Obstructive Pulmonary Disorders

Obstructive Pulmonary Disorders - Chapter 22

General Concepts

• The reason for covering a broad range of material is for future education and careers.
• The instructor will not provide a written list of slides to know, to encourage full engagement with the class material.
• Pulmonary disorders are divided into Obstructive and Restrictive categories:
  • Obstructive: Difficulty getting air OUT (but can get air in, especially early on).
  • Restrictive: Difficulty getting air IN (but can get air out easily).
• Obstructive pulmonary disorders can be caused by:
  • Obstruction in the wall of the lumen.
  • Obstruction of the airway lumen itself (e.g., aspirated object, tumor).
  • Pressure exerted from outside the tube, reducing the lumen's cross-sectional area.

Asthma

• Asthma is considered a paradigm obstructive pulmonary disorder.
• Largely reversible, especially when addressing underlying causes, not just symptoms.
• Characterized by airway inflammation and hyper-reactive airways.
• Triggers for hyper-reactive airways are not always allergens (e.g., smoke inhalation).
• Incidence is higher than 5-12% in the US population.
• Most common chronic disease in children.
• Risk factors:
  • Genetic predisposition (for some individuals).
  • African Americans and inner-city dwellers: Higher risk due to smog, industrial fumes, traffic, which irritate respiratory linings.
  • Premature, low-birth-weight children: Interventions or low O2 presentations can harm respiratory surfaces.
  • Family history of eczema, hay fever, or atopy.
  • People with structurally smaller airways: Any irritation/mucus has profound effect because airways are already small.
  • Allergies.
• Exercise-induced asthma is now referred to differently; consult healthcare providers.
• Extrinsic (allergic) asthma accounts for at least half of all asthma cases.
• Asthma is a lifelong condition with no cure.
• Hyper-reactive airway disease has similar mechanisms to allergic asthma.
• Allergens:
  • IgE attaches to Fc receptors on mast cells.
  • Antigen exposure causes mast cell degranulation.
  • Histamine release (vasodilation, bronchoconstriction).
  • Cytokine release.
  • Mucus production to trap allergens.

Inflammatory Response

• Leukotrienes:
  • Slow-reacting substances of anaphylaxis.
  • Adaptive for those without allergies, causing bronchoconstriction to protect airways from inhaled particles.
  • Inhibitors include Montelukast (Singulair).
• Prostaglandins: Can cause inflammation.
• Bradykinins: Cause inflammation.
• Eosinophilic chemotactic factor: Involved in allergic reactions.
• Serotonin: Causes vasoconstriction.

Normal airway exposed to allergens leads to immune response -> mucus production -> neutrophils releasing chemical mediators which destroy cells (tissue destruction) -> repair leads to collagen deposition (scar tissue).

Long-term, only mitigating symptoms (not the underlying disease) leads to airway remodeling: narrow tube with extra smooth muscle, more goblet cells, and collagen deposition. This is NOT reversible.

Narrower the tube, harder it is to exhale -> Hyperinflated lungs.

Advair: Combines steroid with bronchodilator; works well for some, but some may still experience airway remodeling. Airway remodeling can lead to death.

Key to treating asthmatics: prevent airway remodeling by eliminating triggers.

Tissue destruction leads to exudates and mucosal edema, leading to hypertrophied smooth muscle and edema.

Mucus gland hypertrophy -> extra mucus -> bronchoconstriction -> mucus plugs -> airway remodeling.

Goal with asthma

1. Use rescue inhaler as needed.
2. Address underlying issue.

Common symptoms

• Wheezing: Narrowed lumen in bronchioles, trapping air.
• Chest Tightness: Air trapped in alveoli.
• Dyspnea: Abnormal breathing.
• Cough: May or may not be present. Tries to expel tenacious mucus.
• Accessory Muscles: Use of scalene muscles and pectoralis minor.
• Distant Breath Sounds:
• Inspiratory Wheezing.
• Orthopnea (difficulty laying down).
• Agitation.
• Tachypnea.
• Tachycardia.

Physical Findings

• Cough (may/may not be present).
• Wheezing (early on, may be absent in severe cases).
• Hyperinflated chest.
• Decreased breath sounds.

Chest X-Ray

• Hyperinflation of lungs.
• Flattened diaphragm.

Diagnosis and Treatment

• FEV1/FVC ratio:
  • < 75\% indicates obstructive lung disorder.
• Arterial Blood Gases:
  • Mild attack: Normal.
  • Unfolding: Respiratory alkalosis and hypoxemia.
  • Later: Increased CO_2 levels.
• Skin Testing: Identifies triggers.
• CBC levels: Elevated WBCs and eosinophils.
• Treatment:
  • Avoid triggers.
  • Steroids.
  • Short-acting bronchodilators.
  • Refrigerated air (air conditioning).
  • Desensitization therapy (allergy shots).
    • Introduce small amounts of allergens to teach the immune system.
    • Requires commitment and has variable success rates.
    • Risk of anaphylactic shock.
  • O_2 therapy (if needed).
  • Small volume nebulizers.
  • Beta-2 agonists (bronchodilation).
  • Corticosteroids (reduce inflammation).
  • Leukotriene modifiers.
  • Mast cell inhibitors.

Acute Bronchitis

• Reversible inflammation of trachea and bronchi (not bronchioles).
• Causes: Microbes (viruses, bacteria), heat, chemicals, allergic reactions.
• Inflammatory process:
  • Airways narrow.
  • Capillaries dilate, leading to fluid release and increased mucus production.
  • Potential for paralyzed cilia or denuded cells.
• Clinical Manifestations:
  • Cough.
  • Low-grade fever.
  • Substernal chest discomfort.
  • Sore throat and postnasal drip.
  • Fatigue.
• Diagnosis: Chest x-ray to rule out pneumonia.
• Treatment:
  • Antibiotics (if bacterial).
  • Codeine-containing medications (use cautiously due to opioid addiction risk).
  • Plenty of fluids.
  • Avoid smoke.
  • Use a vaporizer (avoid humidifiers due to thermophilic bacteria risk).

Chronic Bronchitis

• Distinct from acute bronchitis; not related to microbes.
• Associated with smoking.
• Defined as cough with sputum production for at least 3 months in each of 2 consecutive years.
• Leads to death.
• Often coexists with emphysema.
• Etiology: Cigarette smoking, genetic predisposition, physical/chemical irritants.
• Pathophysiology: Inflammatory response, increased mucus production, mucus plugs, increased mucus-producing cells, airway remodeling (permanently narrowed lumens).
• Leads to ventilation-perfusion mismatch, hypercarbia, and hypoxemia.
• Increased pulmonary artery resistance leads to cor pulmonale (right ventricular hypertrophy and right-sided heart failure).
• Clinical Symptoms:
  • Shortness of breath on exertion.
  • Excess mucus and sputum.
  • Chronic cough (worse in the morning).
  • Edema and hypervolemia.
• Historically referred to as "blue bloater" due to distension from fluid retention.
• Diagnosis:
  • Chest x-ray: Extravasations or vascular markings (fluid/edema in the bronchi and lung fields), enlarged horizontal cardiac silhouette (right ventricular hypertrophy).
  • Pulmonary function tests: Decreased FEV1, normal lung capacity, increased residual volume.
  • Blood gases: Elevated arterial CO2, decreased arterial O2.
  • Cardiovascular issues: Secondary polycythemia (increased red blood cells due to low O_2 levels).
• Treatment:
  • Same medications as other obstructive diseases (short-acting bronchodilators, parasympathetic inhibitors, cough suppressants, steroids, antimicrobial agents, theophylline, O_2 therapy).
  • Smoking cessation.
  • Adequate rest.
  • Proper hydration.
  • Physical reconditioning: Parts of the lung that are not yet severely impaired can be reconditioned to improve efficiency.

Emphysema

• Referred to as "pink puffer."
• Uncommon under age 50; often due to alpha-1 antitrypsin deficiency.
• Liver makes Alpha-1 antitrypsin
• Minimizes neutrophil response.

Role of Alpha-1 Antitrypsin

• Alpha-1 antitrypsin dials down the activity of neutrophils to destroying lung tissue.
• People with low alpha-1 antitrypsin counts are not able to dial down the neutrophils resulting in neutrophil influx.
• Neutrophils destroy the alveoli via inflammation.
• Neutrophils release elastase

Elastase

• Also known as protease (protein destroyer).
• Destroys lung tissue (alveoli)
• Elastin are rubber bands wrapped tightly around the alveoli that got stretched when we inhale the air when we inspired. If there is no more drive to inspire, we have higher pressure inside the air wants to go down it's concentration gradient so there is a natural outlet to leave our lungs. Also those rubber bands want to decompress and go back to their resting state. Elastic fibers.

What happens with emphysema that results in permanent inflated Avioli?

• Inflamed alveoli: Neutrophils release protease, and what does that protease do? It digests those elastic fibers.
• Because the alveoli lost the elastic fibers they can never let the air come back out again.
• Someone with emphysema under 50 got it by not having enough alpha-1 antitrypsin, so the body was not able to turn off the neutrophils.
• Pack years not needed.
• If air is constantly filled with smog, people who've never smoked are susceptible to emphysema
• Miners, welders, mold remediation workers are susceptible to emphysema because the particulate triggers neutrophil response which causes emphysema over time.

Clinical Manifestations

• Shortness of breath.
• Very thin, barrel chest.
• Pursed lift breathing. Squeaks out extra centimeters
• Little to no cough because they can't generate enough air going out to get to 100 millimeters of mercury pressure
• Decreased breath sounds.
• Decreased heart sounds.
• Diaphragm is largely flattened, and have decreased diaphragmatic excursion (less movement).

Diagnosis

*Pulmonary function tests are what they are for all obstructive pulmonary disorder.
*Blebs and Bullae (bookmark their mention).

• Narrow Mediastinum.
• Small, Narrow, Heart.

Diagnosis

*Cardiovascular consequences (which you do not need to know). *Shallow P waves.

• Sinus tachycardia. Try to overcome lack of ability to get oxygen in blood.
  *Ventricular arrhythmias. SVTs can lead to heart attacks.
  *Mild increase in arterial O2 because of all the hyperinflation. *Normal arterial CO2 because body gets used to it and adjusts.
  *Unlike chronic bronchitis where early on the CO2 levels go up.
  *

Treatment (same of the other diseases)

*Bronchiectasis only a few thing you need

• Usually occurs in kids.
• Half the cases are directly related to cystic fibrosis.
• Cystic fibrosis is a weirdly prevalent disorder. Recessive only happens when both parents have recessive allele.
  *People with cystic fibrosis don't make chloride channels in their cells (unequal transport of sodium and potassium. And with respect to the lungs, if no chloride then the ability to equalize the gradient of water movement is profoundly impaired, so you make mucous but you can't dilute the mucous so it causes an obstruction (Tenacious mucus). Cystic Fibrosis patients don't live 30 - 32 years old.
  *

Bronchiectasis

There is an infection to the wall of the bronchi and the inflammatory process that got the infection started.
So how did that infection start? Well if you have cystic fibrosis and you have tenacious mucus. Some microbe comes in from whatever source and other people are able to exhale it right away in people who have cystic fibrosis the mucous, is so tenacious, thick, and it sticks in place that the microbe goes there and whenever there is fluid, no matter how thick that is static and not moving in the body in a place where it should not be that brings about infection.

Recurring infection and can lead to persistent dilation of the tissue of a bronchial wall, inflammatory response gets triggered when infection gets set in, destruction of the cell walls. Some can be repaired others cannot. The breath is smells so horrible you just know because their breath it's not bad breath it's like a garbage dump that was sealed and kept in 120 degree weather for months on end with high humidity. It's vile how horrible their breath smells
*

Chronic Productive Cough/Infection

*Clinical Manifestations
*Fever, Night Sweats from infection
*Crackles in the bases of the lungs. Is there purulent exudate from the bacteria inflicts harm on the wall and gathering on the wall , but it is also going down on the lower parts of respiratory tree. The smell of the breath is so bad.
*Malnutrition because work of breathing requires a lot of ATP to do.
*Reoccurring pneumonia, just as a result of the microbes that getting set to that Bronchial walls.
*Not very unusual to see cardiac patients or right ventricle patients because so the increased pulmonary vascular resistance that happens.
*

Treatment

*Antibiotics
*Bronchodilators.
*Vigorous chest percussion.
*Postural drainage: To dislodge the mucus so we do not lose respiratory surfaces so the infection does not get setup.
*Fluids
*

Most often you don't care about Acute tracheobronchial obstruction, where you aspirated an object, unless its the right lung because it is more steep than the left bronchial stem.
Smoke Inhalation is another common cause of acute tracheobronchial obstruction.

Quick Treatment

The key is to open the airway as quickly as open. Hemat maneuver. Then physicians do open tracheostomy.

Pulmonary Function Test

Spirometry: If someone FEV 1 / FVC ratio above 75 percent. No significant obstruction. Below 50 means severe level of medical emergency. This does not mean you do not treat them

If someone has the FEV the the sub-1 improvement of greater than 15% on his face. It's a positive diagnosis that they have obstructive airway disease. Now who knows what the cause is. Often it's, asthma, bronchitis, related to asthma.

• If somebody Sub one to FBC ratio of less than 70%. And they have the improvement of greater than than fifteen percent after the ministry administration of bronchodilator. This is a positive diagnosis of obstructive pulmonary disorder and those same people have increased RVs and increased TRC.