Emphysema and Chronic Bronchitis
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Transcript Emphysema and Chronic Bronchitis
Chronic Obstructive
Pulmonary Disease (COPD)
COPD
Description
Characterized by presence of airflow
obstruction
Caused by emphysema or chronic
bronchitis
Generally progressive
May be accompanied by airway
hyperreactivity
May be partially reversible
Emphysema
Description
Abnormal permanent enlargement of the
air space distal to the terminal bronchioles
Accompanied by destruction of bronchioles
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
COPD
Causes
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
> 1 in 5 deaths is result of cigarette
smoking
COPD
Causes
Cigarette smoking
Nicotine stimulates sympathetic nervous
system resulting in:
HR
Peripheral vasoconstriction
BP and cardiac workload
COPD
Causes
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
COPD
Causes
Secondhand smoke exposure associated
with:
Pulmonary function
Risk of lung cancer
Mortality rates from ischemic heart
disease
COPD
Causes
Infection
Major contributing factor to the aggravation
and progression of COPD
Heredity
-Antitrypsin (AAT) deficiency (produced by
liver and found in lungs); accounts for < 1% of
COPD cases
Emphysema results from lysis of lung tissues by proteolytic
enzymes from neutrophils and macrophages
Pathophysiology of Chronic Bronchitis
and Emphysema
Fig. 28-7
Emphysema
Pathophysiology
Hyperinflation
of alveoli
Destruction of alveolar walls
Destruction of alveolar capillary walls
Narrowed airways
Loss of lung elasticity
Emphysema
Pathophysiology
Two
types:
Centrilobular (central part of lobule)
Most common
Panlobular (destruction of whole lobule)
Usually associated with AAT deficiency
Emphysema
Pathophysiology
Structural changes are:
Hyperinflation of alveoli
Destruction of alveolar capillary walls
Narrowed, tortuous small airways
Loss of lung elasticity
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
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
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
Emphysema
Clinical Manifestations
Dyspnea
Progresses in severity
Patient will first complain of dyspnea
on exertion and progress to interfering
with ADLs and rest
Emphysema
Clinical Manifestations
Minimal
coughing with no to small
amounts of sputum
Overdistention
of alveoli causes
diaphragm to flatten and AP diameter to
increase
Emphysema
Clinical Manifestations
Patient
becomes chest breather, relying
on accessory muscles
Ribs become fixed in inspiratory
position
Emphysema
Clinical Manifestations
Patient
is underweight (despite adequate
calorie intake)
Chronic Bronchitis
Pathophysiology
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
Chronic Bronchitis
Pathophysiology
Chronic inflammation
Primary pathologic mechanism
causing changes
Narrow airway lumen and reduced
airflow d/t
hyperplasia of mucus glands
Inflammatory swelling
Excess, thick mucus
Chronic Bronchitis
Pathophysiology
Greater
resistance to airflow increases
work of breathing
Hypoxemia
and hypercapnia develop
more frequently in chronic bronchitis
than emphysema
Chronic Bronchitis
Pathophysiology
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
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
Chronic Bronchitis
Clinical Manifestations
Earliest
symptoms:
Frequent, productive cough during
winter
Frequent respiratory infections
Chronic Bronchitis
Clinical 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
Chronic Bronchitis
Clinical Manifestations
Hypoxemia
and hypercapnia
Results from hypoventilation and
airway resistance + problems with
alveolar gas exchange
COPD
Complications
Pulmonary hypertension (pulmonary vessel
constriction d/t alveolar hypoxia & acidosis)
Cor pulmonale (Rt heart hypertrophy + RV
failure)
Pneumonia
Acute Respiratory Failure
COPD
Diagnostic 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
COPD
Diagnostic Studies
ABGs
PaO2
PaCO2 (especially in chronic bronchitis)
pH (especially in chronic bronchitis)
Bicarbonate level found in late stages
COPD
COPD
Collaborative Care
Smoking cessation
Most significant factor in slowing the
progression of the disease
COPD
Collaborative Care: Drug Therapy
Bronchodilators – as maintenance therapy
-adrenergic agonists (e.g. Ventolin)
MDI or nebulizer preferred
Anticholinergics
(e.g. Atrovent)
COPD
Collaborative Care:
Oxygen Therapy
O2 therapy
Raises PO2 in inspired air
Treats hypoxemia
Titrate to lowest effective dose
COPD
Collaborative Care:
Oxygen Therapy
Chronic
O2 therapy at home
Improved prognosis
Improved neuropsychologic function
Increased exercise tolerance
Decreased hematocrit
Reduced pulmonary hypertension
COPD
Collaborative 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
COPD
Collaborative Care: Respiratory
Therapy
Huff coughing (Table 28-21)
Chest physiotherapy – to bring secretions
into larger, more central airways
Postural drainage
Percussion
Vibration
Positions
for Postural
Positions
for Postural
Drainage
Drainage
Fig. 28-16
COPD
Collaborative Care
Encourage
as possible
patient to remain as active
COPD
Collaborative Care
Surgical Therapy
Lung volume reduction surgery
Lung transplant
COPD
Collaborative 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
COPD
Collaborative 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
COPD
Collaborative 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
Nursing Management
Nursing Diagnoses
Ineffective airway clearance
Impaired gas exchange
Imbalanced nutrition: less than body
requirements
Disturbed sleep pattern
Risk for infection
Nursing Management
Nursing 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
Nursing Management
Nursing Implementation
Acute Intervention
Required for complications like pneumonia,
cor pulmonale, and acute respiratory failure
Nursing Management
Nursing Implementation
Ambulatory and Home Care
Pulmonary rehabilitation
Control and alleviate symptoms of
pathophysiologic complications of
respiratory impairment
Nursing Management
Nursing 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
Nursing Management
Nursing Implementation
n
n
Ambulatory and Home Care
Explore alternative methods of ADLs
Encourage patient to sit while
performing activities
Coordinated walking
Nursing Management
Nursing Implementation
Ambulatory and Home Care
Slow, pursed-lip breathing
After exercise, wait 5 minutes before
using -adrenergic agonist MDI
Nursing Management
Nursing 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
Nursing Management
Nursing Implementation
Ambulatory and Home Care
Sleep
Nasal saline sprays
Decongestants
Nasal steroid inhalers
Long-acting theophylline
Decreases bronchospasm and airway obstruction
Nursing Management
Nursing Implementation
Ambulatory and Home Care
Psychosocial considerations
Guilt
Depression
Anxiety
Social isolation
Denial
Dependence
Use relaxation techniques and support groups
Nursing Management
Nursing Implementation
Ambulatory and Home Care
Discourage moving to places above 4000
ft.