1. Respiratory Module
C.O.P.D.

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

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

4. 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.

5. 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.

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

7. COPD Includes Does not include Emphysema Chronic bronchitis
Bronchiectasis
Asthma

8. 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

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

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

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

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

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

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

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

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

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

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

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

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

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

22. 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.

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

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

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

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

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

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

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

30. Bronchodilators Frequency Regularly throughout the day & PRN
Prophylactically

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

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

33. 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

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

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

36. What affect do corticosteroids have of blood sugar levels?

37. Glucocorticoids
Examples
Prednisone
Methyprednisone
Beclovent

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

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

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

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

42. Nursing Management Ineffective breathing patterns
Teach and encourage breathing exercises…

43. 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)

44. 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

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

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

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

48. Nursing Management Ineffective coping Set realistic goals Listen
Empathy
Refer

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

50. 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

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

52. Bronchiectasis
Pathophysiology
Form sacs 
Secretion pool 
Infections

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

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

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

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

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

58. 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

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

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

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

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

63. 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

64. Asthma S&S
Primary
Cough
Dyspnea
Wheezing
Expiratory
Nasal flaring

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

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

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

68. Asthma Prevention
Manipulate known triggers
Stress
Pollen
Exercise

69. 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

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

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

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

73. 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

74. 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

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

76. 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

77. 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

78. 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