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