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COLLEGE OF

PHYSICAL AND
RESPIRATORY THERAPY
S.Y. 2016-2017

This written report on

Chronic Obstructive Pulmonary Disease


(COPD)
Is submitted to the
COLLEGE OF PHYSICAL THERAPY AND RESPIRATORY THERAPY
In partial fulfillment to the requirements on the subject
SEMINAR I

SUBMITTED TO:
Mr. Bernardo Tayaban Jr., PTRP, MDA
Ms. Eliza Pinlac, PTRP

SUBMITTED BY:

JOANNA EDEN GURTIZA

Novemeber 11, 2016

Defnition of Terms

The British Thoracic Society guidelines define


chronic obstructive pulmonary disease
(COPD) as a chronic slowly progressive
disorder
characterized
by
airways
obstruction (FEV1 < 80% predicted and
FEV1/VC ratio of < 70%) which does not
change markedly over several months. In
contrast to the airflow obstruction produced
by asthma, airflow obstruction due to COPD
is largely fixed.
Chronic bronchitis is characterized by a
chronic cough with excessive mucus
production that is not due to known specific
causes,
such
as
bronchiectasis
or
tuberculosis, and that is present for most
days of at least 3 months of the year for two
or more consecutive years.
Chronic bronchitis is defined as a cough
productive of sputum for 3 months in a year
for at least 2 consecutive years, in the
absence of other diseases recognized to
cause sputum production.
Emphysema is defined, pathologically, as a
condition
characterized
by
irreversible
dilatation of the air spaces distal to the
terminal bronchiole with destruction of the
alveolar walls, and without fibrosis.
Emphysema consists of several diseases that
ultimately result in permanent overdistension
of the air spaces distal to the terminal
nonrespiratory bronchioles accompanied by
destruction of the alveolar walls and without
obvious fibrosis. Abnormal air spaces, called
bullae and blebs, may be seen on chest
radiograph when the disease is moderately
advanced.
Emphysema may be classified as:
Panacinar: involves all the alveoli
within the acinus equally (as happens

with alpha-1 antitrypsin deficiency);


commonly affects the lower lobes.
Centriacinar: involves the alveoli near
the respiratory bronchioles (as in
smoking-induced
emphysema);
affects mainly the upper lobes.
Paraseptal: involves the peripheral
alveoli.
Asthma is a chronic inflammatory condition
characterized by airway hyperreactivity to
various external and internal stimuli and
manifested
as
recurrent
episodes
of
intermittent reversible airway obstruction.
Bronchiectasis
is
characterized
by
progressive dilation and destruction of
bronchi and bronchioles. It is usually
localized to a few lung segments or an entire
lobe of one lung, although bilateral diffuse
involvement is also common. Before
antibiotic
therapy
and
immunizations,
bronchiectasis usually developed as a
sequela of a chronic necrotizing pulmonary
infection, but now it occurs most often in
patients with underlying systemic disorders
on which airway infection is superimposed,
such as primary ciliary dyskinesia, cystic
fibrosis,
allergic
bronchopulmonary
aspergillosis,
and
immune
deficiency.
Although bronchiectasis can be classified
according to the resultant airway deformities
(e.g.,
cylindrical,
varicose,
or
saccular/cystic), there is little clinical or
pathophysiological difference between the
types. The hallmark of bronchiectasis is a
chronic productive cough, often with copious
amounts of mucopurulent sputum.
Cystic fibrosis (CF) is a genetic disorder
characterized by dysfunction of the exocrine
glands,
especially
the
lungs,
where
abnormally thick, tenacious mucus along
with impaired mucociliary and cough
clearance results in chronic pulmonary
infection and progressive lung destruction

GOLD Classification System for Severity of Female smokers are nearly 13 times as
COPD
likely to die from COPD as women who
Stage
0: At risk

Epidemiology
6th leading cause of death globally
Chronic mucus hypersecretion is
present in 20% of male smokers aged
40 years and 40-45% of male smokers
aged 70 years
Women generally report less than
men
Among middle-aged smokers, 14% of
men and 8% of women have chronic
airflow limitation to a degree
compatible to a degree compatible with
the diagnostic label of COPD

I: Mild COPD

II: Moderate COPD

Characteristics
Normal Spirometry
Chronic symptoms (cough,
sputum production)
FEV1/FVC <70%
FEV1 80% predicted
With or without chronic
symptoms (cough, sputum
production)
FEV1/FVC <70%
50% FEV1 <80% predicted
With or without chronic
symptoms (cough, sputum
production)

III: Severe COPD


IV: Very Severe
COPD

never smoked. In 2000, for the first time,


the number of deaths in the United States
from COPD was greater in women than in
men. Male smokers are nearly 12 times
as likely to die from COPD as men who
never smoked.
COPD causes around 30,000 deaths a In 2003, 10.7 million U.S. adults were
year in the UK. Prevalence increases with
estimated to have COPD.3 However, close
age, with 7.3% of males and 3.2% of
to 24 million U.S. adults with active or
females in the UK between 65 and 74
previous smoking histories have evidence
years of age suffering from the condition.
of
obstructive
lung
dysfunction,
One in eight medical admissions to
suggesting that COPD is underdiagnosed.
hospital in the UK are due to an acute
Inhaled tobacco smoke causes airway
exacerbation of COPD, with the disease
and
lung
inflammation.
However,
costing the NHS an estimated 500
clinically overt, progressive COPD does
million a year.
not develop in approximately 60% of
Worldwide, COPD is the fourth leading
patients
with
significant
smoking
histories. As approximately 40% of those
cause of mortality; it is estimated that by
with previous or ongoing tobacco abuse
the year 2020, COPD will be the 5th most
do
not
develop
COPD,
diagnostic
common cause of disability among adults.
spirometry and/or additional pulmonary
COPD is the fourth leading cause of death
function
tests
of
bronchodilator
in subjects >45 years of age in the United
responsiveness,
lung
volume
States and the fourth most frequent
determinations, and diffusion
cause of death worldwide.1,2 Compared
with declining age-adjusted mortality
Schmitz et. Al
rates from 1965 1998 for other major
chronic diseases such as coronary heart
disease
and
stroke,
COPD-related
mortality increased by 163%.
Smoking is the commonest risk factor for
COPD; approximately 80% to 90% of
COPD deaths are caused by smoking.

ANATOMY, PHYSIOLOGY, KINESIOLOGY


ANATOMY OF THE RESPIRATORY
The
thoracic
cage
consists
of
12
thoracic

vertebrae, 12 ribs, the sternum, and costal


cartilage. The respiratory passages, depicted
in Figure 2-1, consist of the upper airways,
including the nose, pharynx, and larynx; and
the lower airways, referred to as the
tracheobronchial tree, containing (a) the
nonrespiratory conducting airways, or the
anatomic dead space (i.e., the trachea,
bronchi, and bronchioles), that channels
inspired air to the gas exchange areas, and
(b) the respiratory units, or acini, where gas
exchange takes place. The two lungs with
their various lobes and segments are
illustrated in Figure 2-2.
The major airways from the trachea
through the 10 generations of bronchi have
decreasing amounts

of cartilaginous support surrounded by


smooth muscle and elastic fibers; they have
goblet cells for mucus production and are
lined with ciliated columnar

Structure and function of primary organs of the respiratory system


Structure
Description
Function
Nose
Paired
mucosal-lined Conduit that filters, warms,
nasal cavities supported
and humidifies air entering
by
bone
and
cartilage.
lungs.
Pharynx
Passageway connecting Conduit for air and food.
Facilitates exposure of
nasal and oral cavities to
immune
system
to
larynx, and oral cavity to
inhaled
antigens.
esophagus.
Subdivisions
naso-,
Larynx
oro-,,
and
Passageway that prevents
laryngopharynx.
food from entering the lower
Connects
pharynx
to
respiratory tract.
trachea.
Trachea
Voice production.
Opening (glottis) is
covered by vocal folds
Cleans, warms, and moistens
or by the epiglottis
incoming air.
during swallowing.
Flexible tube composed
of C-shaped cartilaginous
Bronchial tree
rings that are connected
posteriorly
to
the
Warms
and
moistens
trachealis muscle.
incoming air from trachea to
Divides into the left
alveoli.
and right main stem
Lungs
Smooth
muscle
bronchi
constriction
alters
airflow.
Right and left main stem

Alveoli

Pleurae

bronchi subdivide within


each lung into secondary
bronchi, tertiary bronchi,
and bronchioles, which
contain smooth muscle.
Paired organs located

within pleural cavities of


the thorax.
The right lung has
three lobes and the
left has two lobes.
Microscopic sacs at the
end of bronchial tree

immediately adjacent to
pulmonary capiliaries.
Functional unit of the
lung.
Doubledlayered,
continuous
serous
membrane
lining
the
inside of the thoracic
cavity.
Divided into parietal
pleura (outer) and
visceral
pleura
(inner).

Contains air passageways


dista to main stem bronchi,
alveoli,
and
respiratory
membranes.
Primary gas exchange site.
Surfactant
lines
the
alveoli
to
decrease
surface
tension
and
prevent complete closure
during exhalation.
Produces lubricating fluid
that allows smooth gliding of
lungs within the thorax
Potential
space
between
parietal and visceral pleura.

epithelium
clearance.

to

facilitate

secretion

The five generations of bronchioles


have no cartilage or goblet cells, but
still have elastic tissue and smooth
muscle fibers; they are lined with
ciliated cuboidal epithelium.
The functional unit of the lungs is
the acinus, which participates in gas
exchange. It includes the respiratory
bronchioles, alveolar ducts and sacs,
and the alveoli, whose walls consist
of a thin epithelial layer over a
connective tissue sublayer.

Control Center of Respiration: Pons


and Medulla oblongata
Trachea

Fibroelastic tube kept patent by a


series of U-shaped hyaline cartilages
commences in the neck below the
cricoid cartilage at the level of the
body of 6th cervical vertebra
ends below in the thorax at the level
of the sternal angle (lower border of
the 4th thoracic vertebra) and divided
into the (L) and (R) primary or main
bronchi

Regulation of Respiration
Neural Control of Breathing

Pulmonary Ventilation

process of bringing atmospheric air


into the lungs down to the alveoli sacs
where gas exchange with pulmonary
capillaries can take place
Air nose and/or mouth larynx
trachea (R) and (L) bronchi
bronchioles alveolar sacs
A pressure gradient develops since
blood to alveoli contain more O2 than

CO2 as compared with blood in the


pulmonary capillaries, therefore gas
will diffuse from area of higher
concentration to area of lower
concentration:
O2 from alveoli to capillaries LA
systemic circulation
CO2 from pulmonary capillaries to
alveoli

Voluntary system
o Located in the cerebral cortex
and send impulses to the
respiratory motor neurons via
the corticospinal tracts
Automatic system
o Located in the pons and
medulla, the efferent output of
which is located in the lateral
and ventral portions of the
spinal cord

*Reciprocal inhibition

Impulses in the descending pathways


that excite the agonists also produce
inhibition of the antagonists
Motor neurons to the expiratory
muscles are inhibited when those
supplying the inspiratory muscles are
active, and vice versa

Apneusis

Pneumotaxic center

Medullary centers
2 types of respiratory neurons

I neurons- discharge during inspiration


E neurons- discharge during expiration

Respiratory center

Area in medulla concerned with


respiration
o Dorsal group
Source of rhythmic drive
to the contralateral
phrenic motor neurons
o Ventral group
Cranial division
Ipsilateral
accessory muscles
of inspiration via
vagus nerves
Caudal division
Intercostal muscles

*Paths from these neurons to expiratory


neurons are crossed but those to the
inspiratory neurons are both crossed and
uncrossed
Pontine and Vagal influences

Rhythmic of the I neurons in the


respiratory center is spontaneous, but
is modified by centers in pons and by
afferents in vagus nerves from the
receptors in the lungs

Arrest of respiration in inspiration

Located in pons; nucleus


parabrachialis and Kolliker Fuse
Nucleus
Responsible for the prevention of
Apneusis

Apneustic center

Area in the caudal pons responsible for


Apneusis

*Complete transection of brain below the


medulla stops all respiration
*Transection of brainstem above pons even
with cranial nerves severed, regular
breathing continues
*Additional transection at the inferior pons:
continuous discharge inspiratory neurons
sustained contraction of the inspiratory
muscles
Transection below the pons + intact vagus
regular respiration continues
*Hering Breuer Reflex

Inflation of the lung inhibits inspiratory


discharge

Complete transection of the pons and


medulla +/- vagus (+) respiration (irregular
and gasping but rhythmic)
Pontine respiratory centers

Make rhythmic discharge of the


medullary neurons smooth and regular

Regulation of Respiratory Center Activity

A rise in PCO2 or H+ concentration in


blood or a drop in its PCO2 increases
the level of respiratory center activity,
and changes in the opposite direction
have a slight inhibitory effect

Carotid and Aortic bodies

Respiratory chemoreceptors that


mediate effects of variations in blood
chemistry on ventilation; initiate

impulses that stimulate respiratory


center
Medullary Chemoreceptors

Secondary mediators of ventilation


when the carotid and aortic receptors
are denervated that respond to
increase in PCO2

MUSCLES OF RESPIRATION
The respiratory muscles, their innervations,
and their functions are listed in Table 2-1.
The primary muscles of inspiration are the
diaphragm, external intercostal muscles, and
parasternal intercostals, as depicted in Figure
2-3. During deep or labored breathing, the
accessory muscles of inspiration are
recruited. At rest, expiration is a passive
process, occurring as the inspiratory muscles
relax and lung elastic recoil takes over.
During forced expiration and coughing, the
abdominal and internal intercostal muscles

are activated. Respiratory muscle weakness


and limited endurance can impair gas
exchange
and
lead
to
respiratory
insufficiency or failure, especially when the
mechanics of breathing are altered by
hyperinflation
of
the
chest
(e.g.,
emphysema, chronic bronchitis, and acute
asthma attack).
NERVOUS CONTROL

The lungs and airways are innervated by the


pulmonary plexus (located at the root of
each lung), which is formed from branches of
the sympathetic trunk and vagus nerve.
Sympathetic nervous system stimulation
results
in
bronchodilation
and
slight
vasoconstriction, whereas parasympathetic
nervous
system
stimulation
causes
bronchoconstriction
and
indirect

The pneumotaxic center in the pons limits


the duration of inspiration and increases the
respiratory rate.
Peripheral receptors provide input to the
respiratory center: stretch receptors in the
lungs
act
to
prevent
overinflation;
chemoreceptors located in the carotid and
aortic bodies respond to hypoxemia and, to a
lesser extent, to rising PCO2 and H
concentration; and proprioceptors in the
joints and muscles excite the respiratory
centers in the medulla to increase
ventilation.
Higher centers in the motor cortex are
responsible for voluntary control of breathing
(e.g.,
voluntary
breath
holding
or
hyperventilation)
and
often
stimulate
respiration in anticipation of exercise.
It is now recognized that the distribution of
neural drive is a major determinant of which
regions of the respiratory muscles are
selectively activated and in what manner
under
various
resting
and
exercise
conditions, and thus of the actions they
produce.

vasodilation. The function of the lungs is


controlled through complex interactions of
specialized
peripheral
and
central
chemoreceptors, as well as the respiratory
center with groups of neurons located in the
medulla oblongata and pons, as illustrated in
Figure 2-4.
The respiratory center in the medulla
contain chemosensitive areas that respond
to changes in carbon dioxide levels (PCO2)
and hydrogen ion (H) concentration, while
other areas receive input from the peripheral
chemoreceptors, baroreceptors, and several
types of receptors in the lungs. They control
inspiration and respiratory rhythm both at
rest and during exercise.

RESPIRATORY PHYSIOLOGY

Disturbances in the control of breathing Goblet cells and bronchial seromucous


will result in abnormal blood gas values. glands produce mucus, which contains
immunoglobulin A, to protect underlying
tissue and trap organisms and particles.
Mucus
production
is
increased
by
inflammation (e.g., asthma and bronchitis)
and its composition may be altered by
various diseases (e.g., asthma and cystic
fibrosis).
Cilia are hairlike structures that wave
mucus up to the carina and throat
(mucociliary transport). Mucociliary transport
is impaired by inhalation of toxic gases (e.g.,
cigarette smoke and air pollution), acute
inflammation, infection, and other disease
processes.
Type II pneumocytes produce surfactant,
which protects underlying tissue and repairs
damaged alveolar epithelium.
Alveolar macrophages roam the surface of
the terminal airways and engulf foreign
matter and bacteria. They also kill bacteria in
situ by means of lysozymes. Their activity
can be impeded by cigarette smoke, air
pollution,
alveolar
hypoxia,
radiation,
corticosteroid therapy, and the ingestion of
alcohol.
B lymphocytes produce gamma globulin
for the production of antibodies to combat
BLOOD SUPPLY TO THE LUNGS
lung infections, and T lymphocytes release a
The bronchial arteries arising from the substance that attracts macrophages to the
descending aorta provide blood supply to the site of an infection.
nonrespiratory
airways,
pleurae,
and
connective tissue, while the pulmonary Polymorphonuclear leukocytes engulf and
arteries supply the respiratory units (acini) kill blood-borne gram-negative organisms.
and participate in gas exchange. Numerous
Mast cells, which are more numerous in
pulmonary vasoactive substances can induce
distal airways, release mediators of the
vasoconstriction or vasodilation of the
inflammatory response to alter epithelial and
pulmonary arterioles. Defense of the Lungs
vascular permeability. Smokers and persons
The lungs have a number of structures that
with asthma have greater numbers of mast
serve to protect the lungs from inhaled
cells.
organisms and particles, and they are
assisted by several different types of cells It is important for physical therapists to
that reside within the lungs.
understand the factors that contribute to
normal functioning of the respiratory system
Nasal mucosa and hairs warm and humidify
in order to appreciate normal versus
inhaled air and filter out particles
abnormal physiological indicators, both at

rest and during exercise, as well as the out of the lungs. During exertion, forced
implications
for
physical
therapy expiration, and coughing, active contraction
interventions.
of the expiratory muscles (plus closure of the
glottis during coughing) causes a marked
BASIC FUNCTIONS OF THE RESPIRATORY rise in intrathoracic pressure so that
SYSTEM
expiration
occurs
more
rapidly
and
completely; in addition, passive relaxation of
The basic functions of the respiratory system
these muscles at end-expiration promotes
include oxygenation of the blood, removal of
descent of the diaphragm and induces an
carbon dioxide, control of acidbase balance,
increase in lung volume toward its neutral
and production of vocalization.
resting position.
MECHANICS OF BREATHING

A NUMBER OF FACTORS DETERMINE


Respiratory gas exchange requires the RESPIRATORY FUNCTION
movement of sufficient volumes of air into
Ventilation (V): The process by which air
the terminal airways to meet the oxygen
moves into and out of the lungs.
needs of the body, whether at rest or during
exercise.
This
occurs
through
active Airway resistance (Raw): The resistance to
contraction of the inspiratory muscles with airflow through the airways; increased airway
enough force to override the elastic recoil of resistance can limit airflow, which is most
the lungs and the resistance to airflow noticeable during expiration when the
offered by the airways. Thus, the respiratory airways are narrower.
cycle consists of:
Pulmonary compliance (C): The ease with
Inspiration, during which active muscle which the lungs expand during inspiration;
contraction results in expansion of the thorax normal lungs are very compliant and easily
and the lungs, a fall in alveolar pressure, and expand during inspiration, according to the
airflow into the lungs. At rest, inspiration is specific compliances of both the lungs and
accomplished primarily by the diaphragm the chest wall and their elastic properties, as
with some assistance from the parasternal well as the adequacy of thoracic pump
and external intercostals and scalenes (the function.
parasternal intercostals and scalenes act to
lift the ribs and expand the upper half of the Diffusion: The movement of gases into and
rib cage, which is important to counteract out of the blood; because CO2 is more
the inward motion of the upper chest that readily diffusible than oxygen, diffusion
would result from an unopposed decrease in abnormalities will result in hypoxemia long
intrapleural
pressure
produced
by before hypercapnia develops.
diaphragmatic descent).10 During exercise
the accessory muscles of inspiration are Perfusion (Q ): The blood flow through the
recruited to increase tidal volume (see Table pulmonary circulation that is available for
2-1), which is assisted by passive relaxation gas exchange; hypoxic vasoconstriction is
of the expiratory muscles that are also stimulated to reduce blood flow to alveoli
activated.The drop in intrathoracic pressure that are not being ventilated (i.e., alveolar
during inspiration also facilitates venous dead space).
return to the heart.
Ventilationperfusion (V /Q) matching: The
Expiration, during which passive relaxation degree of physical correspondence between
of the inspiratory muscles to their resting ventilated and perfused areas of the lungs;
positions and elastic recoil of the lungs cause the optimal V/Q ratio is 0.8 (4 parts
alveolar pressure to rise, resulting in airflow ventilation to 5 parts perfusion) to maintain
normal gas exchange.

Oxygenhemoglobin (O2Hb) binding: The


level of oxygen saturation of the arterial
blood, as shown in Figure 2-5; normal arterial
oxygen saturation (sao2) is 95% or more.

At residual volume (RV), the elastic forces


of the chest wall are balanced by the
maximal expiratory muscle forces at the end
of a forced expiration; it is normally about
20% to 30% of VT.

Because the top portion of the O2


Hb curve is fairly flat, it is not very
sensitive to changes in PO2 (e.g., at
a PO2 of 60, the sao2 is still 90%).
Below a PO2 of 60, the curve is much
steeper and therefore much more
sensitive to decrements in PO2 (e.g.,
at a PO2 of 40, the sao2 drops to 75%
and at a PO2 of 27, the sao2
decreases to 50%).
Different conditions cause the O2Hb
curve to shift to the right or left, which
changes the ease with which oxygen
binds to Hb in the blood and is CIGARETTE S MOKING
released to the tissues.
Smoking accounts for over 90% of all cases
of COPD. While studies in the past have
suggested that only around 1525% of
LUNG VOLUMES AND CAPACITIES
smokers develop COPD, more recent studies
Tidal volume (VT) represents the most indicate that this figure might be nearer
efficient breathing pattern and volume and 50%, and even smokers without symptoms
includes both dead space and alveolar of COPD show a greater age-related decline
volumes.
in lung function than nonsmokers. Cigar and
pipe smokers suffer a lower risk than
Functional residual capacity (FRC) reflects cigarette smokers of developing COPD, but
the balance of the elastic forces exerted by their risk of developing the disease remains
the chest wall and the lungs and is the higher than that of nonsmokers. However,
neutral resting volume of the respiratory the fact that not all smokers develop the
system after a normal expiration.
disease makes it likely that other genetic
and/or environmental factors have a role to
At total lung capacity (TLC), the elastic
play in its development.
forces of the lungs are balanced by the
maximal inspiratory muscle forces during a ALPHA-1 ANTITRYPSIN DEFICIENCY
very deep breath.

IV. ETIOLOGY

Alpha-1 antitrypsin
is
an
enzyme
produced by the liver
that maintains tissue
integrity
by
preventing
uncontrolled
proteolytic
destruction of the
alveolar tissue (see
below). An hereditary
deficiency
of
the
enzyme occurs in 1
in 5,000 live births in
the
UK
and
predisposes
to
destruction of the
alveoli with resulting
tendency
to
emphysema. The disease, which is inherited
as an autosomal recessive condition,
accounts for only 2% of all cases of
emphysema and, even in those subjects who
are homozygous for the condition, clinically
significant emphysema usually occurs only
when the subject is a cigarette smoker.
Emphysema due to alpha-1 antitrypsin
deficiency must be suspected in smokers
who exhibit symptoms and signs of the
disease at a relatively early age (under the
age of 40) and those with a family history of
emphysema.

diagnosis of COPD. Note however that it is


possible to suffer from chronic bronchitis
and/or emphysema without spirometric
evidence of COPD

OCCUPATIONAL FACTORS
Work in dusty environments, in particular
the coal mining industry, is acknowledged as
predisposing to the development of COPD. partridge
Other potential risk factors for developing
COPD include pre-existing bronchial hyperresponsiveness, lower socio-economic status,
and a poor nutritional status in utero.

Airflow obstruction due to chronic bronchitis,


asthma, and chronic obstructive pulmonary
disease (COPD). The central shaded area
denotes patients with airflow obstruction.
Airflow obstruction as reflected by an
FEV1/VC ratio of < 70% is a must for the

ASTHMA

in both the development and exacerbation


of asthma.19 Symptoms of asthma may
begin at any age.
sulivan

The etiology of asthma is not completely


understood. Historically, two types of asthma
have been described. Allergic (or extrinsic)
asthma
has
an
immunologic
(immunoglobulin E [ige]mediated) response
to certain environmental triggers (dust
mites, pollen, mold, animal dander). The
resulting eosinophilic inflammatory response
(an increased number of eosinophils found in
the airway mucosa) produces the common
symptoms and pathophysiological findings of
asthma. Atopy, or allergic sensitivity, is the
strongest factor for the development of
allergic asthma. Nonallergic (or intrinsic)
asthma is a less common form of asthma.
There are no clinical findings of atopy in
nonallergic
asthma;
however,
an
inflammatory response does result from
exposure to an irritant such as smoke,
fumes, infections, or cold air. Literature in
asthma has begun to consider that the two
types of asthma are not all that different:
one has a known and widespread allergic
response (extrinsic) whereas the other has a
more
local
inflammatory
response
(intrinsic).18 The Global Initiative for Asthma
(GINA) does not differentiate allergic from
nonallergic
asthma
in
its
guide
to
management
and
prevention.16
Viral
infections have been suggested to play a role

It is clear from the above that the cause(s)


of asthma is/are unknown. Asthma is best
regarded as a syndrome where the
pathophysiology
relates
to
airway
inflammation.
Airway
inflammation
is
characterized by T-helper cell (TH2)
dysregulation and production of the
interleukins IL-4, IL-5, and IL-13. In atopic
asthma mast cells, by cross linking of high
affinity immunoglobulin E (ige) receptors,
lead to the release of preformed mediators,
e.g. Histamine, tryptase, prostaglandins, and
heparin, and synthesis of other mediators,
including leukotrienes and platelet activating
factors. In nonatopic (intrinsic) asthma there
may be local ige production in the bronchial
mucosa.
Eosinophils,
which
release
tissuedamaging basic proteins, including
major basic protein (MBP), eosinophil cationic
protein (ECP), and eosinophil protein X (EPX),
are thought to be key effector cells despite
recent evidence that anti-IL-5 monoclonal
antibody treatment was able to reduce
greatly circulating eosinophils and reduce
moderately airway eosinophil numbers
without beneficial therapeutic effects in mildto-moderate asthma. Other cell types have
been shown to be activated, e.g. Alveolar
macrophages and epithelial cells, which are
also capable of releasing various cytokines.
Polymorphonuclear neutrophil leucocytes are
thought to be important, particularly in
chronic, severe (steroiddependent) asthma
and about one third of acute exacerbations
of asthma seem to be associated with
increased airway neutrophils rather than
eosinophils. Characteristic structural changes
are present even at an early stage in very
mild disease, and these include patchy
desquamated epithelium and thickening of
the reticular collagen layer of the basement
membrane.
Goblet
cell
hyperplasia,
increased numbers of mucus glands, new

vessel formation, and hypertrophy and PATHOPHYSIOLOGY


hyperplasia of airway smooth muscle are
features of persistent asthma. Functional
abnormalities include increased airway
permeability, plasma exudation, enhanced
parasympathetic
and
inhibitory
nonadrenergic nervous pathways, and airway
hyper-responsiveness.

RESPIRATORY

SYSTEM

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Pathophysiologic changes in the lungs of


COPD patients occur in the proximal airways,
peripheral airways, lung parenchyma, and
pulmonary vasculature.

schimtz

Within proximal and peripheral airway


lumens, increased numbers of neutrophils
accumulate in patients with COPD; activated
macrophages are also increased in airway
lumens in addition to their infiltration of
airway walls. In contrast, CD8+ (suppressor)
T lymphocytes predominate in the lung
parenchyma of COPD patients.14 This
inflammatory cellular phenotype in COPD
differs from asthmatic patients, in which a
predominance of eosinophils and CD4+
(helper) T lymphocytes occurs.
The number of neutrophils in the air spaces
of nonsmokers is normally <3% to 5% on
differential counts of bronchoalveolar lavage
fluid
(BALF),
whereas
smokers
have
increased numbers of BALF neutrophils.
Smoking induces alveolar macrophages to
release neutrophil chemotactic factors, such
as

V. Pathophysiology/Mechanism of Injury/Pathology

Interleukin-8, thus amplifying neutrophil


recruitment. Nicotine is also chemotactic for
neutrophils and smoke activates the
alternative complement pathway.

colonization of the airways is associated with


frequent infections.
Elastase, a potent protease, is secreted by
neutrophils and macrophages. Elastase
degrades parenchymal elastin even as
inflammation is further promoted by the
strongly pro-oxidative effects of inhaled
tobacco smoke and other noxious gases and
particulates.

Tobacco smoke also interferes with the ciliary


action of the respiratory epithelium.

Small peripheral airways <2 mm in


diameter normally account for 10% to 15%
of the total airway resistance; inflammation
of these structures in COPD, typified by
obstructive bronchiolitis, causes increased
airway resistance, even as expiratory
Lung inflammation is promoted by two emptying of distal lung units is impaired from
mechanisms
leading
to
an elastin fiber degradation and abnormal
oxidant/antioxidant
dilation of distal airspaces that culminate in
reduced elastic recoil pressure.
Imbalance: (1) activation of oxidationreduction (redox)-sensitive transcription fa, The thickness of the walls of small airways
which bind to and activate cytokine and in COPD, reflecting inflammation and
chemokine inflammatory genes; and (2) remodeling, correlates with physiological
oxidative inactivation of antiinflammatory measures of reduced expiratory airflow such
proteins
such
as
AAT.
Inflammatory as the forced expiratory volume in 1 second
responses are exaggerated in smokers or (FEV1).
patients exposed to air pollution who develop
COPD, particularly with AAT deficiency.
Progressive expiratory airflow limitation in
COPD and dyspnea on exertion reflect an
Airway inflammation causes hypertrophy accelerated annual rate of decline in the
and hyperplasia of mucus-secreting goblet FEV1. Normally the rate of FEV1 loss is
cells, as well as repeated injury and repair of approximately 30 ml/y in normal adults >30
the respiratory epithelium and related years of age; however in COPD patients the
structures. Airway remodeling involving rate of FEV1 loss is nearly 60 ml/y.
collagen deposition produced fixed airways
obstruction.
Lung hyperinflation is defined by an
elevated residual volume (RV), total lung
Traditionally, COPD was viewed as large capacity (TLC), and RV:TLC ratio during
airway chronic bronchitis versus emphysema pulmonary
function
testing.
In
involving parenchymal destruction distal to moderatesevere
COPD,
hyperinflation
terminal bronchioles. Recent data indicate develops during exercise (ie, dynamic
that COPD actually encompasses varying hyperinflation) from the combined effects of
combinations of small airways inflammatory increased breathing frequency and minute
disease (obstructive bronchiolitis) as well as ventilation, early closure of small airways,
lung parenchymal destruction (Fig. 1121).4
and reduced elastic recoil. Hyperinflation
places the diaphragm and other muscles of
Chronic bronchitis is characterized by
respiration at a mechanical disadvantage by
hypertrophy and inflammation of airway
reducing their radius of curvature and thus,
mucus glands including goblet cells, leading
force generation according to the lengthto increased mucus secretion. Impaired
tension relationship. The work of breathing is
mucociliary
clearance
and
thickened,
therefore increased, leading to exercise
inflamed bronchial walls contribute to
intolerance.
An
increasingly
sedentary
pathologic airway remodeling and luminal
lifestyle
produces
respiratory
muscle
narrowing,
whereas
chronic
bacterial
weakness
and
deconditioning,
which

augment exertional dyspnea for any level of COPD patients who require intubation and
lung function.
mechanical ventilatory support for acute or
acute-on-chronic respiratory failure are at
Reductions in the diffusing capacity of lung risk for autopositive end-expiratory pressure
for carbon monoxide (DLCO) characterize (PEEP). Predisposing factors for auto PEEP
emphysematous COPD. The DLCO is a include tachypnea, which reduces the length
measure of the conductance of carbon of each respiratory cycle (ie, a respiratory
monoxide (CO) from alveolar gas to rate of 20 breaths/ min equals a 3-second
hemoglobin in pulmonary capillary blood.
respiratory cycle length), lower ventilator
peak inspiratory flow rates (which prolong
The pulmonary capillary blood volume is
the duration of the inspiratory phase within
normally approximately 75 ml. Alveolar
each respiratory cycle), and bronchospasm,
capillary loss and destruction in moderatewhich predisposes to incomplete expiratory
severe emphysema reduce capillary blood
lung emptying and higher end-expiratory
volume and thus, the DLCO. Increases in
lung volumes.
ventilation-perfusion ratio (V:Q) mismatching
ensue; most notably, an increase in dead
Pathophysiologic
hemodynamic
space ventilation from ventilation of alveoli consequences of auto PEEP include arterial
without corresponding alveolar capillary hypotension secondary to decreased venous
perfusion. The DLCO may not be a sensitive return and cardiac output. Overestimation of
measure of milder degrees of emphysema.
central venous and/or pulmonary artery
pressures also occurs, as these pressure are
Exertional oxygen (O2) desaturation in
routinely referenced to atmospheric pressure
COPD is increasingly common as the
rather than intrathoracic pressure. Of note,
patients DLCO falls below 40% of predicted
hemodynamic consequences of autoPEEP
values, as in sleep-related O2 desaturation.
result from parallel elevations in intrathoracic
Arterial hypoxemia along with acidosis are or intrapleural pressure; elevated airway
potent
stimuli
for
pulmonary pressure per se causes no hemodynamic
vasoconstriction, which over time results in effects.
abnormal vascular remodeling, luminal
narrowing, and an increased pressure
gradient for pulmonary venous blood flow
(ie, mean pulmonary artery pressure
pulmonary capillary wedge pressure). The
associated increases in pulmonary vascular
resistance
predispose
to
progressive
secondary pulmonary hypertension and right
ventricular hypertrophy (cor pulmonale).
Despite similar degrees of expiratory
airflow limitation in COPD as reflected by
decreased forced vital capacity (FVC) and
FEV1 values, wide ranges in partial pressure
of carbon dioxide (paco2) are observed. Two
main determinants affect arterial paco2
levels in COPD: (1) reductions in the FEV1 of
60% to 70%, and (2) the ventilatory drive
(more
specifically,
the
hypercapnic
ventilatory response to paco2).

Adverse respiratory consequences of auto


PEEP include increased work of breathing
during inspiration because of the patients
need
to
generate
greater
negative
inspiratory
pressures
to
trigger
the
ventilator, and the augmented expiratory
work of breathing.
AutoPEEP cannot be determined by
visualizing displays of the peak inspiratory
pressure because the ventilator circuit is
open to atmosphere. However, the presence
of autoPEEP can be suspected by inspection
of the airway pressure waveforms. Definitive
measurement of autoPEEP is performed
with an endexpiratory pause or brief
occlusion, which causes the ventilator
manometer or digital readout to record the
actual end expiratory pressure.

In certain patients, judicious application of


external PEEP can offset autoPEEP. More
reliable methods to reduce autoPEEP
involve
pharmacologic
treatment
of
bronchospasm and airway inflammation,
limiting tachypnea by increasing each
respiratory cycle length via sedation and
other measures, and increasing ventilator
peak expiratory flow rates to shorten the
inspiratory
phase
and
lengthen
the
expiratory phase of each respiratory cycle.

response

that

stimulates

pathological

CHRONIC BRONCHITIS

Pathophysiology Chronic irritation of the


airways (due to smoking, air pollution,
occupational
exposure,
or
bronchial
infection)
provokes
an
inflammatory

change in the bronchial walls and leads to


a chronic productive cough and recurrent
pulmonary infections.

Chronic inflammation of the airways


induces mucosal edema, hypersecretion of
mucus, and destruction of cilia, all of which
increase airway resistance and produce
expiratory
flow
limitation.
Airway
obstruction and pulmonary dysfunction
develop.
In addition, irritation of the airways can
cause bronchoconstriction, which further
increases airway resistance and expiratory
flow limitation.
During acute exacerbations, sputum
production escalates and more secretions
are
retained,
resulting
in
further
aggravation of _ V/_Q mismatching and
increased work of breathing, and so on.
With severe disease, the excessive work
of breathing and deterioration of gas
exchange, along with polycythemia, lead to
ventilatory failure, cor pulmonale, or both.

As the disease progresses, pulmonary


hyperinflation decreases the efficiency of
the respiratory muscles and increases the
work of breathing
Loss of functional alveoli results in gross
_ V/Q mismatching throughout the lungs,
hyperventilation of well-ventilated, wellperfused alveoli in order to maintain
normal blood gases, increased work of
breathing, and greater risk of ventilatory
muscle fatigue and failure
Also, increased V/Q mismatching with
more advanced disease interferes with gas
exchange, leading to PH, RV failure, and
cor pulmonale.
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ASTHMA
Pathophysiology

Pathophysiology

Hyperreactivity of the airways to various


stimuli provokes bronchial smooth muscle
contraction and hypertrophy, mucosal
edema, and overproduction of viscous
mucus.

Repeated inflammation of the airways


produces
an
imbalance
between
endogenous
proteinases
and
antiproteinases, which causes progressive
lung destruction.

Over time, bronchial airway remodeling


occurs with increased thickness of all
layers of the airways and leads to chronic
stable asthma with intermittent acute
exacerbations.

Loss of elastic recoil due to tissue


destruction leads to expiratory collapse of
distal, poorly supported airways, resulting
in air trapping and alveolar overdistension.
The alveolar walls fragment and attenuate
so that several alveoli coalesce to form
bullae, which can become quite large and
compress adjacent lung tissue.

Because ventilation is significantly


reduced in numerous alveoli and perfusion
is preserved or even increased by
increased cardiac output, V/Q matching is
poor to very poor, which impedes gas
exchange and increases the work of
breathing, as described on pages 72 to 75.

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EMPHYSEMIA

In addition, the loss of large portions of


lung parenchyma reduces the pulmonary
vascular bed, which further increases
pulmonary
vascular
resistance
and
accelerates pulmonary hypertension (PH).

Usually the individual hyperventilates in


order
to
maintain
near-normal
oxygenation, resulting in hypocapnia and
respiratory alkalosis; however, prolonged
or severe attacks may lead to respiratory
muscle fatigue with hypercapnia and
respiratory
acidosis,
necessitating
ventilatory support.

If respiratory distress continues without


response to treatment, status asthmaticus
is present and hospitalization is required.
Occupational asthma develops as a
result of toxic exposure to various
substances in the work place.
In exercise-induced asthma, acute
bronchoconstriction during exercise is
thought
to
be
provoked
by
hyperventilation,
change
in
airway
temperature, or water loss. The resultant
increase in osmolality is proposed to
stimulate activation of mast cells or
afferent
nerve
endings,
leading
to
bronchoconstriction.
BRONCHIECTASIS

epithelium with loss of ciliated cells,


obliteration of the distal bronchi and
bronchioles, and hypertrophy of the
bronchial arteries with anastomosis and
sometimes considerable shunting of blood
to the pulmonary arteries.
During exacerbations, there is increased
obstruction
and
additional
secretion
production,
causing
greater
V/Q
mismatching, which results in impaired gas
exchange and increased work of breathing.
In rare cases in which disease is severe,
increased V/Q mismatching can activate
the two cascades of events that ultimately
lead to respiratory muscle fatigue or failure
and cor pulmonale
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Pathophysiology
Inflammation of the bronchial walls, due
to acute or chronic infection or possibly
defective regulation of the inflammatory
response caused by congenital syndromes,
immune deficiencies, and many other
disorders, results in mucociliary clearance
dysfunction, which leads to a vicious cycle
of persistent bacterial colonization, chronic
mucosal inflammation, and progressive
tissue destruction.
Bronchial dilation and distortion
caused by destruction of the elastic
muscular
airway
components
hypertrophy and hyperplasia of
surrounding undamaged musculature.

are
and
and
the

With long-standing disease there is


damage to the peribronchial alveolar tissue
by inflammation followed by fibrosis,
squamous metaplasia of the bronchial

CYSTIC FIBROSIS
The chronic pulmonary component of CF is
related to the abnormally viscous mucus
secreted in the tracheobronchial tree. The
altered secretions, resulting in airway
obstruction and hyperinflation, impair the
function of the mucociliary transport
system.
Exaggerated
and
sustained
neutrophilic
airway
inflammation
in
response to infection is also a feature of
this disease.24 Partial or complete
obstruction of the airways reduces
ventilation to the alveolar units. Ventilation
and perfusion within the lungs are not
matched. Fibrotic changes are ultimately
found in the lung parenchyma.
sulivan

VI. Clinical Signs and Symptoms/ Physical Disabilities/ Impairment


CLINICAL FEATURES
PRESENTING
FEATURES

SYMPTOMS

CLINICAL

Breathlessness on exertion, cough, and


sputum production are the main presenting
features of COPD. However, significant
COPD and lung dysfunction can exist in the
absence of symptoms, particularly in
sedentary individuals. Recurrent lower

respiratory tract infections in smokers often


draw them to the attention of the health
services and, not uncommonly, a diagnosis
of COPD is considered during such episodes.
Occasionally ankle swelling and
features of cor pulmonale are the presenting
symptoms.
PHYSICAL SIGNS OF COPD
Changes in body habitus: pink puffer
(thin, tachypnoeic, and struggling to breathe
cant breathe) or blue bloater (obese,
cyanosed, drowsy wont breathe).
Ankle oedema and raised JVP in patients
with cor pulmonale (see below).
Hyperinflated (barrel) chest (diminished
distance from the top of the thyroid
cartilage
to
the
suprasternal
notch;
increased anteroposterior diameter of the
thoracic cage).
Symmetrically diminished lung expansion
and air entry in both lung fields; wheeze.
Increased forced expiratory time.

CHRONIC BRONCHITIS

(paco2) (i.e., hypercapnia), respiratory


acidosis 4Clinical manifestations of cor
pulmonale, respiratory failure

Clinical Manifestations
Progressive
exertion

dyspnea,

especially

on

Cough, often severe, with variable degrees


of productiveness
Increased symptoms
respiratory infections

with

acute

Decreased breath sounds with prolonged


expiration, possible end-expiratory wheeze
on forced expiration
With more advanced disease:
Diminished nutritional status, weight
loss from greater energy used for
breathing
Hypoxemia
and
hypercapnia,
respiratory acidosis
Possible signs and symptoms of cor
pulmonale, ventilatory failure, or both
when end-stage disease develops
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Clinical Manifestations
Insidious onset of smokers cough, which
progresses to chronic productive cough
Progressive exertional dyspnea, with
possible respiratory distress late in the
disease

ASTHMA
Clinical Manifestations
Recurrent paroxysmal attacks of cough,
chest tightness, and difficult breathing,
often accompanied by audible wheezing

Increased respiratory symptoms due to


irritants, cold, damp or foggy weather, and
acute pulmonary infections
Normal breath sounds with prolonged
expiratory time and possible crackles or
wheezing
With more advanced disease: 4Hypoxemia
and increased arterial carbon dioxide

EMPHYSEMA

Thick, tenacious sputum, which may be


difficult to expectorate

insufficiency
and
respiratory failure.

Symptom-free between attacks versus


chronic state of mild asthma, with
symptoms particularly noticeable during
periods of exertion or emotional excitement

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Distant
breath
sounds,
prolonged
expiration; high-pitched expiratory and
possibly inspiratory wheezes throughout
both lungs
Tachypnea, possible signs of respiratory
distress (e.g., increased use of accessory
muscles, intercostal retractions, nasal
flaring)
Markedly reduced FEV1, forced expiratory
flow from 25% to 75% of vital capacity
(FEF25%-75%), and maximal expiratory flow
rate at all lung volumes and increased total
lung capacity (TLC) during acute attacks;
increased airway resistance and reduced
maximal expiratory flow rates during
remissions (patients often monitor their
status via daily peak expiratory flowmeter
readings).
During acute attacks, hypoxemia with
hypocapnia is common; normal or increased
paco2 is a serious sign indicating ventilatory

possible

impending

Clinical Presentation
The clinical symptoms of asthma during an
exacerbation may include cough, dyspnea
on exertion or at rest, and wheezing.
The chest is usually held in an expanded
position, indicating that hyperinflation of the
lungs has occurred. Accessory muscles of
ventilation may be used for breathing, even
at rest. Intercostal, supraclavicular, and
substernal retractions (visible inward motion
of the soft tissue) may be present on
inspiration. While expiratory wheezing is
characteristic of asthma, crackles may also
be present. With severe airway obstruction,
breath sounds may be markedly decreased
owing to poor air movement and wheezing
may be present not only during exhalation,
but may also become present on inspiration.
sulivan
BRONCHIECTASIS
Clinical Manifestations

Persistent or intermittent productive


cough with variable amounts of purulent
sputum (often copious)
Dyspnea, particularly if both lungs are
extensively involved; tachypnea
Possible pleuritic chest pain
Fever, loss of appetite, weakness, weight
loss
May be asymptomatic between episodes
of acute infection
Possible blood-streaked sputum or frank
hemoptysis
Adventitious breath sounds, including
crackles and often wheezes
Possible clubbing of digits
Expiratory air flow limitation on pfts, which
correlates with the severity of the disease
and may be reversible with bronchodilators
Possible hypoxemia even in mild disease;
severe hypoxemia with hypercapnia and
acidemia if diffuse disease
If severe disease, signs and symptoms of
pulmonary hypertension and possibly cor
pulmonale
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CYSTIC FIBROSIS
Clinical Presentation
The clinical presentation of CF can be
related to any number of involved systems.
Failure to thrive due to gastrointestinal
dysfunction, diabetes due to pancreatic
dysfunction,
or
frequent
respiratory
infections
and
chronic
cough
from
pulmonary dysfunction are all possible
presentations of the disease. The severity of
the disease, while quite variable, has been
linked to the classification of the CFTR
mutation.

With pulmonary involvement, a patient


presents with thick bronchial secretions that
may be difficult to clear. With advancing
disease, the chest wall will become barreled
with an increased anterior-posterior (AP)
diameter and an increased dorsal kyphosis
due to loss of elastic recoil of the underlying
lungs and hyperinflation.
There is a resultant decrease in thoracic
excursion. Breath sounds may be decreased
with adventitious sounds of crackles and
wheezes.
Hypertrophy of accessory muscles of
ventilation, pursed-lip breathing, cyanosis,
and digital clubbing may all be present.
Pulmonary
function
studies
show
obstructive
impairments
including
decreased FEV1, decreased PEF, decreased
FVC, increased RV, and increased FRC.
The
abnormal
ventilationperfusion
relationship within the lungs results in
hypoxemia and hypercapnea, as shown by
arterial blood gas analysis.
As the disease progresses, destruction of
the alveolar capillary network causes
pulmonary hypertension and cor pulmonale.
In advanced disease, chest radiographs
show diffuse hyperinflation, increased lung
marking, and atelectasis.

Diagnostic Tools/ Procedures or Test


CYTOLOGIC
HEMATOLOGIC
THORACICAND
IMAGING
STUDIES TESTS
Arterial blood is often analyzed to obtain
information
related
to
a
patients
oxygenation, ventilatory, and acidbase
status. Values can be obtained by analysis
of an arterial blood sample or by directreading electrodes after arterial cannulation.

Absorption of light by oxyhemoglobin and

The data obtained from arterial blood


gases (abgs) and normal values are listed in
Table 2-7.
The interpretation of abgs is achieved by
following four simple steps, as presented in
Chapter 6 (see Table 6-5, page 228 and
Figure 6-1, page 229).
Sudden acute changes
paco2 and ph are more
gradual chronic changes
associated with more
manifestations.

in the levels of
dangerous than
and tend to be
serious clinical

It is important for physical therapists to


appreciate normal versus abnormal values
for abgs and how abnormalities affect an
individuals ability to perform exercise and
rehabilitation activities.
Patients with chronic pulmonary disease
and low oxygen saturations often benefit
from the use of supplemental oxygen,
especially during exertion (see page 26).11
Although abgs provide the most accurate
method
of
assessing
a
patients
oxygenation, current technology does not
allow continuous monitoring of a patients
status.
PULSE OXIMETRY
Arterial oxygen saturation of hemoglobin
(sao2) can be estimated via pulse oximetry
(spo2), which employs spectrophotometry in
a sensor typically placed on an ear lobe or
finger to measure the differential

reduced hemoglobin.
Assessment of spo2 is strongly advised for
all patients with an FEV1 less than 50% of
predicted normal or a DLCO less than 60%
of predicted, because of the increased
likelihood of desaturation.
Pulse oximeters tend to have an accuracy
of 2% when resting sao2 is 80% to 100%,
but accuracy may be reduced during
exercise and when oxygen saturation is less
than 70% to 80%.13,22,45 Inaccuracies are
especially likely to occur during rapid or
severe desaturation, in patients requiring
intensive care, and those with poor
peripheral perfusion due to peripheral
arterial disease, vasoconstriction, or low
cardiac output, as well as a number of other
conditions, as listed in Table 2-8 (also refer
to Chapter 6, page 280).
When discrepancies are found between
the spo2 results and the patients clinical
presentation,
blood
gas
analysis
is
indicated.
In infants, transcutaneous oxygen (tcpo2)
electrodes are often used to monitor

oxygenation in neonatal respiratory distress


syndrome and for apnea and sleep studies. .
AMBULATORY OXIMETRY
Ambulatory oximetry monitoring uses a
pulse oximeter with computer software to
continuously record the spo2 and often the
pulse rate waveform for up to 24 hours.
These small, lightweight units typically
collect and store data every 15 seconds via
a finger probe.

In addition, hypoxemia and acidosis are


often associated with atrial and ventricular
arrhythmias.
EXERCISE TESTING
Exercise testing can be performed using
standardized protocols on a treadmill or
cycle ergometer in order to document the
cardiovascular, and sometimes respiratory,
responses to physiological stress for a
description of standard exercise testing).
Alternatively, walk tests are often used to
evaluate functional status.
PULMONARY EXERCISE TESTING

ELECTROCARDIOGRAPHY
12-lead electrocardiogram is commonly
obtained to ascertain the presence of right
ventricular hypertrophy (RVH) and/or strain
in patients with chronic lung disease, acute
asthma, and pulmonary embolism.
Specific indicators of RVH and/or strain
include right axis deviation, P pulmonale (a
tall, peaked P wave >2.5 mm in leads II, III,
and avf), and a dominant R wave in leads
avr and V1

Pulmonary exercise testing, more often


called cardiopulmonary exercise testing
(CPX or CPET), incorporates the analysis of
respiratory
gases,
including
the
measurement of oxygen uptake (_V O2) and
carbon dioxide production (_V CO2), and
other ventilatory parameters, in addition to
the usual parameters monitored during
standard exercise testing (see Chapter 3,
pages 49 to 50), in order to assess the
integrative exercise responses involving the
pulmonary,
cardiovascular,
and
other
systems.3
During testing the patient breathes
through a one-way nonrebreathing valve
with nose plugged so that expired air can be
analyzed and airflow can be measured while
the patient performs graded exercise on a
treadmill or stationary cycle ergometer. CPX
may also include insertion of an arterial line
for periodic blood gas analysis or the use of
pulse oximetry for documentation of oxygen
saturation.
Among the data that can be provided, in
addition to that from a standard exercise
test, are the following:

Respiratory rate (f)


Tidal volume (VT)
Expired, or minute, ventilation (VE)
Maximal oxygen uptake (V O2 max)
CO2 production (VCO2)

Ventilatory or anaerobic threshold (AT)


Respiratory exchange ratio (RER V
CO2/VO2)
Breathing reserve (BR); calculated as
maximal voluntary ventilation (MVV) VE
at maximal exercise
Oxygen
uptakework
rate
(WR)
relationship (VO2/WR) and oxygen
difference
Respiratory dead space (VD) and ratio
to tidal volume (VD/VT)
Alveolar ventilation (VA)
Alveolararterial
oxygen
difference
[P(Aa)O2]
Arterialend
tidal
carbon
dioxide
difference [P(aET)CO2]
Ventilatory equivalents for oxygen (V
E/V O2) and carbon dioxide (V E/V CO2)
Expiratory flow patterns 4Oxygen pulse
(V O2/heart beat)
Maximal MET (metabolic equivalent of
energy expenditure) capacity
Cardiac output (Q )

In addition, blood sampling can be


performed
to
determine
plasma
bicarbonate and acidbase responses
as well as lactate levels.
These data allow for the differentiation of
cardiovascular
versus
pulmonary
limitations as the cause of exerciseinduced dyspnea or impaired exercise
tolerance.
WALK TESTS

Time-based tests (e.g., 6-min walk test


and 12-min walk test)
Fixed-distance tests (e.g., 100-m, halfmile, and 2-kmwalk tests)
Velocity-determined walk tests (e.g.,
self-paced walk test)
Controlled-pacing incremental tests
(e.g., incremental shuttle walk test)
The walk tests used most commonly in the
assessment of patients with lung disease, as
well as other chronic diseases, are the 6-min
and 12-min walk tests (6MWT and 12MWT,
respectively), during which clients are asked
to walk as far as they can during the time of
the test, with rests allowed as needed.
Although these tests are often considered
submaximal, they may be near maximal in
patients with severe obstructive lung
disease.
PULMONARY IMAGING STUDIES
FLUOROSCOPY
Fluoroscopy produces radiographic images
with real-time display of a patients
breathing that may be highlighted with a
radioopaque contrast agent.

Fluoroscopy
offers
a
quick
and
inexpensive method of detecting lesions
that are obscured by ribs or that can be
seen clearly only in an unusual oblique
projection (e.g., some pleural plaques,
retrocardiac nodules), as well as pulsatile
nodules and masses.

Because formal laboratory testing is


complicated, time-consuming, expensive,
and not always available, a number of field
tests have been developed to indirectly
assess exercise capacity. Walk tests are
objective exercise tests that are used to
measure
functional
status,
monitor
treatment effectiveness, and establish
prognosis in patients with limited exercise
tolerance, including those with lung disease.

It is used most commonly to guide


interventional procedures, such as needle or
transbronchial
biopsies
or
catheter
angiography, to detect minor variations in
symmetry of diaphragmatic motion seen in
phrenic nerve damage, and to diagnose air
trapping in small children with suspected
foreign body aspiration.

A variety of walk tests are available35:

With computed tomography (CT), x-ray


beams pass through a body part in multiple

COMPUTED TOMOGRAPHY

projections in order to produce clear


crosssectional images of various body
tissues with good contrast resolution. Chest
CT is valuable in evaluating mediastinal
masses, hilar abnormalities, thoracic aortic
dissection, diffuse lung disease, pleural
abnormalities, presence of metastatic
lesions, and resectability of bronchial
carcinoma, and in quantifying the severity
of emphysema and its appropriateness for
lung reduction surgery.
During conventional CT scanning, patient
movement on the table alternates with data
acquisition via the rotating x-ray source
(i.e., data are acquired from one tissue
plane, and then the patient is moved into
position for the next image plane).
During helical or spiral CT, both the
patient and the x-ray source move
continuously (i.e., the data are acquired
continuously as the x-ray source traces a
spiral path relative to the patient), which
allows a study to be completed during a
single breath-hold.
Multidetector-row CT (MDCT) uses helical
or spiral CT with thinner collimation to
increase the sensitivity of images. Its
accuracy has made it a first-line study in the
diagnosis of pulmonary embolism and
venous thrombosis.37 It is also able to
evaluate all other thoracic structures,
including the lungs and heart, allowing
multiplanar and three-dimensional image
reconstruction.
Interventional CT is widely used to guide
percutaneous biopsy or drainage of thoracic
lesions and to localize fluid collections or
pneumothoraces that are not responding to
blindly placed thoracostomy tubes.
High-resolution CT (HRCT) uses thinner
slices at more frequent intervals to provide
improved visualization of small structures
and detailed anatomic features, producing
images that correlate closely with the
macroscopic appearance of pathologic
specimens. It is most valuable in diagnosing

diffuse lung disease in patients with a


normal
CXR,
detecting
parenchymal
abnormalities involving a small volume of
lung obscured by superimposed structures,
monitoring
disease
processes,
and
indicating which type of biopsy procedure is
likely to be successful in obtaining
diagnostic material.
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging (MRI) uses
radiofrequency pulse sequences with the
patient positioned in a strong magnetic field
to
generate
and
then
amplify
electromagnetic signals. These signals are
spatially mapped to create images of body
tissues. The usefulness of MRI for imaging
the lung parenchyma is limited by
extremely low proton density.
However, thoracic MRI is useful for
imaging mediastinal masses, thromboses of
the superior vena cava and great vessels,
central
pulmonary
emboli,
vascular
stenoses, aneurysms, and dissections, and
soft tissues of the chest wall.
Magnetic resonance angiography (MRA)
and magnetic resonance perfusion studies,
including direct thrombus imaging (MR-DTI),
are valuable tools for assessing suspected
pulmonary embolism, particularly in those
patients with iodinated contrast allergy or
pregnancy. Magnetic resonance methods
are also expected to play a significant role
in the assessment of patients with chronic
thromboembolic hypertension, vasculitis,
and arteriovenous malformations.
ULTRASONOGRAPHY
The use of sound waves (ultrasound) has
limited value in thoracic imaging, because
of the reflection of the ultrasound beam at
the airsoft tissue interface around the
lungs. However, it is useful for detecting,
localizing,
and
characterizing
pleural
effusions and guiding thoracentesis, for
differentiating pleural fluid from pleural
thickening, and for assessing areas of

consolidated lung or masses contacting or


invading the chest wall. In addition, flexible
bronchoscopy with an ultrasound probe is
being investigated as a means of mapping
the airways and surrounding tissues.

NUCLEAR MEDICINE/SCINTIGRAPHIC
IMAGING STUDIES
Scintigraphic studies employ radioactive
imaging agents to light up various tissues
during imaging, using a gamma counter.
VENTILATIONPERFUSION SCANNING
Ventilationperfusion ( V/Q ) scans use
radionuclides to evaluate and compare the
distribution of ventilation and perfusion
within the lungs.
Perfusion and ventilation studies are
obtained separately and then the images
are compare
V/_Q scans are used most commonly to
diagnose pulmonary embolism, predict
postoperative
lung
function
after
pneumonectomy, diagnose early airflow
obstruction, and assess the potential benefit
of surgical excision of emphysematous
bullae.
V/Q scans do not confirm or exclude
pulmonary embolism; rather, they give an
estimate of its likelihood, However, a normal
perfusion scan virtually excludes clinically
relevant
pulmonary
embolism.

Parenchymal
lung
diseases,
whether
obstructive or restrictive, usually produce
matched defects in both ventilation and
perfusion or a reverse mismatch in which
ventilation is reduced compared with
perfusion
Abnormal findings indicate that significant
mismatch between ventilation and perfusion
exists and the patient is likely to have
limited tolerance for activity.

SINGLE-PHOTON EMISSION COMPUTED


TOMOGRAPHY
Single-photon
emission
computed
tomography (SPECT) imaging involves the
injection of a radiolabeled tracer, the photon
emissions of which can be detected much
like x-rays in CT to produce threedimensional images of the distribution of
the tracer in a particular organ; these
images are often shown with a color scale.

SPECT
images
reflect
functional
information, including blood flow, oxygen or
glucose
metabolism,
or
dopamine
transporter concentration.
In pulmonary medicine, SPECT is
commonly used for _ V/Q studies and
produces better characterization of the
lobes and segments than two-dimensional
imaging.
POSITRON EMISSION TOMOGRAPHY
Positron
emission
tomography
(PET)
scanning uses biologically active positron
emission radiopharmaceuticals (i.e., 18Fdeoxyglucose, FDG) to display and quantify
metabolic processes, receptor occupancy,
and blood flow. In pulmonary medicine, PET
is used mostly for evaluating newly
discovered pulmonary nodules, staging of
confirmed nonsmall cell lung cancer, and
sometimes for monitoring response to
therapy.
OTHER
STUDIES

SCINTIGRAPHIC

IMAGING

Gallium scans use radioactive gallium


(67Ga), which has a high affinity for tumor
cells and white blood cells, to detect areas
of hidden inflammation. In pulmonary
medicine, it is used to detect pulmonary
infections, lung involvement in AIDS, and
interstitial lung disease; it is also valuable in
staging pulmonary sarcoidosis.
Other radionuclides can also be used to
detect opportunistic infections seen in
immunocompromised
patients
and
to

measure
mucociliary
clearance
(e.g.,
indium-111labeled white blood cells, 111In
wbcs;
technetium
99mlabeled
diethylenetriaminepentaacetic acid, 99mtcDTPA; or thallium.

INVASIVE DIAGNOSTIC TECHNIQUES


PULMONARY ANGIOGRAPHY
The injection of contrast material into the
thoracic blood vessels allows them to be
depicted on x-ray film. Digital subtraction
angiography uses fluoroscopy and image
intensification,
along
with
computer
processing,
to
subtract
interfering
background body parts, leaving only the
intravascular contrast materials
Pulmonary angiography is used to
diagnose pulmonary emboli, arteriovenous
malformations, pulmonary varices, and
occasionally to delineate the anatomy of the
pulmonary vessels before lung surgery.
It can also be used therapeutically to
inject thrombolytic agents to dissolve
pulmonary emboli and to embolize arteries
supplying the bleeding sites in severe
hemoptysis.
BRONCHOGRAPHY
Images of the bronchopulmonary tree can
be obtained by instilling contrast medium
directly into the airways and then obtaining
radiographs
or
tomographs.
Although
bronchography has been largely replaced by
fiberoptic bronchoscopy, HRCT, and spiral
CT, it is occasionally used in combination
with
bronchoscopy
for
defining
bronchopleural fistulae.
BRONCHOSCOPY
Using a flexible or rigid fiberoptic
endoscope, the larger airways down to the
third or fourth divisions of the segmental
bronchi can be visualized directly.

Because flexible fiberoptic bronchoscopy


requires only topical anesthesia and the
range of visible airways is greater, it is the
more commonly used method,
However, rigid bronchoscopy allows for
greater airway patency; maintenance of
ventilatory support; better removal of blood,
secretions, and tissue samples with less
impairment of ventilation; greater ease and
safety in removal of foreign bodies; and
local tumor therapy (e.g., placement of
radioactive seeds, laser therapy, and
cryotherapy).
If abnormalities are noted during
bronchoscopy,
additional
diagnostic
maneuvers may be performed:
Bronchial brushings are done to obtain
cells for the diagnosis of neoplasms
and infectious pulmonary infiltrates.
Bronchoalveolar lavage is used to
sample cells, inhaled particles, and
infectious agents from the terminal
bronchioles and alveoli in order to
diagnose
infectious
agents
and
sometimes malignant infiltrates. In
addition,
examination
of
cellular
composition and extracellular proteins
is useful in defining sarcoidosis,
extrinsic allergic alveolitis, idiopathic
pulmonary fibrosis, tuberculosis, and
many other lung diseases.
Transbronchial needle aspiration/lung
biopsy can be performed with a smallgauge needle or biopsy forceps passed
through a bronchoscope in order to
acquire tissue samples from within the
walls of the trachea and major bronchi
or
through
these
structures
to
peribronchial
lymph
nodes.
The
diagnostic yield is highest in diffuse
lung
diseases
with
specific
recognizable histologic patterns (e.g.,
sarcoidosis,
metastatic
cancer,
lymphoma,
and
lymphangitic
carcinoma).

Bronchoscopy can also be used as a


therapeutic intervention, such as in
removing retained secretions or aspirated
foreign
bodies,
assisting
in
difficult
intubation
and
bronchodilation,
and
managing malignant obstruction (e.g.,
bronchodilation, placement of stents, laser
therapy, and brachytherapy). In addition,
bronchial
thermoplasty
involving
bronchoscopic radiofrequency ablation of
airway smooth muscle is under investigation
for the treatment of asthma
PERCUTANEOUS
TRANSTHORACIC
NEEDLE ASPIRATION/LUNG BIOPSY
In some cases, a needle is inserted through
the skin to obtain tissue samples from
peripheral lung and sometimes mediastinal
masses,
usually
with
guidance
via
fluoroscopy, CT, or ultrasound imaging. It is
used most commonly to diagnose solitary
pulmonary nodules or masses suspected of
being malignant, particularly in patients
who are clearly inoperable because of
disease extent, significant cardiorespiratory
disease, or poor performance status.
THORACENTESIS AND PLEURAL BIOPSY
The insertion of a needle into the pleural
space allows for the removal of pleural fluid
or acquisition of a pleural biopsy.
Pleural fluid is analyzed to determine
whether it is a transudate or an exudate. In
addition, it may be sent for a variety of
cytologic,
biochemical,
hematologic,
immunologic, molecular, and microbiologic
studies.

Pleurocentesis
is
also
performed
therapeutically
to
relieve
respiratory
impairment caused by pleural effusions.
Blind, or closed, needle biopsy is
performed, usually with image guiding,
when tuberculosis, malignant effusion, or
other pleural pathology is suspected.
Rehabilitation
activities
should
be

postponed until a postprocedure chest


radiograph has ruled out a pneumothorax.
THORACOSCOPY/PLEUROSCOPY
Thoracoscopy, often with video, can be used
to visualize most intrathoracic structures,
including the pleurae. It is used most
commonly as an alternative to open pleural
biopsy when malignant disease is suspected
and a diagnosis has not been made despite
repeated
thoracenteses
and
pleural
biopsies.
Furthermore,
therapeutic
interventions
are
often
performed
thorascopically,
using
video-assisted
thoracic
surgery
(VATS),
including
debridement in tuberculosis and empyema;
diathermy,
laser
coagulation,
or
endostapling in recurrent pneumothorax;
pleurodesis in malignant effusion and
pneumothorax; as well as visual placement
of drains.
MEDIASTINOSCOPY
MEDIASTINOTOMY

AND

Exploration of the mediastinum can be


achieved with an endoscope inserted
through an anterior cervical or parasternal
incision (i.e., mediastinoscopy), using VATS,
or by direct visualization via an anterior
incision
(i.e.,
mediastinotomy).
These
procedures are used most commonly to
detect mediastinal lymph node involvement
by lung cancer and to biopsy abnormal
lymph nodes noted on chest radiography.
OPEN
LUNG
THORACOTOMY

BIOPSY/EXPLORATIVE

Open lung biopsy via an exploratory


thoracotomy is performed in patients with
hilar abnormalities in which overlying
vascular
structures
impede
other
approaches and when transbronchial biopsy
has been unsuccessful in providing a
diagnosis in chronic interstitial lung disease.
It may also useful in determining the nature
of the underlying disease in pulmonary
heart disease.

After surgery, two chest tubes are usually


inserted: a lower one to drain fluids and an
upper one, which requires a water seal and
is often set to gentle suction, to evacuate
air from the pleural space and to create the
negative pressure required for reexpansion
of the lung.

The thoracic cage should be symmetrical


when observed anteriorly, posteriorly, and
laterally.

complaining of poor sleep quality and


daytime sleepiness.

Shape and Dimensions of the Chest

Purposes:

Determine a patients primary and


secondary respiratory and ventilatory
impairments and how they limit
physical function.
Determine the adequacy of the
ventilatory pump and the oxygen
uptake/carbon dioxide elimination
mechanisms to meet the oxygen
demands
at
rest
and
during
functional activities.
Ascertain a patients suitability for
participation
in
a
pulmonary
rehabilitation program.
Develop
an
appropriate
level
intervention plan for the patient.
Establish a baseline to measure a
patients
progress
and
the
effectiveness of the treatment.
Determine when to discontinue
specific interventions and implement
a home program as a basis for selfmanagement.

Components of the Assessment


Analysis
of
Dimensions

Chest

Shape

Symmetry of the Chest and Trunk

and

Mobility of the Trunk


Check active movements in all directions
and identify any restricted spinal motions,
particularly in the thoracic spine.

A-P and lateral dimensions are usually 1:2.


Common chest deformities include:
Barrel Chest
The circumference of the upper chest
appears larger than the lower chest.
The sternum is prominent; A-P chest
diameter is greater than normal.
Upper chest breathers, particularly
patients with COPD, develop a barrel
chest.
Pectus excavatum (funnel chest/funnel
breast)
The lower part of the sternum is
depressed and the lower ribs flare
out.
Patients with this deformity are
diaphragmatic breathers; excessive
abdominal protrusion and little upper
chest
movement
occur
during
breathing.
Pectus carinatum (pigeon breast)
The sternum is prominent and
protrudes anteriorly.
Posture or Preferred Positioning
A patient who has difficulty breathing as the
result of chronic lung disease often leans
forward on hands or forearms to stabilize
and elevate the shoulder girdle to assist
with inspiration.

It is also important to identify a patients


preferred sleeping position. In addition, note
any postural deformities such as kyphosis
and scoliosis and postural asymmetry,
which could restrict chest movements and
ventilation.
Breathing Pattern
Assess the rate, regularity, and
location of ventilation at rest and with
activity.
A normal respiratory rate for a
healthy adult is 12 to 20 breaths per
minute.
The normal ratio of inspiration to
expiration at rest is 1:2 and with
activity 1:1. A patient with chronic
obstructive
pulmonary
disease
(COPD) may have a ratio of 1:4 at
rest, which reflects difficulty with the
expiratory phase of breathing.

To assess the breathing sequence,

above the clavicles. Have the patient


fully exhale and then inhale deeply.

Abnormal Breathing Patterns

Dyspnea. Distressed, labored breathing as the result ofshortness of breath.


Tachypnea. Rapid, shallow breathing; decreased tidal volume but increased
rate; associated with restrictive or obstructive lung disease and use of
accessory muscles of inspiration.
Bradypnea. Slow rate with shallow or normal depth and regular rhythm; may
be associated with drug overdose.
Hyperventilation. Deep, rapid respiration; increased tidal volume and
increased rate of respiration; regular rhythm.
Orthopnea. Difficulty breathing in the supine position.
Apnea. Cessation of breathing in the expiratory phase.
Apneusis. Cessation of breathing in the inspiratory phase.
Cheyne-Stokes. Cycles of gradually increasing tidal volumes followed by a
series of gradually decreasing tidal volumes and then a period of apnea. This
is sometimes seen in the patient with a severe head injury.
have
the
patient
assume
a
To check middle lobe expansion,
comfortable position (semireclining or
continue to face the patient; place
supine). Place your hands on the
the tips of your thumbs at the xiphoid
patients
epigastric
region
and
process and extend your fingers
sternum to observe movements in
laterally around the ribs. Again, ask
these two areas.
the patient to breathe in deeply.
To check lower lobe expansion,
place the tips of your thumbs along
the patients back at the spinous
processes (lower thoracic level) and
Chest Mobility
extend your fingers around the ribs.
Symmetry of Chest Movement
Ask the patient to breathe in deeply.
-

gives information about the mobility


of the thorax and also indirectly
indicates what areas of the lungs may
or may not be responding

Procedure:
Place your hands on the patients chest and
assess the excursion of each side of the
thorax during inspiration and expiration.
Each of the three lobar areas can be
checked.

To check upper lobe expansion,


face the patient; place the tips of
your thumbs at the midsternal line at
the sternal notch. Extend your fingers

Extent of Excursion
Method 1:
Measure the girth of the chest with a tape
measure at three levels (axilla, xiphoid,
lower costal). Document change in girth
after a maximum inspiration and a
maximum expiration.
Method 2:
Place both hands on the patients chest or
back as previously described. Note the
distance between your thumbs after a
maximum inspiration.

Palpation
Palpation of the thorax provides evidence of
dysfunction of the underlying tissues
including the lungs, chest wall, and
mediastinum.

Procedure:
Firmly press against the chest wall with your
hands to identify any specific areas of pain
potentially of musculoskeletal origin. Ask
the patient to take a deep breath and
identify any painful areas of the chest wall.
Chest wall pain of musculoskeletal origin
often increases with direct point pressure
during palpation and during a deep
inspiration. Pain of pulmonary origin is
usually localized to a region of the chest but
also may be felt in the neck or shoulder
region.
Mediastinal Shift
The position of the trachea shifts as the
result
of
asymmetrical
intrathoracic
pressures or lung volumes. For example, if
the patient has had a pneumonectomy
(removal of a lung), the lung volume on the
operated side decreases, and the trachea
shifts toward that side. Conversely, if the
patient has a hemothorax (blood in the
thorax), intrathoracic pressure on the side of
the
hemothorax
increases,
and
the
mediastinum shifts away from the affected
side of the chest.
Procedure:

Tactile (Vocal) Fremitus


-

the vibration felt while palpating over


the chest wall as a patient speaks

Procedure:
Place the palms of your hands lightly on the
chest wall and ask the patient to speak a
few words or repeat 99 several times.
Normally, fremitus is felt uniformly on the
chest wall.
Fremitus is increased in the presence of
secretions in the airways and decreased or
absent when air is trapped as the result of
obstructed airways.
Chest Wall Pain

To identify a mediastinal shift, have the


patient sit facing you with the head in
midline and the neck slightly flexed to relax
the sternocleidomastoid muscles. With your
index finger, gently palpate the soft tissue
space on either side of the trachea at the
suprasternal notch. Determine whether the
trachea is palpable at the midline or has
shifted to the left or right.
Mediate Percussion
-

designed to assess lung density,


specifically, the air-to-solid ratio in
the lungs

Procedure:
Place the middle finger of the nondominant
hand flat against the chest wall along an
intercostal space. With the tip of the middle
finger of the opposite hand, firmly tap on
the finger positioned on the chest wall.
Repeat the procedure at several points on
the right and left and anterior and posterior
aspects of the chest wall. This maneuver
produces a resonance; the pitch varies with
the density of the underlying tissue. The
subjective determination of pitch indicates
the following:
-

The sound is dull and flat if there is


a greater than normal amount of solid
matter (tumor, consolidation) in the
lungs in comparison with the amount
of air.
The
sound
is
hyperresonant
(tympanic) if there is a greater than
normal amount of air in the area (as
in patients with emphysema).
If asymmetrical or abnormal
fndings are noted, the patient
should be referred to the physician
for additional objective tests such as
a chest radiograph.

Auscultation of Breath Sounds

Auscultation
term that

is
a
general
refers to the
process of

listening
sounds
the body,

to
within

specifically
to
breath
sounds during an examination of the lungs.
A stethoscope is used to magnify these
sounds.
Breath sounds should be assessed to:

Identify the areas of the lungs in


which congestion exists and in which
airway clearance techniques should
be performed.
Determine the effectiveness of any
airway clearance intervention.
Determine whether the lungs are
clear and whether interventions
should be discontinued.

Procedure:

Follow a systematic pattern and place the


stethoscope
against
specific
thoracic
landmarks (T2, T6, T10) along the right and
left sides of the chest wall. Ask the patient
to breathe in deeply and out quickly through
the mouth as you move the stethoscope
from point to point. Note the quality,
intensity, and pitch of the breath sounds.
Classifcation of Breath Sounds
Breath sounds are classified by location,
pitch, and intensity as well as the ratio of
sounds heard on inspiration versus those
heard on expiration. Breath sounds also are
identified as normal or adventitious (extra).
Normal breath sounds occur in the absence
of pathology and are heard predominantly
during inspiration. Normal breath sounds are
categorized as vesicular, bronchial, or
bronchovesicular based on the location and
quality of the sound.

stethoscope. Adventitious breath sounds are


categorized as crackles or wheezes.
Breath sounds may be totally absent or
substantially diminished over a portion of
the lungs. This indicates total or partial
obstruction and lack of aeration of lung
tissue. The absence of air and collapse of an
area of lung tissue is known as atelectasis.
Obstruction of airways may be caused by
fluids,
mucus,
bronchospasm,
or
compression by tumor.

Cough and Cough Production


The strength, depth, length, and frequency
of a patients cough must be assessed. In
the patient with current or potential
pulmonary dysfunction a cough can be
described as weak, shallow, soft, or throaty.
A patient may have a weak, shallow cough

Normal Breath Sounds

Vesicular. Soft, low-pitched, breezy but faint sounds heard over most of the
chest except near the trachea and mainstem bronchi and between the
scapulae. Vesicular sounds are audible considerably longer on inspiration than
expiration (about a 3:1 ratio).
Bronchial. Loud, hollow, or tubular high-pitched sounds heard over the
mainstem bronchi and trachea. Bronchial sounds are heard equally during
inspiration and expiration; a slight pause in the sound occurs between
inspiration and expiration.
Bronchovesicular. Softer than bronchial breath sounds; also heard equally
during inspiration and expiration but without a pause in the sound between the
cycles. The sounds are heard in the supraclavicular, suprascapular, and
parasternal regions anteriorly and between the scapulae posteriorly.

Adventitious Breath Sounds

Crackles. Fine, discontinuous sounds (similar to the sound of bubbles popping


or the sound of hairs being rubbed between your fingers next to your ear).
Crackles, which can be fine or coarse, are heard primarily during inspiration as
the result of secretions moving in the airways or in closed airways that are
rapidly reopening. The former term for crackles was rales.
Wheezes. Continuous high- or low-pitched sounds or sometimes musical tones
heard during exhalation but occasionally audible during inspiration.
Adventitious breath sounds are abnormal
as the result of pain or paralysis. A sudden
sounds in the lungs that are heard with a
onset of a cough or a sustained cough often
is described as paroxysmal or spasmodic.

Secretions are checked for:

VIII.

DIFFERENTIAL DIAGNOSIS CONDITIONS

Color (clear, yellow, green, bloodstained)


Consistency (viscous, thin, frothy)
Amount (minimal to copious)
Odor
(no
odor
to
foulsmelling)Production
of
a
small
amount of clear or white secretions
on a daily basis is normal. Copious
but clear
secretions are common
with chronic bronchitis. Yellow, green,
and purulent secretions with a strong
odor are indicative of some type of
infection. Blood-streaked secretions,
known as hemoptysis, is indicative
of some degree of hemorrhage in the
lungs. Frothy, white secretions are
associated with pulmonary edema
and heart failure
kisner

DIFFERENTIAL DIAGNOSIS CONDITIONS

Pulmonary Function Test

Total Lung Capacity (TLC)


Functional Residual
Capacity (FCR)
Residual Volume (RV)
Vital Capacity (VC)
Forced Expiratory Volume
in one second (FEV1)
Forced Expiratory Flow,
Mid expiratory phase
(FEF 25-75%)
FEV1/FVC

Chronic
Bronchiti
s
-

Peripheral
Airway Disease

Emphysema

partridge

paz et. Al

MANAGEMENTS

Kisner
Paz et. Al
watchie

Pharmacological Management
Antihistamines
Antihistamines are used to block histaminemediated
reactions
associated
with
seasonal allergies. They reduce mucosal
congestion, irritation, and discharge caused
by inhaled allergens, and they also reduce
coughing and sneezing associated with the
common cold. They are often combined with
decongestants.
The first-generation antihistamines
readily crossed the bloodbrain barrier to
enter the brain, causing the common side
effects of sedation, fatigue, dizziness, and
blurred
vision.
In
addition,
their
anticholinergic effects may cause drying of
secretions and lead to further airway
obstruction in some patients.

Newer,
second-generation
antihistamines
include
astemizole
(Hismanal), loratadine (Claritin), terfenadine
(Seldane), and fexofenadine (Allegra). They
do not easily cross the blood brain barrier,
so they are far less likely to cause sedation
or other CNS side effects. However, some
may produce cardiotoxicity with serious
arrhythmias.
Antitussives
Antitussives suppress the cough reflex and
are used to treat the irritating, dry, hacking
cough
associated
with
minor
throat
irritations and the common cold. They are
not indicated for productive coughs.
Two main classifications of drugs provide
antitussive effects: nonnarcotic, over-thecounter, cough suppressants (e.g.,

dextromethorphan and
narcotics (e.g., codeine).

benzonate)

and

The most common side effect is sedation,


although some may also cause dizziness
and gastrointestinal distress. Alternatively,
some patients become stimulated by some
codeine antitussives and have difficulty
sleeping.
BRONCHODILATORS
The major determinant of airway caliber
and resistance is the bronchial smooth
muscle encircling the airways. Most
bronchodilators
effect
bronchodilation
through stimulation of the receptors that
cause relaxation of smooth muscle or by
blocking
the
receptors
that
trigger
bronchoconstriction. In general, patients are
prescribed a rescue inhaler for quick relief of
acute attacks of bronchospasm in patients
with asthma or sometimes COPD, and, if
their disease requires the use of this inhaler
more than twice per week, another drug for
long-term control.
Inhaled corticosteroids (ICSs)
are the first-line treatment for mild
persistent to severe asthma (in patients of
age 5 yr) and other bronchoconstrictive
diseases in order to control symptoms,
reduce frequency of exacerbations, and
improve pulmonary function. Treatment
earlier in the course of disease may help
delay disease progression.
Once-daily dosing may be as effective
as the current standard of twice-daily
dosing.
They are not indicated for the relief of
acute bronchospasm.
Low-dose ICSs usually have only local
side effects resulting from deposition on
the posterior pharynx and vocal cords,
causing sore throat, hoarseness, and
oral thrush (Candida infection). These
complications can be minimized by

using a spacer device and rinsing the


mouth after each inhaler use.
Expectorants
Expectorants increase the production of a
thin, watery sputum in the respiratory tract,
probably by increasing the secretion of
mucins, increasing mucus hydration, or both
to such a degree that the volume of
secretions produced is sufficient to allow
patients to cough them up more easily.
These drugs may also be irritants that
promote coughing to dislodge mucus.
The most commonly used expectorant is
guaifenesin, which is found in several
prescription forms and also in over-thecounter
cough
medicines,
often
in
combination with other products, such as
mucolytics and antitussives. It is the only
expectorant that has documented ability to
increase the production of secretions and
thus aid in expectoration.
An expectorant that is found in childrens
cough syrups is ammonium chloride.
There are no major side effects. On
occasion, nausea and vomiting or diarrhea
will occur, particularly with excessive doses
or intake on an empty stomach. Sometimes,
bradycardia occurs due to excess vagal
stimulation induced by coughing.
Mucolytics
Mucolytic agents break up the mucoprotein
molecules that increase the viscosity of
mucus, thus increasing the ease of
expectoration.
Treatment
with
oral
mucolytics is associated with a modest but
significant reduction in acute exacerbations
and days of illness in patients with chronic
bronchitis and COPD.
Nonpeptide (classical) mucolytics, such
as N-acetylcysteine (Mucomyst, Mucosil),
carbocysteine, and mecysteine cleave
disulfide bonds. The beneficial clinical
effects of acetylcysteine may not be due to
its mucolytic or antioxidant activity but

rather to a reduction in bacterial load.92


The most common side effect of these
agents is mild nausea, and sometimes fever
or drowsiness. However, acetylcysteine is
sometimes
associated
with
nausea/vomiting, inflammation of the oral
mucosa (stomatitis), and rhinorrhea and
occasionally induces serious bronchospasm.
Dornase alfa (Pulmozyme) is a genetically
engineered form of the human enzyme
deoxyribonuclease (DNase), which breaks
down the highly polymerized DNA that is
released in large amounts into the airways
from necrotic neutrophils; thus, it reduces
mucus viscosity, facilitating expectoration. It
is approved for use in the long-term
maintenance of patients with CF and is
administered once per day by nebulizer. It
has been shown to improve pulmonary
function and to reduce the incidence of
pulmonary infection requiring antibiotics.
Inhaled hypertonic saline likely works by
reducing the entanglements in airway
mucus gel, and it may also draw liquid
osmotically through the airway epithelium,
producing greater hydration of secretions so
they are easier to mobilize.
watchie

Medical and Surgical Management

paz et al

Physiotherapeutic management

9- Extremely short of breath


10-Maximally short of breath
by metabolic equivalent (MET)

Principles of exercise prescription


determinants of HR,ECG, BP, RPE, VO2
max or MET

Use of 40% of maximum

type of exercise. Intensity, duration,


frequency, and progression of activity

The use of suplemental o2 during exercise


remains controversial. If o2 saturation falls
below 85%, use of o2 may be indicated.

Intensity of exercise

Duration Of Exercise

by heart rate: karvonens formula for


training heart rate (THR)

Warm-up= 5- 15 min

THR= (HRage-adjusted maximumresting) 0.6 to 0.9 + HR resting

HR

by rate of perceived exertion (RPE)


correlated with sensation of SOB
ORIGINAL BORG
SCALE
6
7- very very light
8
9- very light
10
12
14
15- hard
16
17-very hard
18
19- very, very hard

NEW BORG SCALE

progressive exercise with emphasis


on controlled breathing

decrease
musculoskeletal injuries

incidence

of

allows
body
to
gradually
accommodate the CP demands of exercise
aerobic training

0- nothing at all
0.5- very very week
1- very weak
2- weak
3- moderate
4-somewhat strong
5- strong
6
7- very strong
8
9
19-very, very strong
maximal

PERCEIVED SHORTNESS OF BREATH SCALE


1- Rest not short of breath
2- Light activity minimally short of
breath
3- Slightly short of breath
4- Midly short of breath
5- Midly to moderately shorth of breath
6- Moderately short of breath
7- Severe shorthnes of breath
8- Breathing is not in control

frequent rest periods


cool- down= 5-15 min
Frequency of exercise
depends on the intensity that can be
achieved
50% of VO2 max: 3x a week
30%- 40% of VO2 max: >3x a week

BREATHING EXERCISES AND

Diaphragmatic Breathing
Diaphragmatic
Breathing
When
the
diaphragm is functioning effectively in its
role as the primary muscle of inspiration,
ventilation is efficient and the oxygen
consumption of the muscles of ventilation is
low during relaxed (tidal) breathing.When a
patient relies substantially on the accessory
muscles of inspiration, the mechanical work

of
breathing
(oxygen
consumption)
increases and the efficiency of ventilation
decreases. Although the diaphragm controls
breathing at an involuntary level, a patient
with primary or secondary pulmonary
dysfunction can be taught how to control
breathing by optimal use of the diaphragm
and decreased use of accessory muscles.
Procedure

Prepare the patient in a relaxed and


comfortable position in which gravity
assists the diaphragm, such as a semiFowlers position.
If your examination revealed that the
patient initiates the breathing pattern
with the accessory muscles of inspiration
(shoulder and neck musclulature), start
instruction by teaching the patient how
to relax those muscles (shoulder rolls or
shoulder shrugs coupled with relaxation).
Place your hand(s) on the rectus
abdominis just below the anterior costal
margin). Ask the patient to breathe in
slowly and deeply through the nose.
Have the patient keep the shoulders
relaxed and upper chest quiet, allowing
the abdomen to rise slightly. Then tell
the patient to relax and exhale slowly
through the mouth.
Have the patient practice this three or
four times and then rest. Do not allow
the patient to hyperventilate.
If the patient is having difficulty using
the diaphragm during inspiration, have
the patient inhale several times in
succession through the nose by using a
sniffing action.28,60 This action usually
facilitates the diaphragm.
To learn how to self-monitor this
sequence, have the patient place his or
her own hand below the anterior costal
margin and feel the movementThe
patients hand should rise slightly during
inspiration and fall during expiration.
After the patient understands and is able
to
control
breathing
using
a
diaphragmatic pattern, keeping the
shoulders
relaxed,
practice

diaphragmatic breathing in a variety of


positions (sitting, standing) and during
activity (walking, climbing stairs).
Segmental Breathing
Two examples of segmental breathing that
target the lateral and posterior segments of
the lower lobes are described in this section.
However, segmental breathing techniques
also may need to be directed to the middle
and upper lobes if there is accumulation of
secretions or insufficient lung expansion in
these areas.

Lateral Costal Expansion


Procedure
Have the patient begin in a hook-lying
position; later progress to a sitting
position. Place your hands along the
lateral aspect of the lower ribs to direct
the patients attention to the areas
where movement is to occur
Ask the patient to breathe out, and feel
the rib cage move downward and inward.
As the patient breathes out, place
pressure into the ribs with the palms of
your hands. Just prior to inspiration,
apply a quick downward and inward
stretch to the chest. This places a quick
stretch on the external intercostals to
facilitate their contraction.
Apply light manual resistance to the
lower ribs to increase sensory awareness
as the patient breathes in deeply and the
chest expands and ribs flare. Then, as
the patient breathes out, assist by gently
squeezing the rib cage in a downward
and inward direction.
Teach the patient how to perform the
maneuver independently by placing his
or her hand(s) over the ribs or applying
resistance with a towel or belt around
the lower ribs

Posterior Basal Expansion


Procedure

Have the patient sit and lean forward on


a pillow, slightly bending the hips. Place
your hands over the posterior aspect of
the lower ribs, and follow the same
procedure just described for lateral
costal expansion.

Pursed-Lip Breathing
Many therapists believe that gentle pursedlip breathing and controlled expiration is a
useful procedure, particularly to relieve
dyspnea if it is performed appropriately. It is
thought to keep airways open by creating
back-pressure in the airways. Studies
suggest that pursed-lip breathing decreases
the respiratory rate and the work of
breathing (oxygen consumption), increases
the tidal volume, and improves exercise
tolerance
Procedure
Have the patient assume a comfortable
position and relax as much as possible.
Have the patient breathe in slowly and
deeply through the nose and then breathe
out gently through lightly pursed lips as if
blowing on and bending the flame of a
candle but not blowing it out.43 Explain to
the patient that expiration must be relaxed
and that contraction of the abdominals must
be avoided. Place your hand over the
patients abdominal muscles to detect any
contraction of the abdominals.
Glossopharyngeal Breathing
it is used primarily by patients who are
ventilator-dependent because of absent or
incomplete innervation of the diaphragm as
the result of a high cervical-level spinal cord
lesion or other neuromuscular disorders.

tongue pushes the air back and traps it in


the pharynx. The air is then forced into the
lungs when the glottis is opened. This
increases the depth of the inspiration and
the patients inspiratory and vital capacities.

They are designed to maintain or improve


mobility of the chest wall, trunk, and
shoulder girdles when it affects ventilation
or postural alignment. For example, a
patient with hypomobility of the trunk
muscles on one side of the body does not
expand that part of the chest fully during
inspiration.
Exercises
that
combine
stretching of these muscles with deep
breathing improve ventilation on that side of
the chest. Chest mobilization exercises also
are used to reinforce or emphasize the
depth of inspiration or controlled expiration.
A patient can reinforce expiration, for
example, by leaning forward at the hips or
flexing the spine as he or she breathes out.
This pushes the viscera superiorly into the
diaphragm.
Specific Techniques
To Mobilize One Side of the Chest

Procedure
Glossopharyngeal breathing involves taking
several gulps of air, usually 6 to 10 gulps
in series, to pull air into the lungs when
action of the inspiratory muscles is
inadequate. After the patient takes several
gulps of air, the mouth is closed, and the

While sitting, have the patient bend


away from the tight side to lengthen
hypomobile structures and expand that
side of the chest during inspiration
Then, have the patient push the fisted
hand into the lateral aspect of the chest,
bend toward the tight side, and breathe
out
Progress by having the patient raise the
arm overhead on the tight side of the
chest and side-bend away from the tight
side. This places an additional stretch on
hypomobile tissues.

To Mobilize the Upper Chest and Stretch the


Pectoralis Muscles

While the patient is sitting in a chair with


hands clasped behind the head, have
him or her horizontally abduct the arms

EXERCISES TO MOBILIZE THE

(elongating the pectoralis major) during


a deep inspiration
Then instruct the patient to bring the
elbows together and bend forward during
expiration

This same maneuver can be performed


with the patient in a chair . The therapist
or family member can stand in back of
the patient and apply manual pressure
during expiration.

To Mobilize the Upper Chest and Shoulders

Self-Assisted Technique

While sitting in a chair, have the patient


reach with both arms overhead (180
bilateral
shoulder
flexion
and
slight
abduction) during inspiration and then bend
forward at the hips and reach for the floor
during
expiration
Techniques
to Facilitate a Cough
and Improve Airway Clearance

While in a sitting position, the patient


crosses the arms across the abdomen or
places the interlocked hands below the
xiphoid process . After a deep inspiration,
the patient pushes inward and upward on
the abdomen with the wrists or forearms
and simultaneously leans forward while
attempting to cough.
Splinting

An effective cough is necessary to eliminate


respiratory obstructions and keep the lungs
clear. Airway clearance is an important part
of management of patients with acute or
chronic respiratory conditions.
Manual-Assisted Cough
If a patient has abdominal weakness (e.g.,
as the result of a mid-thoracic or cervical
spinal cord injury), manual pressure on the
abdominal area assists in developing
greater intra-abdominal pressure for a more
forceful cough. Manual pressure for cough
assistance can be applied by the therapist
or the patient.

If chest wall pain from recent surgery or


trauma is restricting the cough, teach the
patient to splint over the painful area during
coughing. Have the patient press the hands
or a pillow firmly over the incision to support
the painful area with each cough. If the
patient cannot reach the painful area, the
therapist should assist .
Humidifcation
If secretions are very thick, work with the
patient after humidification therapy or
ultrasonic nebulizer therapy, both of which
enhance the mucociliary transport system
and facilitate a productive cough.

Therapist-Assisted Techniques

Tracheal Stimulation

Tracheal stimulation, sometimes called a


tracheal tickle, may be used with infants or
disoriented patients who cannot cooperate
during treatment.66 Tracheal stimulation is
a somewhat uncomfortable maneuver,
performed to elicit a reflexive cough. The
therapist places two fingers at the sternal
notch and applies a circular motion with
pressure downward into the trachea to
facilitate a reflexive cough.

With the patient in a supine or


semireclining position, the therapist
places the heel of one hand on the
patients abdomen at the epigastric area
just distal to the xiphoid process. The
other hand is placed on top of the first,
keeping the fingers open or interlocking
them. After the patient inhales as deeply
as possible, the therapist manually
assists the patient as he or she attempts
to cough. The abdomen is compressed
with an inward and upward force, which
pushes the diaphragm upward to cause a
more forceful and effective cough.

Suctioning: Alternative to Coughing

Endotracheal suctioning may be the only


means of clearing the airways in patients
who are unable to cough or huff voluntarily
or after reflex stimulation of the cough
mechanism. Suctioning is indicated in all
patients
with
artificial
airways.
The
suctioning procedure clears only the trachea
and the mainstem bronchi.

POSTURAL DRAINAGE
Postural drainage (bronchial drainage),
another intervention for airway clearance, is
a means of mobilizing secretions in one or
more lung segments to the central airways
by placing the patient in various positions so
gravity assists in the drainage process.
When secretions are moved from the
smaller to the larger airways, they are then
cleared by coughing or endotracheal
suctioning. Postural drainage therapy also
includes the use of manual techniques, such
as percussion, shaking, and vibration,
coupled with voluntary coughing.
Percussion
Percussion is used to augment mobilization
of secretions by mechanically dislodging
viscous or adherent mucus from the
airways. Percussion is performed with
cupped hands over the lung segment being
drained. The therapists cupped hands strike
the patients chest wall in an alternating,
rhythmic manner (Fig. 25.24B). The
therapist should try to keep shoulders,
elbows, and wrists loose and mobile during
the maneuver. Mechanical percussion is an
alternative
to
manual
percussion
techniques. Percussion is continued for
several minutes or until the patient needs to
alter position to cough. This procedure
should not be painful or uncomfortable.
Vibration
Vibration, another manual technique, often
is used in conjunction with percussion to
help move secretions to larger airways. It is

applied only during the expiratory phase as


the patient is deep-breathing. Vibration is
applied by placing both hands directly on
the skin and over the chest wall (or one
hand on top of the other) and gently
compressing and rapidly vibrating the chest
wall as the patient breathes out . Pressure is
applied in the same direction as the chest is
moving. The vibrating action is achieved by
the therapist isometrically contracting
(tensing) the muscles of the upper
extremities from shoulders to hands.
Shaking
Shaking is a more vigorous form of vibration
applied
during
exhalation
using
an
intermittent bouncing maneuver coupled
with wide movements of the therapists
hands. The therapists thumbs are locked
together, the open hands are placed directly
on the patients skin, and fingers are
wrapped
around
the
chest
wall. The
therapist

simultaneously compresses and shakes the


chest wall
Postural Drainage Positions

Positions for postural drainage are based on


the anatomy of the lungs and the
tracheobronchial tree (see Figs. 25.2 and
25.4). Each segment of each lobe is drained
using the positions depicted in Figures 25.26
through 25.37. The shaded area in each
illustration indicates the area of the chest
wall where percussion or vibration is
applied.
RIGHT AND LEFT UPPER LOBES

DEANS HIERARCHY FOR TREATMENT OF PATIENTS WITH IMPAIRED

RESPIRATORY EVALUATION FINDINGS AND SUGGESTED PHYSICAL

Chronic Bronchitis

Specific Treatment
Medications include the following
Anticholinergic
bronchodilators
versus long-acting b-agonists
Inhaled corticosteroids
Supplemental oxygen

Specific Treatment
Medications:

EMPHYSEMIA

ASTHMA
Specific Treatment
Medications
Short-acting b2-agonists as rescue
therapy 4Inhaled corticosteroids
If
unsuccessful,
long-acting
bronchodilators,
leukotriene
modifiers, mast cell stabilizers, or
anticholinergic drugs
Avoidance of asthma triggers

Aerobic
conditioning,
relaxation
techniques, and dyspnea positions
BRONCHIECTASIS

Antibiotics for acute exacerbations


4Inhaled corticosteroids
Mucolytics
Possible long-acting b2-agonists,
leukotriene modifiers, oral steroids
Surgical resection if localized disease

REFERENCES

Specific Treatment

Medications:
4Anticholinergic
bronchodilators versus long-acting bagonists
Inhaled corticosteroids
Supplemental oxygen
Surgical interventions
Bullectomy
Lung volume reduction
Lung transplantation, particularly for
a1-PI deficiency

Cardiovascular and pulmonary physical


therapy 2ND Ed. Joanne watchie, pt, ccs
Acute care handbook for physical
therapy 2nd ed. By Jaime c. paz
Acute care handbook for physical
therapy 5th 0ed. By Jaime c. paz
Therapeutic exercise foundations and
technique 5th ed. by kisner and Colby
Physical rehabilitation 6th ed. By o
sulivan
Understanding respirator medicine a
problem oriented approach by martin
patridge

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