Obstructive Lung Diseases and COPD

• Obstructive lung diseases include conditions that make it difficult to inhale or exhale.
• Shortness of breath (SOB) is the most commonly presenting symptom.
• Diagnosis is determined through static pulmonary function tests (PFTs), which assess tidal volume, inspiratory/expiratory reserve volumes, vital capacity, and residual volumes.

Chronic Obstructive Pulmonary Disease (COPD)

• COPD encompasses emphysema, chronic bronchitis, and small airways disease.
• COPD is the third leading cause of death worldwide.
• It is not a specific diagnosis but a combination of progressive chronic diseases.
• More than 16 million Americans have COPD.
• COPD claimed 138,825 American lives in 2020.
• Risk factors include smoking, air pollution, secondhand smoke, occupational dusts and chemicals, heredity/genetic defects, and a history of childhood respiratory infections.
• Presenting symptoms include frequent coughing, excess mucus production, dyspnea/SOB, and difficulty taking a deep breath.
• Complications include activity and participation limitations, inability to work, the need for special equipment, depression, more emergency department visits, and co-existing chronic diseases.

Emphysema

• Emphysema involves the pathologic accumulation of air in the lungs and is a disease of exhalation.
• It is characterized by air trapping.
• Emphysema causes an increase in residual volume (RV) and total lung capacity (TLC), along with a decrease in the FVC1/FVC ratio.
• TLC increase leads to a flattened diaphragm and compromised Length-Tension relationship.
• Alpha-1 antitrypsin (A-1AT) is an enzyme in the blood that protects the body from neutrophil elastase.
• Neutrophil elastase increases elastin degradation and other proteases by coating cells.
• Serum concentrations of A-1AT can rise during acute inflammation, providing protection from inflammatory damage.
• A-1AT deficiency is autosomal recessive.
• One in seven cases of emphysema is not linked to tobacco use.
• Elastase is more active and can degrade elastin more easily, leading to lung damage.
• The condition is difficult to diagnose early.
• Cigarette smoke can change the alpha-1 antitrypsin molecule, limiting its ability to bind to elastase

Association of A-1AT Deficiency and Cigarette Smoking

• A-1AT deficiency and cigarette smoking can cause the destruction of alveoli, development of "super" alveoli, and destruction of connective tissue supports in the smallest airways, leading to collapse during expiration.
• Emphysema creates hyperinflated lungs with enlarged alveoli, leading to loss of alveolar attachments.
• It causes smaller airways to collapse during expiration.
• This leads to air trapping, increased TLC, RV, and FRC, and decreased FEV1/FEV.
• Emphysema is a progressive disease.
• Loss of alveolar attachments, mucosal inflammation and fibrosis, and lumenal obstruction with inflammatory exudate and mucus make the airway obstructed.
• Emphysema often presents with shortness of breath at rest (SOB), apprehensiveness, anxiety, addiction to supplemental oxygen, thin body type, deformed chest with prolonged expiration, and a non-productive cough.
• Clinical manifestations can include cardiac problems (cor pulmonale), mild hypoxemia [reduced O2 concentrations in the blood], worsening hypoxemia, retention of CO2 (hypercapnia), chronic pulmonary metabolic acidosis, and being inactive/deconditioned.
• The most commonly found complications are pneumonia, pneumothorax, chronic atelectasis, cor pulmonale, pulmonary interstitial emphysema and interstitial trapping of air in the lungs, recurrent respiratory infections, respiratory acidosis, hypoxia, and coma.
• Emphysema patients have a poor prognosis.
• The disease is chronic, debilitating, and progressive; it may co-present with lung cancer, and most frequently is diagnosed in the elderly.

Chronic Bronchitis

• Diagnostic criteria includes a productive cough lasting at least 3 months (per year) for 2 consecutive years.
• A ratio of FEV1/FEV less than 75% (suggesting obstruction), accompanied by a chronic cough, increases the likelihood for a bronchitis diagnosis.
• The primary cause is usually long-term exposure to irritants that damage the lungs and airways.
• Chronic bronchitis is characterized by inflammation, excessive mucous production, and scarring of the bronchial lining.
• There is obstructed airflow caused by increased mucous production/reduced mucous clearance.
• Airflow is directly proportional to airway radius4.
• Chronic exposure to irritants causes mucus hypersecretion and hypertrophy of mucus-producing glands in the larger bronchi.
• Destruction of ciliary cells lining airways occurs
• Smooth muscle hypertrophy and atrophy of epithelial cells develops
• Airway collapse may occur, leading to reduced alveoli ventilation, hypoxia, and acidosis (shunt or dead space) and reduced airway radius r4.
• Often, it begins with a recurring morning cough that brings up mucus from the lungs.
• There is increased production of phlegm and chronic coughing, as well as inflammation of the bronchial tubes.
• Symptoms may persist and worsen over the course of the day.
• Patients will experience wheezing and shortness of breath.narrowed due to inflammation, which reduces tidal volume.
• These patients have cough, often with mucus, wheezing, a tight chest, shortness of breath, and tiredness.

Chronic Bronchitis Causes and Treatment

• It is generally worsened over time
• It’s onset can be be triggered by upper- or lower-airway infections.
• The disease can triggered by exposure to environmental irritants, such as dust, fumes, or air pollution.
• Twice as many women get diagnosed with chronic bronchitis as men.
• Patients at with this condition are at greater risk for developing infections.
• Patients tend to be polycythemic, cyanotic, and have peripheral edema from right ventricular failure.
• They may have cor pulmonale secondary to increased pulmonary vascular resistance, shortness of breath (SOB), prolonged expiration, persistent coughing with expectoration, and recurrent infection.
• Treatments include bronchodilators, anti-inflammatory drugs, and oxygen therapy.
• “Blue Bloaters” - this is characterized as decreasing ventilation, increasing RV, V/Q mismatch, hypoxemia, hypercapnia, cyanosis, polycythemia. Cor pulmonale with pulmonary hypertension.

Atelectasis

• Atelectasis is small or large area of lung tissue collapse, resulting in decreased exchange of gases in the lungs.
• These include obstructive and and non obstructive causes
• It causes a Loss of lung volume
• Obstructive atelectasis occurs which results from an obstruction of the bronchus which serves the affected area
• Communication will stops between the alveoli and the trachea and the flow of air is not replaced
• Air still continues to diffuse into the blood, which reduces the alveolar volume, causing the the alveolar to collapses
• Non-obstructive symptoms - Accumulation of fluids or air in the pleural cavity, causing compression on the lungs Cicatricial: Lung tissue scars and prevent normal expansion to occur.

Atelectasis After Surgery

• Atelectasis often occurs after surgery
• Patients must use incentive spirometry and deep breathing exercises
• Complications of atelectasis
• Pneumonia
• Respiratory failure
• Pulmonary edema
• Hypoxemia
• Interventions to limit lung expansion can cause atelectasis:
• processes Hypoventilation associated with decreased pulmonary motion paralysis, pleural disease, diaphragmatic disease, mass
• Failure to breathe deeply postoperatively because of pain leading to muscle guarding and splinting
• Oversedation, coma, immobility
• Loss of surfactant

Atelectasis Implications, Symptoms & Treatment

• Compression of the lung can occur
• Pneumothorax, hemothorax (blood), fluid (hydrothorax) in the pleural cavity
• Abdominal distension may develop
• Frequent gentle position changes, deep breathing, coughing, ambulation sooner rather than later, are all appropriate interventions for the the therapist
• These interventions promote ciliary clearance of, mucus, enhanced lung expansion, permits collateral ventilation
• Asthma is an Episodic, reversible, obstructive lung disease characterized by bronchospasms resulting from an exaggerated inflammatory response of the airway smooth muscles to various stimuli (allergen). Bronchial hyperreactivity

Asthma Symptoms and Clinical Manifestation

• Asthma symptoms include episodic dyspnea, coughing and wheezing

Main Types of Asthma:

Extrinsic (allergic) is asthma from an allergic reaction to specific triggers such as pollen, dust, molds, smoke, automobile exhaust, and animal dander Mast cells, sensitized by IgE antibodies, degranulate and release bronchoactive mediators (histamines) after exposure to a specific antigen Intrinsic (nonallergic/non-Immune causes) - these have no known allergic cause or trigger It Tends to start later in life; is more common in females and is typically more severe The actual pathology is similar to extrinsic asthma but the triggers are a wide range of non-allergy related factors and often occurs secondary to infections of the bronchi, sinuses, or tonsils and adenoids

• Other recognized categories of asthma include adult-onset for exercise-induced. The individual may be sensitive to aspirin, the aspergillus fungus as well as developed developed from an occupational asthma and work

Asthma Pathogenesis

• Pathology includes an inflammatory response consisting of cellular infiltration, epithelial disruption, mucosal edema, inflammatory mediator release and mucous plugging airways leading the body to trigger a production of bronchial smooth muscle production (spasm), vascular congestion, increased vascular permeability, edema formation, production of thick, tenacious mucus, and impaired mucociliary function.
• Bronchial Provocation Test
• Methacholine: Cholinergic stimulant, causes smooth muscle contraction. It’s administered as an inhalant and evaluates airway sensitivity
• Positive test: 20% ↓ FEV1
• Asthma feels like contraction of smooth muscles found in the airways, causing increasing resistance to airflow. The person may feel airway irritability and have a massive inflammation response
• Clinical Course: The patient may have an attack which characterized by dyspnea with wheezing, upper airway obstruction, difficulty with expiration and air trapping in the distal alveoli, leading to hypercapnia or being acidodic and possibly developing hypoxia

Clinical Course

Acutely

• the inside walls of the airways in your lungs can become inflamed and swollen; airway linings may secrete excess mucus.

Chronically

• Repeated attacks cause airway remodeling,air trapping, proliferation of submucosal glands, and hypertrophied smooth muscle.