Respiratory Module C.O.P.D.

COPD - overview COPD? COLD? Broad classifications of disease Chronic Obstructive Pulmonary Disease COLD? Chronic Obstructive Lung Disease Broad classifications of disease

COPD Characterized by airflow limitation Irreversible Dyspnea on exertion Progressive Abn. inflammatory response of the lungs to noxious particles or gases

Pathophysiology Noxious particles of gas  Inflammatory response  (occurs throughout the airways, parenchyma and pulmonary vasculature) Narrowing of airway In COPD the airflow limitation is both progressive and assoc. with abnormal inflammatory response of the lungs to noxious gases. The inflammatory response occurs thorugh the airways, parenchyma and pulmonary vasculature. Because of the chronic inflammation and the body’s attempt to repair it, narrowing occurs in the small peripheral airways.

Pathophysiology Injury  Repair Injury  repair Injury  repair  scar tissue  Narrowing of lumen Over time this injury and repair process causes scar tissue formation and narrowing of the airway lumen.

Pathophysiology Inflammation  Thickening of the wall of the pulmonary capillaries (Smoke damage & inflammatory process)

COPD Includes Does not include Emphysema Chronic bronchitis Bronchiectasis Asthma

COPD - FYI COPD 4th leading cause of death in the US 12th leading cause of disability Death from COPD is on the rise while death from heart disease is going down

COPD Risk Factors for COPD Exposure to tobacco smoke Passive smoking 80-90% of COPD Passive smoking Occupational exposure Air pollution

COPD risk factors #1 Why is smoking so bad?? Smoking ↓ scavenger cell ability ↓ cilia function Irritates goblet cells & Mucus glands  ↑ mucus production

Chronic Bronchitis Disease of the airway Definition: cough + sputum production > 3 months 2 consecutive years

Chronic Bronchitis Pathophysiology Pollutant irritates airway  Inflammation + h secretion of mucus  h goblet cells + h mucus secreting glands + h Mucus i ciliary function

Chronic Bronchitis Plugs become areas for bacteria to grow and chronic infections which increases mucus secretions and eventually, areas of focal necrosis and fibrosis

Chronic Bronchitis Bronchial walls thicken Bronchial Lumen narrows Mucus plugs airway Alveoli/bronchioles become damaged ↑ alveolar macrophages  ↑ susceptibility to LRI

What do you think? Exacerbation of Chronic bronchitis is most likely to occur during? Fall Spring Summer Winter

Emphysema Pathophysiology Affects alveolar membrane Destruction of alveolar wall Loss of elastic recoil Over distended alveoli

Emphysema Pathophysiology Over distended alveoli Damage to adjacent pulmonary capillaries h dead space Impaired passive expiration  Impaired gas exchange

Emphysema Impaired gas exchange impaired expiration Hypoxemia h CO2  Hypercapnia Respiratory acidosis

Emphysema Damaged pulmonary capillary bed h pulmonary pressure  h work load for right ventricle  Right side heart failure (due to respiratory pressure)  Cor Pulmonale

COPD Compare and contrast Chronic Bronchitis is a disease of the ___________? Airway Emphysema is a disease affecting the ___________? Alveoli

C.O.P.D. Risk factors, S&S, treatment, Dx, Rx - same for Chronic Bronchitis & Emphysema

C.O.P.D. Clinical Manifestation (primary) Cough Sputum production Dyspnea on exertion (Secondary) Wt. loss Resp. infections Barrel chest Weight loss because: dyspnea interferes with eating, also the work of breathing is energy depleting.

C.O.P.D. Nrs. Assessment Risk factors Past Hx / Family Hx Pattern of development Presence of comobidities Current Tx Impact

C.O.P.D. Diagnostic exams/procedures Pulmonary function test Tidal Volume i Functional residual h Spirometry / FEV (force of expired vol.)

C.O.P.D. Diagnostic exams/procedures Bronchodilator reversibility test Check FEV Give Bronchodilator If improved FEV = Asthma If no improvement FEV = COPD

Rule out other diseases ABG’s Baseline PaO2 Rule out other diseases CT scan X-ray

C.O.P.D. Medical Management Risk reduction Smoking cessation! (The only thing that slows down the progression of the disease!)

C.O.P.D. Rx. therapy Primary Bronchodilators Corticosteriods Secondary Antibiotics Mucolytic agents Anti-tussive agents

Bronchodilators Action: Route Relieve bronchospasms Reduce airway obstruction ↑ ventilation Route Metered-dose inhaler Nedulizer Oral

Bronchodilators Frequency Regularly throughout the day & PRN Prophylactically

Bronchodilators Examples Albuterol (Proventil, Ventolin, Volmax) Metaproterenol (Alupent) Ipratropium bromide (Atrovent) Theophylline (Theo-Dur)* * Oral

Glucocorticoids Action Route Potent anti-inflammatory agent Inhaled Systemic (oral or intravenous)

Endocrine Flashback Which of the following is an iatrogenic event secondary to prolonged use of corticosteroid medications? SIADH Diabetes Insipidus Cushing disease Addison’s disease Acromegaly

What electrolyte imbalance is assoc with Cushing Syndrome? Hypercalcemia Hypocalcemia Hypernatremia Hyponatremia Hyperkalemia Hypokalemia

Corticsteriods S/E Cushing Never discontinue abruptly Moon face Na+ & H20 retention Never discontinue abruptly

What affect do corticosteroids have of blood sugar levels?

Glucocorticoids Examples Prednisone Methyprednisone Beclovent

C.O.P.D. Medical Management Treatment O2 When PaO2 < 60 mm Hg Pulmonary rehab Breathing exercises Pulmonary hygiene

Nursing Management Impaired gas exchange Ineffective airway clearance Ineffective breathing patterns Activity intolerance Deficient knowledge about self-care Ineffective coping

Nursing Management Impaired gas exchange Bronchodilators Corticosteroids Monitor for side effects Measure FEV (force of expired volume) Assess dyspnea Smoking cessation

Nursing Management Ineffective airway clearance Eliminate pulmonary irritants Directed cough Chest physiotherapy Fluids Aerosol mists

Nursing Management Ineffective breathing patterns Teach and encourage breathing exercises…

Nursing Management Breathing exercises Diaphragmatic breathing  (usually have shallow, rapid, inefficient breathing) Diaphragmatic breathing  ↓rate ↑ventilation ↑expelled air Pursed lip breathing Slows respiration Prevents collapse of small airways Helps control rate and depth Relax (↓ anxiety)

Nursing Management Activity intolerance Activity pacing More fatigued in AM Plan activities for “best times” Physical conditioning Exercise training ↑tolerance ↓dyspnea ↓fatigue Graded exercise Regular vs. sporadic

Nursing Management Deficient knowledge about self-care ↑participation (ĉ ↑ improvement) Coordinate diaphragmatic breathing with activities Avoid fatigue Fluids always available

Knowledge Deficit O2 therapy Flow rate # hours required No smoking Regular blood oxygenation levels Regular ABG’s

Knowledge Deficit Set realistic goals Modify life style Avoid temperature extremes Heat  ↑ O2 demand Cold  ↑ bronchospasms

Nursing Management Ineffective coping Set realistic goals Listen Empathy Refer

C.O.P.D. Nursing Management Imbalanced Nutrition: Less than Body requirement (frequently weight loss and protein breakdown) Monitor weight ↑Protein Nutritional supplements

Question? Deep breathing techniques to increase O2 levels A patient is getting discharged from a SNF facility. The patient has a history of severe COPD and PVD. The patient is primarily concerned about their ability to breath easily. Which of the following would be the best instruction for this patient? A.  Deep breathing techniques to increase O2 levels. Cough regularly and deeply to clear airway passages. Cough following bronchodilator utilization Decrease CO2 levels by increase oxygen tank output during meals. Deep breathing techniques to increase O2 levels Need to increase CO2 removal not O2 intake Cough regularly and deeply to clear airway passages Too often  fatigue Cough following bronchodilator utilization Decrease CO2 levels by increase oxygen tank output during meals More O2  Hypoventilation  hypercapnia

Bronchiectasis Pathophysiology Chronic, irreversible, dilation of the bronchi and bronchioles Inflammatory process  Damage of bronchial wall  Permanently distended

Bronchiectasis Pathophysiology Form sacs  Secretion pool  Infections

Bronchiectasis Etiology 2nd chronic disorder Pulmonary infection Aspiration Bronchus obstruction Genetic disorder Cystic fibrosis

Bronchiectasis Clinical Manifestations Recurrent LRI Cough Sputum Copious (>200ml) Purulent Foul smelling Auscultation Wheezes Crackles

Bronchiectasis If wide spread  Clubbing of the fingers Dyspnea Clubbing of the fingers  h pulmonary blood pressure  Cor pulmonale

Bronchiectasis Dx S&S Sputum cultures r/o TB CT*

Bronchiectasis Tx Bronchodilators Mucolytic agents Antibiotics Surgery If hypoxemia Postural drainage Chest physiotherapy Smoking cessation

Asthma Pathophysiology Characterized by intermittent airway obstruction In response to variety of stimuli  Epithelial lining of the airway respond by becoming inflamed and edematous Bronchospasms Secretions increase in viscosity

Asthma Pathophysiology The airway hyper-responsiveness, mucosal edema & h mucus production leads to Recurrent episodes of symptoms Cough Chest tightness Wheezing dyspnea

Asthma What is the strongest predisposing factor for asthma? Smoking Family history Allergy Having a weird middle name

Asthma Pathophysiology Mast-cells play a key role in the inflammatory process Alpha– adrenergic receptors trigger broncho-constriction

What is the action of a mast-cell stabilizer Reduces histamine release Increases the effectiveness of the white blood cells Increase WBC production Bronchodilatation

Thought question? Why is Asthma not considered a form of C.O.P.D? Smoking is not a risk factor It is not irreversible It doesn’t start with the letter “C” It is not a chronic disease It is not an obstructive disease

Asthma S&S Primary Cough Dyspnea Wheezing Expiratory Nasal flaring

Asthma Assessment & Dx History Co-mobid conditions Gastro-esophageal reflux

Asthma Respiratory rate During an Acute episode Increased (initially) CO2? Decreased  Resp. alkalosis Tired  Decreased Resp. rate CO2 ? Increased  Resp acidosis

Asthma O2 Sats? Heart rate Blood Pressure Decreased Cyanosis Heart rate Increased Blood Pressure Anxious, feeling of impending doom!

Asthma Prevention Manipulate known triggers Stress Pollen Exercise

Asthma Rx therapy 2 general classes of asthma medications Quick-relief Long-acting Because of the underlying pathology of asthma is inflammation, controlled primarily with anti-inflammatory meds

Asthma Rx therapy Bronchodilators Anticholinergics Corticosteriods Aminophylline Anticholinergics Atropine Sulfate Atrovent Corticosteriods Prednisone Decreased inflammation Mucolytic agents Acetylcysteine

Asthma Diet Activity Fluids Rest periods Relaxation techniques Not overexert self Sit down and sip warm water

Status Asthmaticus Pathophysiology Attack lasting > 24 hours Do not respond to normal treatment

The term “pink puffer” refers to the client with which of the following conditions? ARDS Asthma Chronic obstructive bronchitis Emphysema So much energy to breath - cachetic thin (blue bloaters  bronchitis

A 66 year old client has marked dyspnea at rest, is thin and uses accessory muscles to breathe. He’s tachypneic, with a prolonged expiratory phase. He has no cough. He leans forward with his arms braced on his knees to support his chest and shoulders for breathing. This client has symptoms of which disease? Asthma Chronic Bronchitis Emphysema

It’s highly recommended that clients with asthma, chronic bronchitis and emphysema have Pneumovax and flu vaccinations for which of the following reasons?

All clients are recommended to have these vaccines These vaccines produce bronchodilation and improve oxygenation These vaccines can reduce tachypnea Respiratory infections can cause severe hypoxia and possible death in these clients

Exercise has which of the following effects on clients with asthma, chronic bronchitis and emphysema? It enhances cardiovascular fitness It improves respiratory muscle strength It reduces the number of acute attacks It worsens respiratory function and is discouraged

Clients with Chronic Obstructive Bronchitis are given diuretics Clients with Chronic Obstructive Bronchitis are given diuretics. Which of the following best explains why? Reducing fluid volume reduces oxygen demand Reducing fluid volume improves the clients mobility Reducing fluid volume reduces sputum production Reducing fluid volume improves respiratory function