2. COPD
Definition - a disease state characterized by
airflow limitation that is not fully reversible
COPD includes.
Emphysema - an anatomically defined condition
characterized by destruction and enlargement of
the lung alveoli.
Chronic bronchitis- a clinically defined
condition with chronic cough and mucus.
Small airways disease - a condition in which
small bronchioles are narrowed.
3. COPD is present only if chronic airflow
obstruction occurs; chronic bronchitis
without chronic airflow obstruction is not
included within COPD .
EPIDEIMOLOGY
fourth leading cause of death in US
affects >16 million persons in US
GOLD estimates suggest that COPD will
rise from the sixth to the third most
common cause of death worldwide by
2020.
5. Natural History
.The effects of cigarette smoking on
pulmonary function appear to depend on
– The intensity of smoking exposure
– Timing of smoking exposure during growth
– The baseline lung function of the individual
.Genetic factors likely contribute to the level
of pulmonary function achieved during
growth and to the rate of decline in
response to smoking and potentially to
other environmental factors as well.
7. Pathophysiology(2)
Airflow Obstruction
-Persistent reduction in forced expiratory
flow rates .reduced FEV1
.reduced ratio of FEV1/FVC
Hyperinflation
-Increases in the residual volume and the
residual volume/total lung capacity ratio
Gas Exchange
-Non uniform distribution of ventilation
-Ventilation-perfusion mismatching
9. Clinical Presentation
History
Risk factors
Cough, sputum production, and exertional dyspnea
Symptoms for months or years before seeking
medical attention
Activities involving significant arm work, particularly
at or above shoulder level, are particularly difficult
for patients with COPD
Activities that allow the patient to support the arms
and use accessory muscles of respiration are better
tolerated
Worsening dyspnea on exertion is the principal
feature of advanced COPD
10.
11. Physical Findings
Early stages of COPD:
Normal physical examination
Current smokers - signs of active smoking
( an odor of smoke or nicotine staining of
fingernails ).
12. severe disease :
Prolonged expiratory phase and
expiratory wheezing
Signs of hyperinflation ( a barrel chest
and enlarged lung volumes with poor
diaphragmatic excursion)
Use of accessory muscles of respiration,
sitting in the characteristic "tripod"
13. Advanced disease:
Systemic wasting - significant weight loss,
and diffuse loss of subcutaneous adipose
tissue .
Paradoxical inward movement of the rib
cage with inspiration (Hoover's sign)
Signs of overt right heart failure.
14. Laboratory Findings
Arterial blood gases and oximetry
Hematocrit – Secondary polycythemia
Pulmonary function testing
-reduction in FEV1 and FEV1/FVC
-lung volumes may increase, resulting in
an increase in total lung capacity,
functional residual capacity, and residual
volume
19. Management of COPD
• Desired outcomes
▫ prevent disease progression
▫ relieve symptoms
▫ improve exercise tolerance
▫ improve overall health status,
▫ prevent and treat exacerbations,
▫ prevent and treat complications, and
▫ reduce morbidity and mortality
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20. Non-pharmacologic Therapy
Avoidance of risk factors -
– smoking cessation
– reduction of indoor pollution
– reduction of occupational e
Pulmonary Rehabilitation
Lung Volume Reduction Surgery (LVRS)
Lung Transplantation
Influenza vaccination
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21. Pharmacologic Therapy
A. Bronchodilators
Central to the symptomatic management
Prescribed on an as needed or on a regular basis to prevent or
reduce symptoms.
ß2-agonists, anticholinergics, and methylxanthines
used singly or in combination
Long-acting bronchodilators are more effective and
convenient than treatment with short-acting bronchodilators.
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22. ß2-agonists
• Cause relaxation of bronchial smooth
muscle and bronchodilation
• Improve mucociliary clearance
▫ short-acting agents (4 – 6 hrs)
Albuterol, levalbuterol, and terbutaline , salbutamol
▫ long-acting (dosed every 12 hours)
Formoterol and salmeterol
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23. Anticholinergics
Produce bronchodilation by competitively
inhibiting cholinergic receptors in bronchial
smooth muscle
Ipratropium bromide: slower onset
Tiotropium bromide: long acting
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24. Combination of Anticholinergics and ß2-
agonists
• Used when the disease progresses and symptoms
worsen over time
• Allows use of the lowest effective doses and
reduces adverse effects from individual agents
• albuterol and ipratropium (Combivent) is available
as an MDI for chronic maintenance therapy of
COPD.
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25. Methylxanthines
produce bronchodilation by:
– inhibition of phosphodiesterase
– inhibition of calcium ion influx into smooth muscle,
– prostaglandin antagonism,
– stimulation of endogenous catecholamines,
– adenosine receptor antagonism, and
– inhibition of release of mediators from mast cells and
leukocytes
Theophylline and aminophylline
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26. Theophylline
Not used as first-line therapy
– Risk for drug interactions and the inter-
patient variability in dosage requirements
– Used for patients who are intolerant or
unable to use an inhaled bronchodilator
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27. B. Corticosteroids
Anti-inflammatory mechanisms
▫ reduction in capillary permeability to decrease mucus,
▫ inhibition of release of proteolytic enzymes from
leukocytes, and
▫ inhibition of prostaglandins
• chronic, systemic corticosteroids should be avoided
if possible
▫ To decrease adverse effects
• Appropriate situations to consider corticosteroids
▫ Short term systemic use for acute exacerbations
▫ inhalation therapy for chronic stable COPD
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28. • Several studies have shown an additive
effect with the combination of inhaled
corticosteroids and long-acting
bronchodilators.
• Combination therapy with salmeterol plus
fluticasone or formoterol plus budesonide is
associated with greater improvements in
FEV1, health status, and exacerbation
frequency than either agent alone.
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29. Therapy at Each Stage of COPD
III: Severe
II: Moderate
I: Mild
FEV1/FVC < 70%
FEV1 > 80%
predicted
FEV1/FVC < 70%
50% < FEV1 < 80%
predicted
FEV1/FVC < 70%
30% < FEV1 <
50% predicted
FEV1/FVC < 70%
FEV1 < 30%
predicted
or FEV1 < 50%
predicted plus
chronic respiratory
failure
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
treatments
IV: Very Severe
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30. Treatment Of COPD Exacerbation
Desired Outcomes
Prevention of hospitalization or reduction
in length of hospital stay,
Prevention of acute respiratory failure and
death,
Resolution of symptoms,and a return to
baseline clinical status and quality of life.
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31. Non-pharmacologic Therapy
Oxygen therapy should be considered for
any patient with hypoxemia
– Noninvasive positive-pressure ventilation
(NPPV): using a face or nasal mask
– Intubation and mechanical ventilation
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32. Pharmacologic Therapy
• Bronchodilators
▫ Increased dose and frequency of bronchodilators
are used in exacerbation
▫ Short-acting β2-agonists are preferred
rapid onset of action.
▫ Anticholinergic agents may be added if symptoms
persist despite increased doses of β2-agonists.
• Corticosteroids
▫ Short course of IV or oral corticosteroids
▫ If treatment is continued for longer than 2 weeks, a
tapering oral schedule should be employed to
avoid hypothalamic-pituitary-adrenal axis
suppression.
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33. • Antimicrobial Therapy
▫ Most exacerbations of COPD are thought to be caused by
viral or bacterial infections
▫ Antibiotics should be initiated if at least two of the following
three symptoms are present:
Increased dyspnea
Increased sputum volume
Increased sputum purulence(prsence of pus)
• Selection of empiric antimicrobial therapy should be
based on the most likely organisms.
▫ Haemophilus influenzae,
▫ Moraxella catarrhalis,
▫ Streptococcus pneumoniae, and
▫ H. parainfluenzae.
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34. • Therapy should be initiated within 24 hours and continued for
at least 7 to 10 days
• For uncomplicated exacerbations recommended therapy
includes:
▫ a macrolide (azithromycin, clarithromycin)
▫ second- or third-generation cephalosporin, or doxycycline
▫ Trimethoprim-sulfamethoxazole: an increasing pneumococcal
resistance.
▫ Amoxicillin and first- generation cephalosporins : β-lactamase
susceptibility.
▫ Erythromycin: insufficient activity against H. influenzae.
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35. Complicated exacerbations
– If drug-resistant pneumococci, β-lacta-mase-
producing H. influenzae and M. catarrhalis
amoxicillin/clavulanate
fluoroquinolone
– Pseudomonas aeruginosa
a fluoroquinolone with enhanced pneumococcal
and P. aeruginosa activity (levofloxacin)
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36. Acute exacerbations
– white blood cell count, vital signs, chest x-ray,
and changes in frequency of dyspnea, sputum
volume, and sputum purulence
In more severe exacerbations, arterial
blood gases and oxygen saturation should
also be monitored
Patient adherence to therapeutic
regimens, side effects, potential drug
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