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Chronic Obstructive Pulmonary Disease (COPD)

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Chronic Obstructive Pulmonary Disease (COPD) COPD Description Characterized by presence of airflow obstruction Caused by emphysema or chronic bronchitis Generally ... – PowerPoint PPT presentation

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Title: Chronic Obstructive Pulmonary Disease (COPD)


1
Chronic Obstructive Pulmonary Disease (COPD)
2
COPDDescription
  • Characterized by presence of airflow obstruction
  • Caused by emphysema or chronic bronchitis
  • Generally progressive
  • May be accompanied by airway hyperreactivity
  • May be partially reversible

3
Emphysema Description
  • Abnormal permanent enlargement of the air space
    distal to the terminal bronchioles
  • Accompanied by destruction of bronchioles

4
Chronic Bronchitis Description
  • Presence of chronic productive cough for
  • 3 or more months in each of 2 successive years
    in a patient whom other causes of chronic cough
    have been excluded

5
COPDCauses
  • Cigarette smoking
  • Primary cause of COPD
  • Clinically significant airway obstruction
    develops in 15 of smokers
  • 80 to 90 of COPD deaths are related to tobacco
    smoking
  • gt 1 in 5 deaths is result of cigarette smoking

6
COPDCauses
  • Cigarette smoking
  • Nicotine stimulates sympathetic nervous system
    resulting in
  • ? HR
  • Peripheral vasoconstriction
  • ? BP and cardiac workload

7
COPDCauses
  • Cigarette smoking
  • Compounds problems in a person with CAD
  • ? Ciliary activity
  • Possible loss of ciliated cells
  • Abnormal dilation of the distal air space
  • Alveolar wall destruction
  • Carbon monoxide
  • ? O2 carrying capacity
  • Impairs psychomotor performance and judgment
  • Cellular hyperplasia
  • Production of mucus
  • Reduction in airway diameter
  • Increased difficulty in clearing secretions

8
COPDCauses
  • Secondhand smoke exposure associated with
  • ? Pulmonary function
  • ? Risk of lung cancer
  • ? Mortality rates from ischemic heart disease

9
COPDCauses
  • Infection
  • Major contributing factor to the aggravation and
    progression of COPD
  • Heredity
  • ?-Antitrypsin (AAT) deficiency (produced by liver
    and found in lungs) accounts for lt 1 of COPD
    cases
  • Emphysema results from lysis of lung tissues by
    proteolytic enzymes from neutrophils and
    macrophages

10
Pathophysiology of Chronic Bronchitis and
Emphysema
Fig. 28-7
11
Emphysema Pathophysiology
  • Hyperinflation of alveoli
  • Destruction of alveolar walls
  • Destruction of alveolar capillary walls
  • Narrowed airways
  • Loss of lung elasticity

12
Emphysema Pathophysiology
  • Two types
  • Centrilobular (central part of lobule)
  • Most common
  • Panlobular (destruction of whole lobule)
  • Usually associated with AAT deficiency

13
Emphysema Pathophysiology
  • Structural changes are
  • Hyperinflation of alveoli
  • Destruction of alveolar capillary walls
  • Narrowed, tortuous small airways
  • Loss of lung elasticity

14
Emphysema Pathophysiology
  • Small bronchioles become obstructed as a result
    of
  • Mucus
  • Smooth muscle spasm
  • Inflammatory process
  • Collapse of bronchiolar walls
  • Recurrent infections production/stimulation
    of neutrophils and macrophages release
    proteolytic enzymes alveolar destruction
  • inflammation, exudate, and edema

15
Emphysema Pathophysiology
  • Elastin and collagen are destroyed
  • Air goes into the lungs but is unable to come out
    on its own and remains in the lung
  • Causes bronchioles to collapse

16
Emphysema Pathophysiology
  • Trapped air ? hyperinflation and overdistention
  • As more alveoli coalesce, blebs and bullae may
    develop
  • Destruction of alveolar walls and capillaries ?
    reduced surface area for O2 diffusion
  • Compensation is done by increasing respiratory
    rate to increase alveolar ventilation
  • Hypoxemia usually develops late in disease

17
EmphysemaClinical Manifestations
  • Dyspnea
  • Progresses in severity
  • Patient will first complain of dyspnea on
    exertion and progress to interfering with ADLs
    and rest

18
Emphysema Clinical Manifestations
  • Minimal coughing with no to small amounts of
    sputum
  • Overdistention of alveoli causes diaphragm to
    flatten and AP diameter to increase

19
Emphysema Clinical Manifestations
  • Patient becomes chest breather, relying on
    accessory muscles
  • Ribs become fixed in inspiratory position

20
Emphysema Clinical Manifestations
  • Patient is underweight (despite adequate calorie
    intake)

21
Chronic BronchitisPathophysiology
  • Pathologic lung changes are
  • Hyperplasia of mucus-secreting glands
  • in trachea and bronchi
  • Increase in goblet cells
  • Disappearance of cilia
  • Chronic inflammatory changes and narrrowing of
    small airways
  • Altered fxn of alveolar macrophages infections

22
Chronic BronchitisPathophysiology
  • Chronic inflammation
  • Primary pathologic mechanism causing changes
  • Narrow airway lumen and reduced airflow d/t
  • hyperplasia of mucus glands
  • Inflammatory swelling
  • Excess, thick mucus

23
Chronic BronchitisPathophysiology
  • Greater resistance to airflow increases work of
    breathing
  • Hypoxemia and hypercapnia develop more frequently
    in chronic bronchitis than emphysema

24
Chronic BronchitisPathophysiology
  • Bronchioles are clogged with mucus and pose a
    physical barrier to ventilation
  • Hypoxemia and hypercapnia d/t lack of ventilation
    and O2 diffusion
  • Tendency to hypoventilate and retain CO2
  • Frequently patients require O2 both at rest and
    during exercise

25
Chronic Bronchitis Pathophysiology
  • Cough is often ineffective to remove secretions
    because the person cannot breathe deeply enough
    to cause air flow distal to the secretions
  • Bronchospasm frequently develops
  • More common with history of smoking or asthma

26
Chronic BronchitisClinical Manifestations
  • Earliest symptoms
  • Frequent, productive cough during winter
  • Frequent respiratory infections

27
Chronic BronchitisClinical Manifestations
  • Bronchospasm at end of paroxysms of coughing
  • Cough
  • Dyspnea on exertion
  • History of smoking
  • Normal weight or heavyset
  • Ruddy (bluish-red) appearance d/t
  • polycythemia (increased Hgb d/t chronic
    hypoxemia))
  • cyanosis

28
Chronic BronchitisClinical Manifestations
  • Hypoxemia and hypercapnia
  • Results from hypoventilation and ? airway
    resistance problems with alveolar gas exchange

29
COPDComplications
  • Pulmonary hypertension (pulmonary vessel
    constriction d/t alveolar hypoxia acidosis)
  • Cor pulmonale (Rt heart hypertrophy RV failure)
  • Pneumonia
  • Acute Respiratory Failure

30
COPDDiagnostic Studies
  • Chest x-rays early in the disease may not show
    abnormalities
  • History and physical exam
  • Pulmonary function studies
  • reduced FEV1/FVC and ? residual volume and total
    lung capacity

31
COPDDiagnostic Studies
  • ABGs
  • ? PaO2
  • ? PaCO2 (especially in chronic bronchitis)
  • ? pH (especially in chronic bronchitis)
  • ? Bicarbonate level found in late stages COPD

32
COPDCollaborative Care
  • Smoking cessation
  • Most significant factor in slowing the
    progression of the disease

33
COPDCollaborative Care Drug Therapy
  • Bronchodilators as maintenance therapy
  • ?-adrenergic agonists (e.g. Ventolin)
  • MDI or nebulizer preferred
  • Anticholinergics (e.g. Atrovent)

34
COPDCollaborative Care Oxygen Therapy
  • O2 therapy
  • Raises PO2 in inspired air
  • Treats hypoxemia
  • Titrate to lowest effective dose

35
COPD Collaborative Care Oxygen Therapy
  • Chronic O2 therapy at home
  • Improved prognosis
  • Improved neuropsychologic function
  • Increased exercise tolerance
  • Decreased hematocrit
  • Reduced pulmonary hypertension

36
COPDCollaborative Care Respiratory Therapy
  • Breathing retraining
  • Pursed-lip breathing
  • Prolongs exhalation and prevents bronchiolar
    collapse and air trapping
  • Diaphragmatic breathing
  • Focuses on using diaphragm instead of accessory
    muscles to achieve maximum inhalation and slow
    respiratory rate
  • See text re how to teach

37
COPDCollaborative Care Respiratory Therapy
  • Huff coughing (Table 28-21)
  • Chest physiotherapy to bring secretions into
    larger, more central airways
  • Postural drainage
  • Percussion
  • Vibration

38
Positions for Postural Drainage
Positions for Postural Drainage
Fig. 28-16
39
COPDCollaborative Care
  • Encourage patient to remain as active
  • as possible

40
COPDCollaborative Care
  • Surgical Therapy
  • Lung volume reduction surgery
  • Lung transplant

41
COPDCollaborative Care
  • Nutritional therapy
  • Full stomachs press on diaphragm causing dyspnea
    and discomfort
  • Difficulty eating and breathing at the same time
    leads to inadequate amounts being eaten

42
COPDCollaborative Care
  • Nutritional therapy
  • To decrease dyspnea and conserve energy
  • Rest at least 30 minutes prior to eating
  • Use bronchodilator before meals
  • Select foods that can be prepared in advance
  • 5-6 small meals to avoid bloating
  • Avoid foods that require a great deal of chewing
  • Avoid exercises and treatments 1 hour before and
    after eating

43
COPDCollaborative Care
  • Nutritional therapy
  • Avoid gas-forming foods
  • High-calorie, high-protein diet is recommended
  • Supplements
  • Avoid high carbohydrate diet to prevent increase
    in CO2 load

44
Nursing ManagementNursing Diagnoses
  • Ineffective airway clearance
  • Impaired gas exchange
  • Imbalanced nutrition less than body requirements
  • Disturbed sleep pattern
  • Risk for infection

45
Nursing ManagementNursing Implementation
  • Health Promotion
  • STOP SMOKING!!!
  • Avoid or control exposure to occupational and
    environmental pollutants and irritants
  • Early detection of small-airway disease
  • Early diagnosis of respiratory tract infections

46
Nursing ManagementNursing Implementation
  • Acute Intervention
  • Required for complications like pneumonia, cor
    pulmonale, and acute respiratory failure

47
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Pulmonary rehabilitation
  • Control and alleviate symptoms of
    pathophysiologic complications of respiratory
    impairment

48
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Teach patient how to achieve optimal capability
    in carrying out ADLs
  • Physical therapy
  • Nutrition
  • Education
  • Activity considerations
  • Exercise training of upper extremities to help
    improve function and relieve dyspnea

49
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Explore alternative methods of ADLs
  • Encourage patient to sit while
  • performing activities
  • Coordinated walking

50
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Slow, pursed-lip breathing
  • After exercise, wait 5 minutes before using
    ?-adrenergic agonist MDI

51
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Sexual activity
  • Plan during part of day when breathing is best
  • Slow, pursed-lip breathing
  • Refrain after eating or other strenuous activity
  • Do not assume dominant position
  • Do not prolong foreplay

52
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Sleep
  • Nasal saline sprays
  • Decongestants
  • Nasal steroid inhalers
  • Long-acting theophylline
  • Decreases bronchospasm and airway obstruction

53
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Psychosocial considerations
  • Guilt
  • Depression
  • Anxiety
  • Social isolation
  • Denial
  • Dependence
  • Use relaxation techniques and support groups

54
Nursing ManagementNursing Implementation
  • Ambulatory and Home Care
  • Discourage moving to places above 4000 ft.
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