Chronic Obstructive

Pulmonary Disease ( COPD)

• COPD is a disease state characterized by
the presence of airflow obstruction due to
chronic bronchitis or emphysema

• The airflow obstruction is generally

progressive, may be accompanied by
airway hyper-reactivity, and may be
partially reversible

• Most patients with COPD have features of

both emphysema and chronic bronchitis
COPD
 Chronic bronchitis

• It is a clinical diagnosis

• Defined by excessive secretion of bronchial

mucus

• Manifested by daily productive cough occuring

on most days for at least 3 consecutive
months or more in at least 2 consecutive
years
 Emphysema

• It is a pathologic diagnosis

• Denotes abnormal permanent

enlargement of air spaces distal to the
terminal bronchiole, with destruction of
their walls and without obvious fibrosis
 Etiology
Cigarette smoking
• The most important cause of COPD

• Nearly all smokers suffer an accelerated

decline in lung function that is dose- and
duration-dependent

• Fifteen percent develop progressively

disabling symptoms in their 40s and 50s

• It is estimated that 80% of patients seen for

COPD have significant exposure to tobacco
smoke
 Other Exposures
• Combination of exposures to
environmental tobacco smoke
• Occupational dusts and chemicals
• Indoor air pollution from biomass
fuel used for cooking and heating
in poorly ventilated buildings
• Outdoor air pollution
• Airway infection
• Familial factors
• Allergy
 Hereditary factors
• Deficiency of α 1-antiprotease

Other Factors
• Low socioeconomic status
• Maternal smoking
• Low birth weight
 Pathogenesis
• Enlargement of mucous secreting gland and
increased number of goblet cells contribute to
enhanced secretion of airway mucous that manifests
as chronic bronchitis

• Loss of elastic tissue, inflammation and fibrosis in

airway wall result in premature airway closure, gas
trapping and dynamic hyperinflation leading to
changes in pulmonary and chest wall compliance

• Excessive lysis of elastin and other structural

proteins in the lung matrix by elastase and other
proteases derived from lung neutrophils,
macrophages, and mononuclear cells causes
destruction of alveoli and appearance of emphysema
Emphysematous dysfunction
in COPD
 Clinical Findings
Symptoms and Signs
• Patients with COPD characteristically present in
the fifth or sixth decade of life

• Complaining of excessive cough, sputum

production, and shortness of breath

• Symptoms have often been present for 10 years or

more

• Dyspnea is noted initially only on heavy exertion,

but as the condition progresses it occurs with mild
activity. In severe disease, dyspnea occurs at rest
• A hallmark of COPD is frequent
exacerbations of illness that result in
absence from work and eventual disability

• Pneumonia, pulmonary hypertension, cor

pulmonale, and chronic respiratory failure
characterize the late stage of COPD

• Death usually occurs during an

exacerbation of illness in association with
acute respiratory failure
• Clinical findings may be completely
absent early in the course of COPD

• As the disease progresses, two

symptom patterns tend to emerge,
historically referred to as "pink puffers"
and "blue bloaters"
• They represent pure forms of
emphysema and bronchitis

• Most COPD patients have pathologic

evidence of both disorders
 Patterns of disease in
advanced
Type A: Pink
COPD.
Type B: Blue
Puffer Bloater
(EmphysemaPredomi (BronchitisPredominant
nant) )
History •Major complaint is dyspnea, •Major complaint is chronic
often severe cough, productive of
and mucopurulent sputum, with
•Usually presenting after age
physical frequent exacerbations due to
50 chest infections
examinati •Cough is rare, with scant •Often presents in late 30s and
on clear, mucoid sputum 40s
•Patients are thin, with recent •Dyspnea usually mild, though
weight loss common patients may note limitations to
•They appear uncomfortable, exercise
with evident use of accessory •Patients frequently overweight
muscles of respiration and cyanotic but seem
•Chest is very quiet without comfortable at rest
adventitious sounds •Peripheral edema is common
•No peripheral edema •Chest is noisy, with rhonchi
invariably present; wheezes are
 Type A: Pink Puffer Type B: Blue
(EmphysemaPredominan Bloater (Bronchitis
t) Predominant)

Laborato •Hemoglobin usually •Hemoglobin

ry normal (12–15 g/dL) usually elevated
studies •PaO2 normal to (15–18 g/dL)
slightly reduced (65– •PaO2 reduced
75 mm Hg) but SaO2 (45–60 mm Hg)
normal at rest and PaCO2 slightly
•PaCO2 normal to to markedly
slightly reduced (35– elevated (50–60
40 mm Hg) mm Hg)
•Chest radiograph •Chest radiograph
shows hyperinflation shows increased
with flattened interstitial
diaphragms markings ("dirty
lungs"), especially
 Chest film. Chronic Bronchitis
Irregular bronco-vascular markings as sign of
chronic inflammation of the walls of the bronchi.
 Emphysema
p.a. and lateral:
- Hypertransparency
of lung fields,
- straightened
vascular markings
- The peripheral zone
in the p.a. chest film
where one can see
no vessels
- Small, droplet-
shaped heart, barrel
chest,
- widened intercostal
spaces,
- sudden transition of
wide central
pulmonary arteries to
small vessels.
Unilateral emphysema
Chronic Bronchitis
 Type A: Pink Type B: Blue
Puffer Bloater
(Emphysema (Bronchitis
Predominant) Predominant)
Pulmonary •Airflow •Airflow
function obstruction obstruction
tests ubiquitous ubiquitous
•Total lung •Total lung
capacity capacity
increased, generally
sometimes normal but may
markedly so be slightly
•DLCO reduced increased
•Static lung •DLCO normal
compliance •Static lung
increased compliance
normal
Special Type A: Pink Type B: Blue
evaluations Puffer (Emphysema Bloater (Bronchitis
Predominant) Predominant

V/Q Increased ventilation to Increased perfusion to

high V/Q areas, ie, high low V/Q areas
matching dead space ventilation.

Hemodynami Cardiac output normal to Cardiac output normal.

slightly low. Pulmonary Pulmonary artery
cs artery pressures mildly pressures elevated,
elevated and increase sometimes markedly so,
with exercise and worsen with exercise

Nocturnal Mild to moderate degree Severe oxygen

of oxygen desaturation desaturation, frequently
ventilation not usually associated associated with
with obstructive sleep obstructive sleep apnea.
apnea.

Exercise Increased minute Decreased minute

ventilation for level of ventilation for level of
ventilation oxygen consumption. oxygen consumption.
PaO2 tends to fall, PaCO2 PaO2 may rise; PaCO2
 Investigations
Laboratory Findings
Spirometry:

• Pulmonary function tests early in the course of COPD

reveal only evidence of abnormal closing volume and
reduced midexpiratory flow rate

• Reductions in FEV1 and in the ratio of forced expiratory

volume to vital capacity (FEV1% or FEV1/FVC ratio) occur
later

• In severe disease, the FVC is markedly reduced

• Lung volume measurements reveal a marked increase in

residual volume (RV)

• Increase in total lung capacity (TLC), Elevation of the

RV/TLC ratio, indicative of air trapping, particularly in
emphysema
 Arterial blood gas
measurements
• Arterial blood gas measurements characteristically
show no abnormalities early in COPD other than an
increased A–a–DO2

• They are necessary if

• (1) hypoxemia or hypercapnia is suspected
• (2) the FEV1 is < 40% of predicted
• (3) there are clinical signs of right heart failure

• Hypoxemia occurs in advanced disease, particularly

when chronic bronchitis predominates

• Compensated respiratory acidosis occurs in patients

with chronic respiratory failure, particularly in chronic
bronchitis, with worsening of acidemia during acute
exacerbations.
 Examination of the
sputum
• Examination of the sputum may reveal
Streptococcus pneumoniae, H
influenzae, or Moraxella catarrhalis

• Positive sputum cultures are poorly

correlated with acute exacerbations,
and research techniques demonstrate
evidence of preceding viral infection in
a majority of patients with
exacerbations.
 ECG
• The ECG may show sinus tachycardia, and in
advanced disease, chronic pulmonary
hypertension may produce electrocardiographic
abnormalities typical of cor pulmonale

• Supraventricular arrhythmias (multifocal atrial

tachycardia, atrial flutter, and atrial fibrillation)
and ventricular irritability also occur
 Imaging
• Radiographs of patients with chronic bronchitis
typically show only nonspecific peribronchial
and perivascular markings

• Plain radiographs are insensitive for the

diagnosis of emphysema; they show
hyperinflation with flattening of the diaphragm
or peripheral arterial deficiency in about half of
cases

• Parenchymal bullae in the setting of either of

these findings are diagnostic of emphysema

• Doppler echocardiography is an effective way

to estimate pulmonary artery pressure if
pulmonary hypertension is suspected
Emphysema
Centrilobular emphysema. CT
scan
Paraseptal emphysema. CT scan,
magnified view
 Differential Diagnosis
• Bronchial asthma
• Bronchiectasis
• Cystic fibrosis
• Bronchopulmonary mycosis
• Central airflow obstruction
 Complications
• Acute bronchitis, pneumonia, pulmonary
thromboembolism, and concomitant left ventricular
failure may worsen otherwise stable COPD

• Pulmonary hypertension, cor pulmonale, and chronic

respiratory failure are common in advanced COPD

• Spontaneous pneumothorax occurs in a small

fraction of patients with emphysema. Hemoptysis
may result from chronic bronchitis or may signal
bronchogenic carcinoma.
 Prevention
• COPD is largely preventable through elimination of
long-term exposure to tobacco smoke

• Smokers with early evidence of airflow limitation can

alter their disease by smoking cessation. Smoking
cessation slows the decline in FEV1 in middle-aged
smokers with mild airways obstruction

• Vaccination against influenza and pneumococcal

infection may also be of benefit
 Treatment
Ambulatory Patients
Smoking cessation
• The single most important
intervention in smokers with COPD is
to encourage smoking cessation
• Nicotine transdermal patch, nicotine
gum, and bupropion increase
cessation rates in motivated smokers
 Oxygen therapy
• The only drug therapy that is documented to
improve the natural history of COPD is
supplemental oxygen in those patients with
resting hypoxemia

• Survival in hypoxemic patients with COPD treated

with supplemental oxygen therapy is directly
proportionate to the number of hours per day
oxygen is administered

• Oxygen by nasal prongs must be given at least 15

hours a day unless therapy is intended only for
exercise or sleep
• Arterial blood gas analysis is used to
guide initial oxygen therapy

• Hypoxemic patients with pulmonary

hypertension, chronic cor pulmonale,
erythrocytosis, impaired cognitive
function, exercise intolerance, nocturnal
restlessness, or morning headache are
particularly likely to benefit from home
oxygen therapy

• For most patients, a flow rate of 1–3

L/min achieves a PaO2 greater than 55
mm Hg
 Bronchodilators
• Bronchodilators are the most important agents in the
pharmacologic management of patients with COPD

• Bronchodilators offer some patients improvement in

symptoms, exercise tolerance, and overall health
status

• Aggressiveness of bronchodilator therapy should be

matched to the severity of the patient's disease

• In patients who experience no symptomatic

improvement, bronchodilators should be
discontinued.
• The two most commonly prescribed bronchodilators:

• Anticholinergic ipratropium bromide

• Short-acting β 2-agonists eg, albuterol,

metaproterenol

• Ipratropium bromide is generally preferred to the short-

acting β2-agonists as a first-line agent because of its longer
duration of action and absence of sympathomimetic side
effects
• Typical doses are two to four puffs (36–72 mcg) every 6
hours
• Short-acting β2-agonists are less expensive and have a
more rapid onset of action, commonly leading to greater
patient satisfaction
• At maximal doses, β2-agonists may cause tachycardia,
tremor, or hypokalemia
• Oral theophylline:

• It is a third-line agent in COPD patients who fail

to achieve adequate symptom control with
anticholinergics and β2-agonists

• Sustained-release theophylline improves

arterial oxygen hemoglobin saturation during
sleep in COPD patients and is a first-line agent
for those with sleep-related breathing disorders
 Corticosteroids
• Apart from acute exacerbations, COPD is not
generally a corticosteroid-responsive disease

• Empiric trials of oral prednisone for 14–21

days and inhaled corticosteroids for 6–12
weeks of therapy are common

• The drug should be discontinued unless there

is a 20% or greater increase in FEV1 after the
trial of therapy.
 Antibiotics
• Antibiotics are commonly prescribed to outpatients
with COPD for the following indications:

• (1) to treat an acute exacerbation

• (2) to treat acute bronchitis
• (3) to prevent acute exacerbations of chronic
bronchitis (prophylactic antibiotics)

• Common agents include trimethoprim-

sulfamethoxazole (160/800 mg every 12
hours), amoxicillin or amoxicillin-clavulanate
(500 mg every 8 hours), or doxycycline (100
mg every 12 hours) given for 7–10 days

• Broader spectrum therapy may be indicated in

patients with more severe baseline airflow
obstruction.
 Other measures
• In patients with chronic bronchitis, increased
mobilization of secretions may be accomplished
through the use of adequate systemic
hydration, effective cough training
methods, or use of a hand-held flutter
device and postural drainage, sometimes
with chest percussion or vibration

• Expectorant-mucolytic therapy has generally

been regarded as unhelpful in patients with
chronic bronchitis

• Cough suppressants and sedatives should be

avoided as routine measures.
• Human α 1-antitrypsin:

• It is available for replacement therapy in

emphysema due to congenital deficiency of
α1-antitrypsin

• Patients over 18 years of age with airflow

obstruction by spirometry and levels less than
11 mcmol/L are potential candidates for
replacement therapy

• α1-Antitrypsin is administered intravenously in

a dose of 60 mg/kg body weight
• Graded aerobic physical exercise
programs (eg, walking 20 minutes three
times weekly, or bicycling) are helpful to
prevent deterioration of physical condition
and to improve the patient's ability to carry
out daily activities

• Training of inspiratory muscles

• Pursed-lip breathing to slow the rate of

breathing and abdominal breathing
exercises to relieve fatigue of accessory
muscles of respiration may reduce
dyspnea in some patient
 Hospitalized Patients

Hospitalization is indicated for acute

worsening of COPD that fails to respond
to measures for ambulatory patients

Patients with acute respiratory failure or

complications such as cor pulmonale and
pneumothorax should also be
hospitalized
 Management of the hospitalized
patient with an acute exacerbation of
COPD includes:

• Supplemental oxygen
• Inhaled ipratropium bromide
• Inhaled 2-agonists
• Broad-spectrum antibiotics
• Corticosteroids
• Chest physiotherapy
• Theophylline should not be initiated in the acute setting,
but patients taking theophylline prior to acute
hospitalization should have their theophylline serum
levels measured and maintained in the therapeutic
range

• Oxygen therapy should not be withheld for fear of

worsening respiratory acidemia; hypoxemia is more
detrimental than hypercapnia

• Cor pulmonale usually responds to measures that

reduce pulmonary artery pressure, such as
supplemental oxygen and correction of acidemia

• Cardiac arrhythmias, particularly multifocal atrial

tachycardia, usually respond to aggressive treatment of
COPD itself. Atrial flutter may require DC cardioversion
after initiation of the above therapy

• If progressive respiratory failure ensues, tracheal

intubation and mechanical ventilation are necessary
 Surgery for COPD
Lung transplantation
• Requirements for lung transplantation are severe
lung disease, limited activities of daily living,
exhaustion of medical therapy, ambulatory
status, potential for pulmonary rehabilitation,
limited life expectancy without transplantation,
adequate function of other organ systems, and a
good social support system

• Substantial improvements in pulmonary function

and exercise performance have been noted after
transplantation
 Lung volume reduction
surgery
• Lung volume reduction surgery (LVRS), or reduction
pneumoplasty, is a surgical approach to relieve dyspnea
and improve exercise tolerance in patients with
advanced diffuse emphysema and lung hyperinflation

• Bilateral resection of 20–30% of lung volume in selected

patients results in modest improvements in pulmonary
function, exercise performance, and dyspnea
 Bullectomy

• Bullectomy is an older surgical procedure for

palliation of severe dyspnea in patients with
severe bullous emphysema

• In this procedure, the surgeon removes a

very large emphysematous bulla that
demonstrates no ventilation or perfusion on
lung scanning and compresses adjacent
lung that has preserved function

• Bullectomy can now be performed with a

CO2 laser via thoracoscopy
 Prognosis
• The outlook for patients with clinically
significant COPD is poor

• The median survival of patients with severe

COPD (FEV1 1 L) is about 4 years

• The degree of pulmonary dysfunction (as

measured by FEV1) at the time the patient
is first seen is probably the most important
predictor of survival