory acidosis is an alarm for impending respiratory failure.
  • ABGs obtained early in the course of acute asthma may not reflect oxygenation changes that can occur rapidly.

Asthma – Clinical Manifestations

  • Symptoms:
    • Severe dyspnea
    • Chest tightness
  • Signs:
    • Non-productive cough
    • Expiratory wheezing
    • Tachycardia
    • Tachypnea
    • Decreased PaO_2
  • With severe asthma:
    • Labored breathing with expiratory and inspiratory wheezing
    • Status Asthmaticus
      • Severe respiratory distress
      • Unresponsive to initial therapy
      • Worsening hypoxemia
      • Worsening acidosis
      • Can be FATAL!

Chronic Obstructive Pulmonary Disease (COPD)

  • Airflow limitation not fully reversible
  • Progressive and abnormal inflammatory response of the lung to respiratory irritants.
  • Chronic bronchitis and Emphysema usually coexist so this combination is called COPD.
  • Common clinical manifestations
    • Dyspnea
    • Wheezing

Chronic Bronchitis

  • Chronic inflammation of the airways from inhaled irritants
  • Neutrophils, macrophages, and lymphocytes congregate in bronchial walls
  • Airway edema from the inflammatory response
  • Normal ciliary function is impaired
  • Large amount of thick secretions cannot be cleared
  • Overproduction of mucus interferes with effective breathing
  • Clinical Manifestations
    • Productive cough
    • Fever
    • Recurrent respiratory infections
    • Anorexia
    • Weight loss
    • Fatigue
    • Clubbing of fingers
      • Occurs with any condition that produces chronic hypoxemia

Emphysema - Types

  • Primary
    • 1 – 3% of cases
    • Genetic
    • α1 antitrypsin deficiency
  • Secondary
    • 97-99% of cases
    • Cigarette smoke inhalation

Emphysema - Pathophysiology

  • Abnormal permanent enlargement of acini
  • Destruction of alveolar walls
  • Decreased alveolar-capillary membrane surface area
  • Destruction of alveolar cells
  • Loss of elastic recoil
  • Decreased surface area for gas exchange

Emphysema – Clinical Manifestations

  • Dyspnea
  • Increased pCO_2 – Hypercarbia
  • Increased anterior-posterior chest diameter
  • Bleb – lung blister from atmospheric air in the airway
  • Bulla – blister in the skin or mucosa with serous or purulent fluid
  • Flattened diaphragm on X-Ray