Copd

By- Dr. Akshita Juneja (PT)

MPT-Cardiopulmonary

D.C.PT
Certified BLS & ACLS
 INTRODUCTION
OBSTRUCTIVE LUNG DISEASE
• Several abbreviations can be found in the
literature for a pulmonary disorder characterized
by increased airway resistance, particularly
noticeable by a prolonged forced expiration.
• Some of these are chronic obstructive pulmonary
disease (COPD), chronic obstructive airway
disease (COAD), chronic airway obstruction
(CAO), and chronic obstructive lung disease
(COLD).
• Chronic obstructive pulmonary disease (COPD) is a
generic term that refers to lung diseases that result
in air trapping in the lungs, causing hyperinflation of
the lungs, and a barrel-chest deformity.

• There are two entities in COPD namely-

(i) Chronic Bronchitis
(ii) (ii) Emphysema
.
 Chronic
Bronchitis
 Chronic Bronchitis
• Chronic bronchitis is a
disease of the airways. It is
characterized by excess
mucus secretion and
productive cough. The
cough is called a smokers'
cough in the early stages but
once mucus production has
been excessive for 3 months
a year for over 2 years, this
becomes the inadequate but
traditional definition of
chronic bronchitis.
• Cigarette smoking is the most important risk factor in
the development of chronic bronchitis.

• The cause of chronic bronchitis is believed to be

related to long-term irritation of the trachea-bronchial
tree.
• The most common cause of irritation is cigarette
smoking.
• Repeated inhalation of tobacco smoke irritates the
sensitive lining of the airways, leading to inflammation,
mucus hyper secretion and sometimes bronchospasm.
Inflammation is the key process. It causes narrowing
first in the distal small airways and then in the proximal
large airways.
• Inhaled cigarette smoke stimulates the goblet cells and
mucous glands to secrete more mucus. This smoke also
inhibits cilliary action. The hyper secretion of mucus
and impaired cilia lead to a chronic productive cough.

• Pathologically, there is an increase in the size of the

tracheo-bronchial mucous glands and goblet cell
hyperplasia (an increase in the number of cells in an
organ or tissue). Mucous cell metaplasia of bronchial
epithelium results in a decreased number of cilia.
• In the peripheral airways, bronchiolitis, bronchiolar
narrowing, and increased amounts of mucus are
observed.
• In addition, the irritation of smoke in the
tracheo-bronchial tree causes broncho-
constriction.
• Although smoking is the most common cause
of chronic bronchitis, other agents that have
been implicated are air pollution, bronchial
infections, and certain occupations.
 Characterstics

1)Excess mucus secretion and productive cough, excessive for

3 months a year for over 2 years.

2)Stocky in build and dusky in color.

3)The patient exhibits significant use of accessory muscles of

respiration.

4)Wheezing may be audible or noted by auscultation.

5)Intercostal or sternal retraction of the chest wall may be

noted.
6)Edema in the extremities, particularly around the ankles, and
neck vein distention reflect decompensated right heart
failure.

7)The patient may report that breathing difficulty began with

increased amounts of secretions (with a change in their
normal color), which is often difficult to expectorate, and
increased cough productivity.

8)Pao2 is reduced, Paco2 increased, and pH reduced.

9) Pulmonary function tests may indicate reduced vital

capacity, FEV1, maximum voluntary ventilation, and diffusing
capacity and increased FRC and residual volume.
• These patients are referred to as "blue
bloaters,“ because they usually have stocky
body build and are "blue" as a result of
hypoxemia
• Although many of these patients have a high
arterial partial pressure of carbon dioxide
(Pac02), the pH is normalized by renal retention
of bicarbonate (HC03).
• In the patient with chronic bronchitis, bone
marrow tries to compensate for chronic
hypoxemia by increased production of red
blood cells, leading to polycythemia.
• Polycythemia, in turn, makes the blood more
viscous, forcing the heart to work even harder to
pump it. Long-term hypoxemia leads to
increased pulmonary artery pressure and right
ventricular hypertrophy.
• Individuals with bronchitis often expectorate
mucoid brownish-colored sputum.
• In an exacerbation, usually from infection, they
have an even greater amount of purulent
sputum.
• Ventilation-perfusion abnormalities are common,
which increase hypoxemia and Paco2 retention
• The respiratory rate increases, as does the use of
accessory muscles. The resultant increased work
of breathing requires greater oxygen consumption
by these muscles, with a greater production of
carbon dioxide (C02) than the respiratory system
can adequately meet. This contributes to a further
drop in the arterial partial pressure of oxygen
(Pao2) and a rise in Paco2.

• The hypoxemia and acidemia increase pulmonary

vessel constriction, which raises pulmonary artery
pressure and ultimately leads to right heart failure
(cor pulmonale).
Emphysema
 Emphysema
• Emphysema is the second most prevalent disease
within the category of COPD.
• It is primarily a disease of alveoli and smallest
airways, with secondary effects on other airways.
• It is usually caused by damage to the alveoli from
smoking.
• There are following types of emphysema :-
1) Centrilobular Emphysema
2) Paraseptal emphysema
3)Panlobular Emphysema
Normal Alveoli VS Alveoli with Emphysema
 Centrilobular emphysema

• Centrilobular emphysema is characterized by

- Destruction of the respiratory bronchiole.
-Edema
-Inflammation
-Thickened bronchiolar walls.
• These changes are more common and more
marked in the upper lobes and superior
segments of the lower lobes.
• Centrilobular emphysema involves the
enlargement and destruction of the first- and
second-order respiratory bronchioles, and the
alveoli remain intact (mainly the respiratory
Bronchioles).
• This form of emphysema is found more often
in men than in women, is rare among
nonsmokers, and is common among patients
with chronic bronchitis.

Male > Females

 Paraseptal emphysema
• Paraseptal emphysema involves the periphery
of the secondary lobule along the septum.
• Paraseptal emphysema is not typically
associated with the progression of end-stage
COPD but can be associated with an increased
risk of pneumothorax (PTX)
 Pan lobular emphysema

• Pan lobular emphysema, on the other hand, is

characterized by destructive enlargement of the
alveoli, distal to the terminal bronchiole.
• It most often involves the lower lobes.
• This type of emphysema is also found in subjects
that have ALPHA-ANTITRIPSIN deficiency.
• Airway obstruction in these individuals is caused
by loss of lung elastic recoil or radial traction on
the bronchioles.
• When individuals with normal lungs inhale,
the airways are stretched open by the
enlarging elastic lung, and during exhalation
the airways are narrowed as a result of the
decreasing stretch of the lung.
• However, the lungs of patients with
panlobular emphysema have decreased
elasticity because of disruption and
destruction of surrounding alveolar walls. This
in turn leaves the bronchiole unsupported and
vulnerable to collapse during exhalation.
• Bullae, emphysematous
spaces larger than 1 cm in
diameter, may be found in
patients with emphysema.
• It is thought that bullae
develop from a coalescence
of adjacent areas of
emphysema or an
obstruction of the
conducting airways that
permits the flow of air into
the alveoli during inspiration
but does not allow air to flow
out again during expiration.
• This causes the alveoli to become hyperinflated and
eventually leads to destruction of the alveolar walls
with a resultant enlarged air space in the lung
parenchyma. These bullae can be more than 10 cm in
diameter, and by compression, can compromise the
function of the remaining lung tissue .

• If this happens, surgical intervention to remove the

bulla is often necessary.

• Pneumothorax, a serious complication, can result

from the rupture of one of these bullae.
• The principal pathophysiological deficits include
irreversible alveolar damage resulting from loss of
elastic recoil and the normal tethering of the alveoli,
which renders the lung parenchyma excessively
compliant and floppy. Excessive distension and
dilatation of the terminal bronchioles and destruction
of alveoli reduces the surface area for gas exchange.

• Hence diffusing capacity is correspondingly reduced.

The dead space in the lungs and total lung capacity
increase significantly. Breathing at normal tidal volume,
the patient's airways close beyond that which normally
• In its non acute, chronic stages the primary
problems include inadequate and inefficient gas
exchange resulting from the structural damage to
the lungs and altered respiratory mechanics of
the lungs, chest wall, and their interaction. The
lungs are - hyperinflated, the chest wall
becomes rigidly fixed in a hyperinflated position,
the normal bucket handle and pump handle
motions of the chest wall are impaired, the hemi
diaphragms are flattened, the mediastinal
structures are shifted, and the heart is displaced
and rotated, making its function inefficient
• The emphysema patient's most common complaint
is dyspnea.

• Physically, these patients appear thin and have an

increased anteroposterior chest diameter.

• Typically, they breathe using the accessory muscles

of inspiration. These patients are often seen leaning
forward, resting their forearms on their knees or
sitting with their arms extended at their sides and
pushing down against the bed or chair to elevate
their shoulders and improve the effectiveness of
the accessory muscles of inspiration.
• They may breathe through pursed lips during the
expiratory phase of breathing. These patients
have been referred to as "pink puffers" because
of the increased respiratory work they must do to
maintain relatively normal blood gases.

• On auscultation, decreased breath sounds can be

noted throughout most or all of the lung fields.

• Radiologically, the emphysema patient has

overinflated lungs, a flattened diaphragm, and a
small, elongated heart.
 Medical
Management
 EMPHYSEMA
• Treatment of progressive emphysema that
requires hospitalization often includes IV
fluids, antibiotics, and low-flow oxygen
(Snider, Faling, and Rennard, 1994). Some of
these patients also receive bronchodilators,
corticosteroids, diuretics, and digitalis.
Pursed-lip breathing can relieve dyspnea and
improve arterial blood gasses (Muller, Petty,
and Filley, 1970;Petty and Guthrie, 1974).
• Emphysema is associated with a prolonged
history of smoking and chronic bronchitis and
indicates significant irreversible lung damage. A
less common type of emphysema not associated
with smoking is alpha-antitrypsin deficiency.
• Antitrypsin is essential in balancing elastin
production and degradation and in preserving
optimal lung parenchymal compliance.
• A deficiency of antitrypsin reduces lung elasticity
and contributes to the characteristic increase in
lung compliance that is the hallmark of
emphysema.
• Oxygen therapy can reduce hypoxaemia and some of its
effects, such as oedema (Howes et ai., 1 995).

• Long-term oxygen reduces mortality for patients with

persistent hypoxaemia .
• Bronchodilators reduce airflow obstruction in two-thirds
of patients with chronic disease, thereby reducing
hyperinflation and possibly breathlessness (Tantucci et ai.,
1 99 8) (Huib, 1 999). , but should be used according to
need because continuous use can worsen lung function.
• Combination therapy with different classes of
bronchodilator may be the most beneficial approach
(Manning, 2000). A quarter of patients respond to
theophylline (Mahon, 1 999).
• Steroids have been advised for exacerbations but in the
chronic state they reduce airways obstruction in only
10% of patients, and continued use is associated with
myopathy (Davies et ai., 1 9 99). However, individuals
vary and should be individually assessed (Yildiz, 2000).

• Drug assessment should include quality of life scores,

peak flow monitoring and sequential testing of different
bronchodilators, steroids, combinations and various
delivery systems .

• Short-term reversibility studies should not be substituted

for long-term assessments.
• Inhalers are indicated for acute and chronic disease
unless nebulizers are objectively found to be more
effective (BTS, 1 997). Some patients respond to· drugs
for breathlessness .

• Many COPD patients have disturbed sleep, for which the

hypnotic drug zolpidem has been found to be beneficial
without affecting oxygenation, ventilation or physical
performance (Girault et at., 1 996). Severe exacerbations
may indicate the need for non-invasive (Poponick, 1 999)
or invasive ventilation. Severe chronic emphysema may
indicate the need for surgery, varying from laser ablation
of giant bullae to lung volume reduction
 Physical
Therapy
Management
 Principles of physical therapy management

The goals of long-term management for the patient with

chronic bronchitis include the following:-

• Maximize the patient's quality of life, general health, and

well-being and hence physiological reserve capacity.

• Educate about chronic bronchitis, self-management, effects

of smoking, nutrition, weight control, smoking reduction or
cessation, other lifestyle factors, medications, infection
control, and role of a rehabilitation program.
• Facilitate mucociliary transport.
• Optimize secretion clearance.
• Optimize alveolar ventilation.
• Optimize lung volumes and capacities and flow
rates.
• Optimize ventilation and perfusion matching
and gas exchange.
• Reduce the work of breathing.
• Reduce the work of the heart
• Maximize aerobic capacity and efficiency of
oxygen transport.
• Optimize physical endurance and exercise
capacity.
• Optimize general muscle strength and
thereby.
• peripheral oxygen extraction.
 TREATMENT
• Education,
• Aerobic exercise,
• Strengthening exercises,
• Chest wall mobility exercises,
• Range of motion,
• Body positioning,
• Breathing control and
• Coughing maneuvers,
• Airway clearance techniques,
• Activity pacing, and
• Energy conservation.
• An ergonomic assessment of the patient's work and home
environments may be indicated to minimize oxygen demand and
energy expenditure in these settings.
• Supplemental oxygen
Supplemental oxygen is not usually required
until lung damage becomes extreme (i.e., the
morphological changes are consistent with the
irreversible changes associated with
emphysema).
THANK
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