Ch 35- Alterations of Pulmonary Function

Site of Aspiration

• Aspiration involves fluid and solid particles entering the lung
• This happens when swallowing and coughing are impaired due to decreased LOC or CNS issues
• Predisposing factors include altered LOC from drug abuse, sedation, anesthesia, seizure disorders, neuromuscular disorders causing dysphagia, esophageal disorders, nasogastric tubes, and intubation of the trachea
• The right lung, particularly the lower lobe, is more prone to aspiration due to the straighter branching angle of the right mainstem bronchus
• Most foreign bodies aspirated by children end up in a bronchus (75%)
  • Presents as persistent unexplained cough and refractory parenchymal infiltrates
  • Complete occlusion of a lung segment, visible as atelectasis on a chest radiograph
  • Air trapped distally to the obstruction, acting like a ball-valve mechanism
• Upper trachea obstruction causes inspiratory stridor
• Lower intrathoracic airway obstruction causes wheezing

Hypoxemia

• Hypoxemia refers to reduced oxygenation of arterial blood (PaO2) caused by respiratory alterations, leading to tissue hypoxia
• Hypoxia refers to reduced oxygenation of cell tissues

Chronic Bronchitis

• Chronic bronchitis is defined by hypersecretion of mucus and a productive cough for at least 3 months a year for 2 consecutive years
• Pathophysiology involves chronic irritant exposure, which recruits neutrophils, macrophages, and lymphocytes, leading to progressive lung damage
• Tobacco smoke directly harms airway epithelial cells
• Inflammation from irritants causes bronchial edema, increased mucus glands, goblet cells, smooth muscle hypertrophy/fibrosis, and narrowed airways
• Excessive thick mucus (from impaired ciliary function) compromises lung defense, leading to injury and ineffective repair
• Frequent bacterial infections complicate damaged airways, causing bronchospasm, dyspnea, and productive cough
• Initially, only larger bronchi are affected, but eventually all airways become involved
• Thick mucus and smooth muscle hypertrophy cause airway narrowing and obstruction
• Expiration becomes difficult due to airway obstruction
• Airway collapse occurs early during expiration
• Air trapping leads to increased chest expansion, respiratory muscle disadvantage, increased work of breathing, decreased tidal volume, hypoventilation, and hypercapnia
• Persistent inflammation leads to bronchial hyperreactivity and bronchoconstriction
• It is associated with weight loss, muscle weakness, and increased susceptibility to comorbidities
• Etiology is linked to noxious particles/gases, tobacco smoke, occupational exposures, and indoor/outdoor air pollution
• There is no reversal of pathologic changes
• Prevention involves smoking cessation and vaccinations
• Clinical manifestations include productive cough ("smoker's cough") and airway obstruction (decreased FEV1)
• Other symptoms include decreased exercise tolerance, wheezing, and shortness of breath
• Hypoxemia may occur with exercise
• Disease progression includes increased sputum and frequent infections
• FVC and FEV1 values markedly reduce
• Air trapping increases FRC and residual volume
• Airway obstruction causes decreased ventilation and increased PaCO2
• Marked hypoxemia causes polycythemia and cyanosis
• Untreated hypoxemia leads to pulmonary hypertension, cor pulmonale, disability, or death
• Evaluation relies on history, physical examination, chest radiograph, pulmonary function tests, and blood gas analyses
• Hypoxemia occurs first with exercise, then at rest
• Air trapping worsens, increasing the work of breathing and leading to hypercapnia
• Chest radiography shows changes in thoracic diameter, distended lung fields, and flattening of the diaphragm
• High-resolution CT scans are performed if radiography is not definitive
• Treatment includes bronchodilators and expectorants and aims to reduce dyspnea and control cough
• Bronchodilators include long-acting anticholinergics or beta agonists for symptomatic patients with COPD and low FEV1
• Mucolytics reduce cough and have anti-inflammatory and antioxidant effects
• Inhaled corticosteroids diminish exacerbations and slow the decline in quality of life and FEV1
• Corticosteroids can cause oral candidiasis and increase pneumonia risk
• Oral corticosteroids are considered a last resort
• Acute exacerbations involving infection and bronchospasm require antibiotics and corticosteroids and may require mechanical ventilation
• Phosphodiesterase-4 (PDE4) inhibitors reduce inflammation, cough, and sputum production
• Macrolides are anti-inflammatory and reduce neutrophil-elastase-induced mucous stasis
• Chest physical therapy involves deep breathing and postural drainage
• Long-term oxygen therapy and ventilation are used for progressive pulmonary dysfunction for severe hypoxemia and CO2 retention
• In COPD, chronic elevation of PaCO2 diminishes the sensitivity of central chemoreceptors, shifting breathing stimulus to peripheral chemoreceptors
• Apnea may result if oxygen therapy causes PaO2 to increase above 60mmHg
• Severe hypoxemia must be reversed, especially if there are comorbidities
• Mechanical ventilation is needed if oxygen titration cannot be achieved without causing respiratory depression
• Teaching includes nutritional counseling, respiratory hygiene, infection recognition, and pursed-lip breathing
• Complications include exacerbations frequently worsened by bacterial/viral infections and increased susceptibility to respiratory tract infections
• Additional complications involve heart disease, lung cancer, GERD, and osteoporosis

Adult Asthma

• A chronic inflammatory disorder of the bronchial mucosa, causes bronchial hyper-responsiveness, constricted airways, and reversible airflow obstruction
• Can start at any age and is becoming more common
• Adult onset has high mortality in adult females, black persons and adults >65 years old
• Considered a familial disorder; more than 100 genes implicated in susceptibility, pathogenesis, and treatment outcomes
• Key players are IgE, eosinophils, mast cells, adrenergic receptors, leukotrienes, nitric oxide, and transmembrane proteins in the endoplasmic reticulum
• Risk factors include exposure to allergens, pollution, tobacco smoke, viral infections, esophageal reflux, and obesity
• Asthma’s cause is increased bronchial smooth muscle spasm and increased vascular permeability
• Asthma involves persistent inflammation with Immunoglobulin E (IgE) Dendritic cells, T helper 2 (Th2) lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils

Early Asthmatic Phase

• Acute bronchoconstriction peaks in 30 minutes and resolves within 1 to 3 hours
• Bronchial mucosa exposed to antigen, activates dendritic cells, which present the antigen to T helper cells
• T helper cells differentiate into Th2 cells, which release inflammatory cytokines and activate inflammatory cells
• Results in vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), mucus production, and airway narrowing

Late Asthmatic Phase

• Begins 4-8 hours after the early response, increasing airway hyperresponsiveness
• Includes inflammatory mediators such as cysteinyl leukotrienes and prostaglandin D2
• Chemotactic recruitment happens as lymphocytes, eosinophils, neutrophils, basophils accumulate during an acute response
• Results: bronchospasm, edema, mucus obstruction
• Eosinophils cause direct tissue injury with pulmonary scarring and inflammation
• Release of neuropeptides leads to heightened airway sensitivity
• Ciliated epithelial cell damage causes impaired function and debris plugs
• Increased reactive nitric oxide, oxidative injury occurs, and chronically inflames
• Decreased function from T regulatory cells occurs

Airway Remodeling

• Untreated inflammation causes permanent damage
• Airway obstruction increases resistance, decreases flow, causes air trapping, and increases work of breathing
• Non-uniform resistance causes uneven distribution of inspired air
• Alveolar gas pressure increases, ventilation decreases, and decreased perfusion from lung segments
• Lung volume and obstruction triggers lung receptors, hyperventilation, and CO2 retention Persistent hypoxemia stimulates breathing, but decreases PaCO2 and creates respiratory alkalosis
• Progressive obstruction causes hyperinflation
• Respiratory acidosis reduces left ventricle filling
• It compromises cardiac output during hyperinflation

Asthma Management & Prevention

• Management: allergens, irritants and control symptoms
• Inflammatory Mediators

Inflammatory Mediators of Adult Asthma

• IL-4: Activates B lymphocytes and eosinophils
• IL-5: Stimulates eosinophils, which cause tissue injury, increase bronchial sensitivity, fibroblast proliferation, epithelial injury, and airway scarring
• IL-8: Activates neutrophils
• IL-9: Promotes mast cell growth and differentiation, which increases by IgE production through B cells
• IL-13: Impairs mucociliary clearance, enhances fibroblast secretion, increases number of eosinophils, contributes to bronchoconstriction, and airway remodeling
• IL-17: Increases neutrophilic inflammation
• IL-22: Stimulates smooth muscle, important in innate and adaptive responses and bronchoconstriction
• IL-25: Promotes remodeling
• IL-33: Contributes to remodeling
• Clinical Manifestation of Adult Asthma
  • Symptom Free with normal pulmonary function tests. Between attacks
  • Symptom Free with abnormal pulmonary function tests: Partial remission
  • Initial Response: Chest constriction, wheezing, dyspnea, coughing, prolonged expiration, tachycardia/tachypnea status -Late stage: Worsening hypoxemia and increased PaCO2 levels severe and that the asthma is still in bronchial spasm
  • May show no air flow making it a very dangerous case Accessory muscles: Use of accessory muscles Wheezing when inspiring/expiring Pulsus can show decrease during SBP during inspiration if > 10mmHg Make sure the O2 is still at high 90% and above

Evaluation & Treatment

• Testing recommended by the National Asthma Education and Prevention Program;
• The biomarkers and Epigenetic markers can help determine treatment plans
• Bronchodilators to widen the airway
• Mild with Beta-2-agonist inhaler

Acute and Chronic Treatments

• Acute: Inhaled medication including corticosteroids along with checking the O2
• Chronic Essential: Anti-Inflammatory and corticosteroid meds Alternative: Monoclonal antibodies, help with adjunctive therapy, Inhaled Leukotriene Severe: Aggressively using beta agonist

Asthma

• It is manageable with extensive education, use of peak flow meters and action plans
• Complications can include; pneumonia
• collapsing of the lung and or respiratory failure
• status asthmaticus

Childhood Asthma

• Has reversible Obstructions by hyperreactivity and hypersensitivity usually related to an allergen
• There are genes that produce and increase the amount of cytokine mediators. For example: IL(4,5,6,13,leukiotrienes), adrenaline receptors and TM Proteins.
• Riskfactors Allergens, tobacco, urban area, viral infection Vitamin D suppression Hygiene

Asthma pathophysiology

• Early onset allergic asthma - starts with hypersensitivity which is managed by T2 lymphocytes with cytokines, increased synthesis of leukocytes, and increase of B type cell for the IgE production
• Long Term implications can lead to the blocking production of Th1 leading to the Th2 becoming dominate in asthma responses
• Airway limitations and obstruction/ breath will be more severe in young children than older children -Education with family will assist with treatment during asthma triggers

Childhood Clinical Presentation of Asthma

• Most have viral respiratory infections as a reason
• Most are mild to normal fever grade

Acute Asthma

• Harsh and painful wheezing and breathing
• Increase heart and breathing rates along with signs of flared nostrils.

Chronic

• Abnormal structure of thorax with a widened barrel chest
• Exercise should still be encouraged but caution for severe intolerant of underlying causes for asthma still apply
• Abnormal findings will need tested in other ways

What Can Help Control Childhood asthma

• The mAPI can reduce effects by controlling what the causes are
• Medication and treatment can help by reducing the allergic reaction
• Make certain of the pulmonary functions, including spirometer use on the correct age of child

Childhood Asthma Treatments

• Environmental education to reduce allergens
• Pharmacology treatment should have the same effects
• Postures that relief from breathing difficulties -Lean forward while bracing and opening airways

Defined

• Pulmonary edema: excess fluid in the lung.
• Normal lung balance: lymphatic drainage and a balance among pressure
• Predisposing Factor: Ards, heart complications

Edema Cause & Treatment

• Cardiac: Left Side Failure with filling and pressure Give medication and improve output with the heart
• Aids: Membrane damage with toxins Prevent agent intake and ventilate

Rare Pulmonary Contradictions

• Obstruction with lypmhatic system issues: Dependant on what is restricting and causing the issue to continue
• The Posted Obstructive Edema Air way extraction Assistance with Airway pressure
• Elevation of altitude Take prevention by medication of slow descents

Pulmonary Fibrosis

• Def: high density of tissue and scarring Etiology: Scarring may happen after getting ARDS, from tuberculosis or autoimmune disorders or inhalation of dust or contaminates (asbestos)

What are the pathophysiology behind these diseases Stiff tissue that decreases the transfer Inflammation Complications will most likely lead into fatal/poor outcome

How Processes cause Hypoxemia

• Reduction in arterial How is it caused/result Alveoli issue's and low O1, The ventilation of the alveoli The issue of O2 and Q vs P of all other systems

Main factors hypoxia comes from

 Ischemia-Low O2
 Tissue does occur but not all the time with other abilities like lower cardiac output

Causes

• The decrease of Inhalant agents
• Neurotic simulation
• Mismatch of the systems by
• In rare cases, capillary perfusion may be the issue

Key Notes

• Ventilation will help when we breath better and more open

Air Delivery

1. Ventilation

• How much is being inhaled/exhaled (TV-Tidal Volume with RR-RespiratoryRate)
• Shallow Slow breaths = Hypoventaliation -High CO2 -More acidic results

2. Inspired Aid

• Fraction of insired are (23-31 percent)

Keynotes that both can apply One leads to lack of O2

Blood Transportation

1. With (V) Ventilation Transportation and balancing oxygen and air (V/Q) will help reduce the effects by Body: Vasoconstriction to open. Improve O2 and prevent issues Potentially: High blood flow and more blood Overtime the failure of those may cause greater harm that then has to go onto Right Heart Failure with (Cor-pulmonary)

Transfer

• Thicker membrane can reduce the intake
• Membrane with edema, scar tissue

Transport & Effects

1. When blood bypasses air then you will have: Hypoxia or Oxygen therapy

EMPYEMA

Def: infected pleural space and presence of pus

Etiology: may grow after infection such as pneumo Can also grow by s-aur and e-coli

Patho: blocks fluids 3 Stages Eutative Fin Org

Manifestations & Examination:

 Blue discoloration,
 chest pain if tapped
 Chest X-rays

ARDs & what we should know!

Def: Spectrum that can hurt a lung Symptoms bilateral and can cause fluid

2 key points

• Partial pressure and inhaled o2 rates will have an effect
• All can lead to being a threat.
• Can also limit the delivery of a person's How is AARDs related when not causing: Aspiration of the body

All will include these steps

 Acute cell with inflammation- Immune issues
 Edema and High proteins -

Phases

• exulative will most of the time involve the major Mediators which can also
• Include, releasing inflammation proteins that make sure cells can protect in a better mode - These release neutrophils that will be used for cap, and increase the risk in Pulmonary -HTN - Edema - vasoconstrict

All of that then has the domino effect of AARDS like issues with

 Surfactant protein being inactivated
 Hemorrhagic

Alveoli

• It then gets to fibrotic issue

Symptoms,

• Dyspnea
• Tidal Volume will lower since less air is being taken in.

ARDs vs Berlins Definition

• Depends on all these points to catertorize the effects Treatment focuses on: High O2 and low levels of radiation with what the patient body need

What if the body becomes to damaged from ards Then most likely it will cause MODS and end up causing a fatality Complications may arise but only the near normals are often found and then its almost like another issue

What happens to children

• Underlying diseases and trauma to the infant are most likely fatal
• Infants tend to lack most air due to compliant walls since all the cells are going where they are more accessible
• The goal is the same- To reduce complications

How and what to do with the Smoke

• Tobacco causes damage and inflammation to the area
• Leads in thickening membranes
• And can lead to an infection
• Tobacco comes a main factor in lung injuries and lung tumors.
  • Smoke has almost 30 C.A that can create C to the Larynx

1. Carcinogen will help with lung cancer
2. And over time mutations may as well!