Alterations of Pulmonary Function Notes

Review of Pulmonary Structures

• Restrictive Disorders

  • Definition: Decreased compliance of lung tissue.
  • Increased effort required to expand lungs during inspiration.
  • Decreased Vital Capacity and Total Lung Capacity.
  • Increased lung stiffness.
  • Shallow, rapid breathing.
  • Alveolar hypoventilation.
  • 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.
    • Portion of the rib cage is separated from the rest of the chest wall.
    • Injured area cannot contribute to lung expansion.

Pneumothorax

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

Pleural Effusion

• Definition: Fluid in 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 leading to hypoxemia.

Pneumoconiosis

• Definition: Inhalation of non-biodegradable substances - Coal, silica, asbestos, talc, textiles, metals.
• Chronic inflammation in lung tissues.
• Scarring of 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, lungs can be stretched with greater ease.
• Increased use of accessory muscles for breathing.
• Air is trapped in the lungs that results 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 of 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.

Asthma 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 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 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

Chronic Bronchitis – 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 airway
• Bulla – blister in skin or mucosa with serous or purulent fluid
• Flattened diaphragm on X-Ray