Copd

Copd
By- Dr. Akshita (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
.

• → Nose—warms the air breathed in and filters out
bacteria and debris. Nasal breathing is important for
best lung function.
• ↓ Pharynx—is an oval fibro-muscular sac located
behind the nasal cavity, mouth, and larynx, it is
passageway that conducts air from the nose to the
voice box. The pharynx also conducts food from the
mouth to the esophagus, the tube that leads to the
stomach. It is approx. 12to 14 cm long. It opens into
the nasal cavity (nasopharynx), mouth (oral pharynx)
and larynx (laryngopharynx).

-The nasopharynx is a continuation of the nasal
cavities . It lies behind the nose and above the soft
palate.
-The oral pharynx extends from the soft palate to
the epiglotis It opens into the mouth anteriorly
through the oropharyngeal isthmus.
-The laryngopharynx lies behind the larynx and
extends from the epiglotis above to the inlet of
the esophagus.

• ↓ Larynx—The larynx is a complex structure
composed of cartilages and cords moved by
sensitive muscles. It acts as a sphincteric valve
with its rapid closure, preventing food, liquids,
and foreign objects from entering the airway.
It controls airflow, and at times closes so that
thoracic pressure may be raised and the upper
airways cleared by a propulsive cough when
the larynx opens. Expiratory airflow vibrates
as it passes over the contracting vocal chords,
producing the sounds used for speech.

• ↓ Trachea—windpipe. The trachea is a semi-rigid,
cartilaginous tube approximately 10 to II cm long
and 2.5 cm wide. It lies infront of the esophagus,
descending with a slight inclination to the right
from the level of the cricoid cartilage.It travels
behind the sternum into the thorax to the sternal
angle (opposite the fifth thoracic vertebra), where
it divides to form the right and left main-stem
bronchi.

• ↓ Bronchi—two tubes that lead from the trachea to the
lungs. The bronchi divide into many smaller airways,
called bronchioles. The bronchi of the airways continue to
divide until there are approximately 23 generations .
- The main, lobar, and segmental bronchi are made up of
the first four generations.
-The sub segmental bronchi extend from the fifth to the
seventh generation.

-The terminal bronchioles extend from the twelfth
to the sixteenth generation.
-The respiratory bronchioles extend from the
seventeenth to the nineteenth generation.
-They are considered a transitional zone between
bronchioles and alveoli. Alveolar ducts extend
from the twentieth to the twenty-second
generation.
-The twenty-third generation of air passages is
called alveolar sacs. They are essentially the same
as alveolar ducts, except that they end as blind
pouches.

• ↓ Lungs—Two lungs, each covered with its otherwise
free in the thoracic cavity.
-The lungs are light, soft spongy organs, pleurae-the
visceral pleura and the parietal pleura-lie within the
thoracic cavity.
-Each lung is attached to the heart and the trachea by its
root and the pulmonary ligament. It is whose color
darkens with age as they become impregnated with
inhaled dust

-They are covered with the visceral pleura, a
thin, glistening serous membrane that covers
all surfaces of the lung.
- Each lung has an apex, base, arid three
surfaces (costal, medial, and diaphragmatic).
-There are also three borders (anterior, inferior,
and posterior). Each lung is divided by fissures
into separate lobes

• In the right lung the oblique fissure separates the lower
lobe from the middle, whereas the horizontal fissure
separates the upper lobe from the middle. The right lung is
heavier and wider than the left lung. It is also shorter
because of the location of the right lobe of the liver.
• The left lung is divided into upper and lower lobes by the
oblique fissure. It is longer and thinner than the right lung,
because the hem1 and pericardium are located in the left
thorax.
• The lungs are connected to the upper airways by the
trachea and main-stem bronchi.

• ↓ Alveoli—millions of tiny air sacs in the lungs,
surrounded by tiny blood vessels called capillaries.
This is where the exchange of oxygen and carbon
dioxide takes place. These sacs look like bunches of
grapes.
• → Pleura—a membrane that covers the lungs and
helps them move freely.

MOVEMENTS OF THE THORAX
• The frequency of movement of the bony thorax
joints is greater than that of almost any other
combination of joints in the body.
• Two types of movements have been described-the
pump-handle movement and the bucket-handle
movement.
• The upper ribs are limited in their ability to move.
Each pair swings like a pump handle, with elevation
thrusting the sternum forward. This forward
movement increases the anteroposterior diameter
and the depth of the thorax and is called the pump-

• In the lower ribs, there is little antero-
posterior movement. During inspiration, the
ribs swing outward and upward, each pushing
against the rib above during elevation. This
bucket handle movement increases the
transverse diameter of the thoracic cage.
• Thus during inspiration, the thorax increases
its volume by increasing its anteroposterior
and transverse diameters.

Inspiration
• Inspiration- is an active movement involving the
contraction of the diaphragm and intercostals.
Additional muscles may come into play during
exertion in health. The accessory muscles
include the sternocleidomastoids, scalenes,
serratus anterior, pectoralis major and minor,
trapezius, and erector spinae

Expiration
• Expiration is a passive process, occurring
when the intercostals and diaphragm relax.
Their relaxation allows the ribs to drop to
their pre-inspiratory position and the
diaphragm to rise. These activities compress
the lungs, raising intra thoracic pressure
above atmospheric pressure, and thereby
contributing to air flow out of the lungs.

Respiratory muscles (anteriorly)

Respiratory muscles(posteriorly)

MUSCLES OF RESPIRATION
Diaphragm
• The diaphragm is the principal muscle of respiration.
During quiet breathing, the diaphragm contributes
approximately two thirds of the tidal volume in the
sitting or standing positions, and approximately three
fourths of the tidal volume in the supine position. It is
also estimated that two thirds of the vital capacity in
all positions is contributed by the diaphragm. The
diaphragm is a large, dome-shaped muscle that
separates the thoracic and abdominal cavities.

• This large muscle can be divided into right and left halves.
Each half is made up of three parts-sternal, lumbar, and
costal.
• These three parts are inserted into the central tendon,
which lies just below the heart. The sternal part arises from
the back of the xiphoid process and descends to the central
tendon.
• The position of the diaphragm and its range of movement
vary with posture, the degree of distention of the stomach,
size of the intestines, size of the liver, and obesity.
• The average movement of the diaphragm in quiet
respiration is 12.5 mm on the right and 12 mm on the left.
This can increase to a maximum of 30 mm on the right and
28 mm on the left during increased ventilation.

• Each half of the diaphragm is innervated by a
separate nerve-the phrenic nerve on that side.
• Contraction of the diaphragm increases the
thoracic volume vertically and transversely. The
central tendon is drawn down by the diaphragm
as it contracts. As the dome descends, abdominal
organs are pushed forward, as far as the
abdominal walls will allow.
• When the dome can descend no farther, the
costal fibers of the diaphragm contract to
increase the thoracic diameter of the thorax.

Intercostals
• The external intercostals extend from the
tubercles of the ribs, above, down, and forward
to the costochondral junction of the ribs below,
where they become continuous with the anterior
intercostal membrane.
• There are 11 external intercostal muscles on
each side of the sternum.
• They are thicker posteriorly than anteriorly, and
thicker than the internal intercostal muscles.
• They are innervated by the intercostal nerves,
and contraction draws the lower rib up and out
toward the upper rib. This action increases the
volume of the thoracic cavity.

• There are also 11 internal intercostals per
side.
• These are considered primarily expiratory in
function. Studies have shown that the
intercartilaginous or parasternal portion of the
internal intercostals contracts with the
external intercostals during inspiration to help
elevate the ribs.
• Besides their respiratory functions, the
intercostal muscles contract to prevent the
intercostal spaces from being drawn in or
bulged out during respiratory activity.

• Contraction of the interosseous portions of
the intercostals depresses the ribs and may
aid in forceful exhalation. This muscle is
innervated by the adjacent intercostals
nerves.

Sternocleidomastoid
• The sternocleidomastoids (SCMs) are strong neck muscles
arising from two heads, one from the manubrium and one
from the medial part of the clavicle.
• These two heads fuse into one muscle mass that is inserted
behind the ear into the mastoid process.
• It is innervated by the accessory nerve and the second
cervical nerve.
• There are two of these muscles, one on each side of the
neck.

• When one SCM contracts, it tilts the head toward the
shoulder of the same side and rotates the face toward
the opposite shoulder.
• If the two SCM muscles contract together, they pull the
head forward into flexion. When the head is fixed, they
assist in elevating the sternum, increasing the
anteroposterior (AP) diameter of the thorax.
• The SCMs are the most important accessory muscles
of inspiration. Their contractions can be observed in all
patients during forced inspiration and in all patients
who are dyspneic. These muscles become visually
predominant in patients who are chronically dyspneic.

Scalenes
• The anterior, medial, and posterior scalenes are three
separate muscles that are considered as a functional
unit.
• They are attached superiorly to the transverse
processes of the lower five cervical vertebrae and
inferiorly to the upper surface of the first two ribs.
• They are innervated by related cervical spinal nerves.
• These muscles are primarily supportive neck muscles,
but they can assist in respiration through reverse
action. When their superior attachment is fixed, the
scalenes act as accessory respiratory muscles and
elevate the first two ribs during inspiration.

Serratus Anterior
• The serratus anterior arises from the outer
surfaces of the first eight or nine ribs.
• It curves backward, forming a sheet of muscle
that inserts into the medial border of the scapula.
• It is innervated by the long thoracic nerve
(cervical nerves CS, C6, and C7).
• There are two of these muscles, one on each side
of the body. Normally, they assist in forward
pushing of the arm (as in boxing or punching).
When the scapulae are fixed, they act as
accessory respiratory muscles and elevate the
ribs to which they are attached.

Pectoralis Major
• The pectoralis major is a large muscle arising from the
clavicle, the sternum, and the cartilages of all the true ribs.
•
• This muscle sweeps across the anterior chest to insert into
the intertubercular sulcus of the humerus.
• It is innervated by the lateral and medial pectoral nerves
and cervical nerves CS, C6, C7, C8, and T1.
• There are two of these muscles, one on each side of the
body.

• This muscle acts to rotate the humerus
medially and to draw the arm across the
chest.
• In climbing and pull-ups, it draws the trunk
toward the arms.
• In forced inspiration when the arms are fixed,
it draws the ribs toward the arms, thereby
increasing thoracic diameter.

Pectoralis Minor
• The pectoralis minor is a thin muscle originating
from the outer surfaces of the third, fourth, and
fifth ribs near their cartilages.
• It inserts into the coracoid process of the
scapula.
• It is innervated by the pectoral nerves (cervical
nerves C6, C7, and C8).

• There are two of these muscles, one on each side of
the body.
• They contract with the serratus anterior to draw the
scapulae toward the chest.
• During deep inspiration, they contract to elevate the
ribs to which they are attached.

Trapezius
• The trapezius consists of two muscles that form a diamond-shaped
sheet extending from the head down the back and out to both
shoulders .
• Its upper belly originates from the external occipital protuberance
and curves around the side of the neck to insert into the posterior
border of the clavicle.
• The middle part of the muscle arises from a thin diamond-shaped
tendinous sheet, the supraspinous ligaments and the spines o f the
upper thoracic region, and runs horizontally to insert into the
spine of the scapula.
• Its lower belly arises from the supraspinous ligaments and the
spines of the lower thoracic region, and runs upward to be
inserted into the lower border of the spine of the scapula.

• This large muscle is innervated by the external or
spinal part of the accessory nerve and cervical
nerves C3 and C4.
• Its main function is to rotate the scapulae in
elevating the arms and to control their
gravitational descent.
• It also braces the scapulae and raises them, as in
shrugging the shoulders. Its ability to stabilize the
scapulae makes it an important accessory muscle
in respiration. This stabilization enables the
serratus anterior and pectoralis minor to elevate
the ribs.

Erector Spinae
• The erector spinae is a large muscle extending
from the sacrum to the skull.
• It originates from the sacrum, iliac crest, and
the spines of the lower thoracic and lumbar
vertebrae.
• It separates into a lateral iliocostalis, an
intermediate longissimus, and a medial spinalis
column. This muscle mass inserts into various
ribs and vertebral processes all the way up to
the skull.

• It is innervated by the related spinal nerves.
• These muscles extend, laterally flex, and rotate
the vertebral column.
• They are considered accessory respiratory
muscles through their extension of the vertebral
column.
• In deep inspiration, these muscles extend the
vertebral column, allowing further elevation of
the ribs

Rectus Abdominis
• The rectus abdominis rises from the pubic
crest and extends upward to insert into the
xiphoid process and the costal margin of the
fifth, sixth, and seventh costal cartilages .
• It is innervated by related spinal nerves, and
its action is considered within the context of
the other abdominal muscles.

Obliqus Extenus Abdominis
• This muscle arises in an oblique line from the fifth
costal cartilage to the twelfth ribs. Its posterior fibers
attach in an almost vertical line with the iliac crest.
The other fibers extend down and forward to attach
to the front of the xiphoid process, the linea alba,
and below with the pubic symphysis.
• It is innervated by the lower six thoracic spinal
nerves.

Obliquus Intemus Abdominis
• This muscle originates from the lumbar fascia, the
anterior two thirds of the iliac crest, and the
lateral two thirds of the inguinal ligament. Its
posterior fibers run almost vertically upward to
inselt into the lower borders of the last three ribs.
The other fibers join an aponeurosis attached to
the costal margin above, the linea alba in the
midline and the pubic crest below.
• It is innervated by the lower six thoracic nerves
and the first lumbar spinal nerves.

Transversus Abdominis
• The transversus abdominis arises from the inner
surface of the lower six costal cartilages, the lumbar
fascia, the anterior two thirds of the iliac crest, and
the lateral one third of the inguinal ligament .
• It runs across the abdomen horizontally to insert into
the aponeurosis extending to the linea alba.
• It is innervated by the lower six thoracic nerves and
the first lumbar spinal nerves.

Pulmonary Volumes
and Capacities
1. The tidal volume is the volume of air inspired or expired
with each normal breath; it amounts to about 500
milliliters in the adult male.
2. The inspiratory reserve volume is the extra volume of air
that can be inspired over and above the normal tidal
volume when the person inspires with full force; it is
usually equal to about 3000 milliliters.

3. The expiratory reserve volume is the maximum extra
volume of air that can be expired by forceful
expiration after the end of a normal tidal expiration;
this normally amounts to about 1100 milliliters.
4.The residual volume is the volume of air remaining in
the lungs after the most forceful expiration; this
volume averages about 1200 milliliters.
5.The inspiratory capacity equals the tidal volume plus
the inspiratory reserve volume. This is the amount of
air (about 3500 milliliters) a person can breathe in,
beginning at the normal expiratory level and
distending the lungs to the maximum amount.

6. The functional residual capacity equals the
expiratory reserve volume plus the residual
volume. This is the amount of air that remains in
the lungs at the end of normal expiration (about
2300 milliliters).
7.The vital capacity equals the inspiratory reserve
volume plus the tidal volume plus the expiratory
reserve volume. This is the maximum amount of
air a person can expel from the lungs after first
filling the lungs to their maximum extent and
then expiring to the maximum extent (about4600
milliliters).

8. The total lung capacity is the maximum
volume to which the lungs can be expanded
with the greatest possible effort (about 5800
milliliters); it is equal to the vital capacity plus
the residual volume.
• All pulmonary volumes and capacities are
about 20 to 25 per cent less in women than in
men, and they are greater in large and athletic
people than in small and asthenic people.

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
tracheobronchial 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 (increased Reid
index) and goblet cell hyperplasia (Mitchell, 1968; Reid,
1960; Stoller and Wiedemann, 1990). Mucous cell
metaplasia of bronchial epithelium results in a
decreased number of cilia. Cilliary dysfunction and
disruption of the continuity of the mucous blanket are
common. In the peripheral airways, bronchiolitis,
bronchiolar narrowing, and increased amounts of
mucus are observed (Cosio, 1978; Wright, 1992).

• The fact that smokers secrete an abnormal
amount of mucus makes them susceptible to
respiratory infections, and it takes them
longer to recover from these infections. 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 (Dornhorst,
1955; Filley et ai, 1968; Fishman, 1988; Nash,
Briscoe, and COUl·nand, 1965).
• 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
(Rochester and Brown, 1976).

• 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 ox ygen (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 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.

• Centriacinar or 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 ALPHAj-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 normal mucocilliary transport system is
ineffective because years of smoking destroy
the cilia, reduce their number, and alter their
configuration and orientation; thus their
function is correspondingly obliterated or
impaired.
• In addition, these patients are unable to
generate high transpulmonary pressures and
forced expiratory flow rates because of altered
respiratory mechanics. Consequently,
coughing maneuvers are weak and ineffective.

• 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 (Fig.

• Pulmonary function tests show a decreased vital
capacity, FEY" maximum voluntary ventilation
and a greatly reduced diffusing capacity.
• The total lung capacity is increased, while the
residual volume and functional residual capacity
are even more increased.
• Arterial blood gases reflect a mildly or
moderately lowered Pao2, a normal or slightly
raised Paco2 and a normal pH.
• These patients, unlike patients with chronic
bronchitis, normally will develop heart failure in
the end stage of the disease

CARDIO-RESPIRATORY ASSESSMENT
DEMOGRAPHIC DATA
• Name:
• Gender:
• Address:
• Marital status:
• Religion:
• Occupation:
• Date of assessment:

• Occupation: Note the patient’s present job
and, if he is retired,
• whether this was premature due to ill-health. Note
should be made if there has been any exposure to
asbestos or coal dust (as these can cause fibrosing
lung disease later in life), or if the patient has worked
in a bakery or on a farm (as yeasts and spores can
produce allergic responses).

•CHIEF COMPLAINTS:
- always in patients
language

• The six key symptoms/complaints of
respiratory disease are:
● chest pain (that may be extended to chest
sensations)
● dyspnoea/ breathlessness
● cough
● wheeze
● sputum production
● haemoptysis.

• Present medical history
Breathlessness –
Description of onset
o Date
o Time
o Type : sudden/gradual
Setting
o Cause
o Circumstances
o Activities surrounding onset

Severity
o How bad it is
o How it affects activities of daily living
Frequency
o How often
Duration
o How long
o Constant/intermittent
Course
o Better/worse/same

Associated symptoms
o Sweating
o Cough
o Chest discomfort
Aggravating factors
o Position/weather/temperature/anxiety/exercise
Reliving factors
o Position/hot/cold/rest

During the status of episode
o Can you continue to do what you were doing
o Do you have to sit down or lie down
o Can you continue to speak
Do the attack cause your lips or nail bed to turn blue

• Social history:
• Note the type of living accommodation and
whether there are stairs to encounter: whether
there is dampness; and how far he lives from
shops and social amenities. The patient should be
asked Whether he has pets - as there may be an
allergy problem; and about his hobbies, as the
physiotherapist may be able to advise on suitable
breathing patterns for gardening or swimming,
etc., each depending on the patient’s disability.

• Family history: If there is a history of allergy,
such as hay fever or skin problems, the
patient should be asked whether there is any
relevant family history.
• If the patient is married, note the health of
the spouse.
• Smoking habits: The patient must be
questioned carefully as to how many
cigarettes are smoked, whether they are
home-made and, if he has given up, when he
did so.

• Past medical history : Note any operations,
accidents or illnesses such
• as rheumatic fever which can cause heart
problems; pulmonary
• tuberculosis which leaves scarring and
possible cavities (apparent on
• the chest radiograph); whooping cough and
measles which can cause
• bronchiectasis through plugging of the small
airways.

• Past medical history
Surgeries & hospitilisation
o Injuries & accidents
o Immunization
o Allergies
o Medications

• Personal history :
History of smoking - Yes/no
• Types of tobacco
• How old when the patient begin smoking
• How many years the patient smoked
• How many cigarettes smoked each day
• Any variation in smoking habits
• Any attempt to stop smoking
• Date when the patient last smoked
• Pack year:

History of alcohol intake - yes/no
• How old when the patient started alcohol
• How many years the patient consumed
• How many pegs each day
• Any variation in alcoholic habits
• Any attempt to quit alcohol
• Date when the patient last taken

Subjective evaluation of
cardinal symptoms

Chest pain
• Ask about the onset, character, severity, duration,
radiation, and any previous history of chest pain.
• A history of chronic pleuritic chest pain going back
several months or years could indicate an inflammatory
disorder resulting in pleurisy. This can occur in a variety
of collagen vascular disorders but is a relatively rare
cause of pleuritic chest pain.
• Chest pain that is dull and persistent in one area, and
especially if it is keeping the patient awake at night,
could indicate a malignant process within the chest
that is affecting the chest wall. Such pains have usually
been going on for weeks or more and get progressively
worse, and may or may not be augmented by palpation
of the chest.

Chest pain
o Location
o Onset
o Date
o Time
o Type Sudden/gradual
o Pattern
o Frequency : How
o Severity
o Recurrence
o Duration How long it lasts
o Constant or intermittent
o Course :better/worse/staying the same

Provoked symptoms(aggravating factors)
o Breathing
o Positions :Lying flat/side lying
o Movement with arms
o Rest/exercise
o Sleeping/stress/after eating
o Stress/anxiety

Quality
• Dull/ aching/pin prickling/throbbing/knife
like/sharp/constricting/sticking/burning/shooting
Radiating
Referred
Relieving factors
• Rest
• Positions
• Analgesics
• Antacids
• Hot
• cold

Severity
• How it affects ADL
• VAS scale
Associated symptoms
• Coughing/breathlessness/palpitations/
hemoptysis /vomiting/ leg
pain/weakness/muscle fatigue
Time frame
• Acute/chronic

Dyspnoea
• Dyspnea, breathlessness or shortness of breath, can be
defined as the sensation of difficulty in breathing
• If there has been an increase in breathlessness, does
it vary with position or change of position and has it
affected the patient’s lifestyle?
• Analysis of dyspnoea should be approached in a similar
way to that of chest pain, so ask about severity,
duration, onset, precipitating factors, and previous
history. It is absolutely crucial to ask about the onset.
Ask the patient what they were doing at the time when
the breathlessness started in order to get some idea as
to how sudden the onset was.

Types of dyspnea
• Restrictive dyspnea
• Obstructive dyspnea
• Cardiac dyspnea
• Psychogenic dyspnea
• Acute dyspnea
• Chronic dyspnea
• Recurrent dyspnea
• Progressive dyspnea
• Paroxysmal dyspnea
• Episodic dyspnea
• Inspiratory dyspnea
• Expiratory dyspnea
• Orthopnea one P / Two P/ Three P
• Treopnea
• Platypnea
• PND

• Orthopnoea: How many pillows does the
patient require in order to sleep or he
comfortably? (This may influence the choice
of starting position for the treatment session.)
If the patient suffers from paroxysmal
nocturnal dyspnoea which may be caused by
slipping down the bed, the physiotherapist
can suggest types of back rest or, perhaps,
seek advice from the occupational therapist.

Paroxysmal Nocturnal Dyspnea
• Paroxysmal nocturnal dyspnea (PND) is an
important type of shortness of breath. This
symptom has strong predictive value as a sign of
CHF (Hurst, etai, 1990). The patient usually falls
asleep in the recumbent position, and 1 or 2
hours later, awakens from sleep with acute
shortness of breath.
• The patient sits upright on the side of the bed or
goes to an open window to breathe "fresh air" to
get relief from shortness of breath.

• The mechanism of PND is the transfer of fluid
from extravascular tissues into the bloodstream
(or intravascularly) during sleep (Constant, 1993).
The intravascular volume of fluid gradually
increases until the compromised left ventricle can
no longer manage it. The left atrial pressure rises
when the rate of lymphatic drainage from the
lungs is unable to keep up with the increased
volume of tluid. The increased atrial pressure
leads to a sufficiently elevated pulmonary
capillary pressure to produce interstitial edema.
Patients who are light sleepers awaken early with
dyspnea.

Platypnea
• Platypnea is the onset of dyspnea when assuming
the sitting position from the supine position
(Sharf, 1989).
• This unusual phenomenon is often found in
patients with basilar pulmonary fibrosis or basilar
arteriovenous malformation.
• It can be related to the redistribution of blood
flow to the lung bases in the sitting position with
resultant ventilation-perfusion mismatching and
hypoxemia.

Trepopnea
• Trepopnea refers to dyspnea in one lateral position but
not the other (Snider, 1994). It is often produced by
unilateral respiratory system pathology such as lung
disease, pleural effusion, or airway obstruction.
• It also is commonly seen in patients with mitral
stenosis (Constant, 1993). Occasionally it may be the
result of a fall in blood pressure in the left lateral
decubitus position.
• If the patient has ischemic heart disease, the reduction
in coronary perfusion can cause either angina or
dyspnea.

Breathlesnes
Description of onset
o Date
o Time
o Type : sudden/gradual
Setting
o Cause
o Circumstances
o Activities surrounding onset

American Thoracic Society Dyspnea
Scale
GRADE DEGREE
0 NONE Not troubled with
breathlessness except with
strenuous exercise
1 SLIGHT Troubled by shortness of
breath when hurrying on
the level or walking up a
slight hill
2 MODERATE Walks slower than people
of the same age on the
level because of
breathlessness or has to
stop for breath when
walking at own pace on the
level

GRADE DEGREE
3 SEVERE Stops for breath after
walking about 100 yards or
after a few minutes on the
level
4 VERY SEVERE Too breathless to leave the
house or breathless when
dressing or undressing

visual analogue scale
No breathlessness
Greatest Breathlesness
• The visual analogue scale
is a vertical line of 100
mm in length.
• The patient is asked to
make a mark along this
line that represents his
level of breathlessness.
• The distance of the
patient's mark above zero
represents the
measurement of dyspnea

• During the status of episode
• Can you continue to do what you were doing
• Do you have to sit down or lie down
• Can you continue to speak
• Do the attack cause your lips or nail bed to
turn blue

Tick the activities disturbed by breathlessness
o Climbing stairs ( ) if yes how many steps
o Walking ( ) if yes how much distance
o Bathing ( )
o Toileting ( )
o Dressing ( )
o Combing ( )
o Shopping ( )
o Grooming ( )
o Speaking ( )
o Any other activities
• Exposure to the patients with tuberculosis
• Exposure to asbestos/sand blasting/pigeon feeding

Wheeze:
• Ask whether this has increased recently. Is it so bad as to
be audible from the foot of the bed?
• a wheeze is a musical note generated from the lungs that
may be a single note (monophonic wheeze) or multiple
different notes (polyphonic wheeze).
• Ask about the onset, duration and periodicity of wheeze.
Wheeze that occurs more at night and first thing in the
morning, and that may be exacerbated by exercise, is
suggestive of asthma and COPD. A pronounced variation in
the severity of wheeze (worse at night and in the morning
compared to daytime) is more suggestive of asthma, but by
no means excludes COPD.

Cough
• Cough is the commonest symptom that is associated
with pure respiratory disease. The function of cough is
to expel unwanted elements from the respiratory tract;
that includes both foreign elements and substances
generated by the host. Thus cough is a prominent
feature of upper respiratory infections, inhalation of
irritants such as dusts and chemicals, as a result of
lower respiratory infections, and the result of
accumulation of products within lung (e.g. in
pulmonary oedema). In addition to this, cough
receptors within the lung can be stimulated as happens
in interstitial lung disease or in endobronchial
sarcoidosis.

A quick guide to the causes of chronic cough
(more than 6 months)
Asthma Worse at night/early morning
History of chest heaviiness as a child
Family history of atopy
Relief by salbutamol (not always)
Copd Longstanding smoking
Chronic bronchitis
Rhinosinusitis Tickly, irritating cough
Post-nasal drip sensation
History of sinusitis – frontal headache,
nasal discharge
History of recurrent rhinitis – nasal
discharge and blockage
Gastro-oesophageal
reflux
Tickly, irritating cough
Acid reflux symptoms
Response to proton pump inhibitor

Laryngeal
hypersensitivity
Tickly, irritating cough
Voice disturbance
Cough precipitated by talking
No nocturnal symptoms
Vigorous cough
Unresponsive to medication
other Includes lung cancer, bronchiectasis,
interstitial lung disease, eosinophilic
bronchitis
Requires specialist investigation

Characteristics of sputum production
in relation to diagnosis
Characteristic Likely Diagnosis
Acute onset, purulent sputum,
clearing after 1–3 weeks
Acute bronchitis
Pneumonia
Regular sputum production,
more than a half egg-cupful,
varying in purulence
Bronchiectasis
Occasionally chronic bronchitis
‘Chronic productive cough for
more than 3 months in each of
2
consecutive years...’
Medical Research Council
criteria for definition of chronic
bronchitis

Clear or slightly opaque
sticky sputum, white
yellow or green
Asthma
Colour of purulent
sputum and organism
Lime green – Haemophilus influenzae
‘Rusty’ – Streptococcus pneumoniae
Dark green – Pseudomonas aeruginosa
Foul smell and taste Chronic pulmonary sepsis with cavities in
the lung
Infection from rotting teeth and
associated gum disease

Description
• Mucoid /mucopurulent/purulent/blood tinged
• GRADES
Color
• Clear/colorless like egg
white/black/brownish/frothy white/pink/sand
• Greenish/red jelly/rusty/
Consistency
• Thin/thick/viscous/tenacious/frothy

Quantity
• Scanty/ teaspoon / cup /copious /pint or
more
Time of the day
• Morning/evening
Odor

Associated symptoms
• Hemoptysis
• Hoarseness
• Voice changes
• Dizziness/fainty syncope
• Head ache
• Altered sensorium
• Ankle swelling
• Cyanosis

Hemoptysis
Amount : clot/massive
Odor
Color
Appearance
Acute/chronic

Frequency
Streaky/Non streaky/FROTHY BLOOD TINGED
Associated symptoms
o Warmth
o Bubbling sensation
o With chest pain/dyspnea
o WITHOUT COUGHING
o Nausea/vomit/cough

Constitutional symptoms
• Fever
• Excessive sweating
• Loss of appetite
• Nausea
• Vomiting
• Weight loss
• Fatigue
• Weakness
• Exercise intolerance
• Altered sleep pattern

Objective assessment
• Height:
• Weight:
• BMI:
• Clinical presentation:
• o General appearance: cardiopulmonary
distress/anxiety/pain
• o Awake /alert(conscious)/attentive/comprehensive

• Body type:
-Ectomorphic/endomorphic/mesomorphic
• Vital signs:
o Temperature
o Pulse rate
o Respiratory rate
o Blood pressure
• Pulse Rhythm:
o regular,
o regularly irregular, bigeminy or trigeminy
o irregularly irregular if yes
• check heart rate ___

Inspection & observation
• HENT (head, eyes, nose, and throat)
Head
 Facial expression
Forehead
Eyes-PERRLA
Eyes-Sclera clear/muddy,palor,ictrus
Eyelid -ptosis
Nose –nasal flaring
Lips- Cyanosis Lips-Pursed lip breathing

Neck
Position of trachea: midline/right/left
Jugular venous pressure:
normal/increased/markedly increased
Use of accessory muscles- SCM/PMi/Tr
 Prominence of accessory muscles
 Trail sign
Tracheal tug or oliver sign

Thorax
 COPD Posture: rounded shoulders, protruded neck,
kyphosis, outstretched hands
 AP:T Ratio: 5:5/5:6/5:7 barrel chest: present/absent
 Chest wall deformities: Pectus carinatum/Pectus
excavatum/ kyphosis/ scoliosis/ kyphoscoliosis
 Type of breathing: rapid/shallow/deep
 Effort of breathing: minimal on inhalation and passive
on exhalation
 Pattern of breathing: Thoraco abdominal/abdomino
thoracic
 Abnormal breathing pattern: Apnea/Biot’s//Cheyne-
stokes/ Kussmauls/ paradoxical/ asthmatic/flail chest

 Labored Breathing signs:
• Intercostals indrawing/retractions
• Supra clavicular indrawing
• Sub costal indrawing
• Hoovers sign
• Harrisons sulcus

• Abdomen: abdominal paradox
Extremities
• Upper limb
o Clubbing: schamroth window test___,
grade___,clubbing index__
o Cyanosis:
o Nicotine stain:
o Capillary filling time:
o Tremor
• Lower limb
• oedema

Palpation
o Tracheal position –
o Subcutaneous emphysema –
o Tenderness on accessory muscles –
o Palpation of lymph nodes: axillary /cervical/supraclavicular-
o Symmetry: symmetrical/asymmetrical -
• Upper zone
• Middle zone
• Lower zone

o Tactile Vocal fremitus
Upper zone
Middle zone
Lower zone
o Tactile rhonchial fremitus –
o Percussion -
• Type of note: resonant/hyper resonant/ stony
dullness/woody dullness
• Level of right border
• Level of left border
• Level of heart border
• Level of diaphragmatic excursion

o Pedal oedema -
• Pitting/non pitting
• Grade
• Level or extent of oedema
• o Peripheral skin temperature

Auscultation
• Quantity of breath sound-
• Quality of breath sound –
• Added sound-
o Inspiration : early/mid /late, fine/coarse
o Expiration : wheeze/rhonchi
• Vocal resonance:
whispering pectoriloquy,aegophony

• Chest expansion-
Upper zone
Middle zone
Lower zone

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 at Pa02 < 8 kPa (60 mmHg; Leach and
Treacher, 1 998). Bronchodilators reduce airflow obstruction
in two-thirds of patients with chronic disease, thereby
reducing hyperinflation and possibly breathlessness (Tantucci
et ai., 1 99 8) , but should be used according to need because
continuous use can worsen lung function (Huib, 1 999).
• 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

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.

• The primary interventions for maximizing
cardiopulmonary function and oxygen transport
in patients with chronic bronchitis include some
combination of education, aerobic exercise,
strengthening exercises, chest wall mobility
exercises, range of motion, body positioning,
breathing control and coughing maneuvers,
airway clearance techniques, relaxation, 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.

• The use of supplemental oxygen depends on
the severity of the disease. Some patients
have no need for supplemental oxygen, some
need it only during exercise, and some
patients require continuous oxygen with
proportionately more delivered during activity
and exercise compared with rest.
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).

• Education is a principal focus of the long-term
management of the patient with chronic bronchitis.
Education includes the reinforcement of preventative
health practices (e.g., smoking reduction and
cessation, cold and flu prevention, flu shots, aerobic
exercise, strengthening exercises, nutrition, weight
control, hydration, pacing of activities, energy
conservation, relaxation, and stress management).
• Chronic bronchitis and emphysema are often
associated with sleep disturbances. Obstructive sleep
apnea is increasingly prevalent with disease severity.
Thus activity and sleep patterns need to be assessed to
ensure sleep is maximally restorative and is not
contributing to the patient's symptoms.

• Aerobic exercise is an essential component of
the long-term management of the patient
with chronic bronchitis to optimize the
efficiency of oxygen transport overall and
mobilize and remove secretions (Oldenburg,
Dolovich, Montgomery, and Newhouse, 1979).

• Physical therapy is one component of a
comprehensive rehabilitation program in the
long-term management of emphysema.
• Such a program also needs to include
information on health promotion and
maintenance, ongoing review and log of
medications, respiratory support (e.g., oxygen
aerosol therapy, and mechanical ventilatory
support),

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