OBSTRUCTIVE

LUNG DISEASE

CHARLEMAGNE B. PULGAN, RN
 CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
a long-term lung disease that obstructs airflow
and makes breathing difficult
is an umbrella term that could refer to
emphysema and chronic bronchitis
Asthma was once classified as a type of COPD
but it’s now considered a distinct chronic
inflammatory disorder- characterized primarily by
reversible inflammation
COPD is an irreversible chronic obstructive airway
disease that includes airway limitation and airflow
obstruction
Preventable and treatable respiratory disease
involving:
Both airways and pulmonary parenchyma (lung
tissues, bronchioles, bronchi, blood vessels,
interstitium, and alveoli)
Emphysema, Chronic Bronchitis (COPD)
Cystic Fibrosis, Bronchiectasis and Asthma (Chronic
Inflammatory Disease
a. Chronic bronchitis
Involves long-term inflammation and
swelling of the airways, leading to
excessive mucus production and
coughing
b. Emphysema
Involves damage to the alveoli (tiny air
sacs) in the lungs, reducing their
elasticity and making it harder for the
lungs to take in oxygen and expel carbon
dioxide.
A patient with COPD will have elevated
carbon dioxide levels
Over time, the elevated carbon dioxide
levels will make the patient dependent on
the lower partial pressure of Oxygen level
changes (hypoxia) to regulate ventilation.
Therefore, if you deliver high-flow oxygen,
the patient will lose his or her hypoxic
respiratory drive and stop breathing
Risk Factors
1. Cigarette smoking (90% of all cases)
The most common cause of COPD is smoking
2. Long-term Exposure/Occupational Exposure
long-term exposure to other lung irritants, such as air
pollution, chemical fumes, and dust, can also
contribute to the disease
3. Familial and Hereditary Factors
4. Genetic
Alpha-1 Antitrypsin Deficiency - (AAT) is a protein
normally found in the liver and the bloodstream (it
protects the lungs from the damage caused by
inflammation)
 How alpha-1
antitrypsin
deficiency can
lead to COPD?
Role of Alpha-1 Antitrypsin
Alpha-1 antitrypsin (AAT) is a protein produced by
the liver.
Its primary function is to protect the lungs from
damage caused by inflammation.
Specifically, AAT inhibits an enzyme called
neutrophil elastase, which is released by white
blood cells during inflammation to fight infections.
If left unchecked, neutrophil elastase can degrade
the elastic tissue in the lungs, causing significant
damage.
How AAT Deficiency Leads to COPD
In people with AAT deficiency, there is
either not enough AAT in the bloodstream
or the AAT protein is dysfunctional.
Without adequate AAT, the neutrophil
elastase enzyme is not properly regulated,
and over time, it begins to break down the
elastic fibers in the lungs.
This leads to lung tissue destruction—
primarily in the alveoli (tiny air sacs)—
causing emphysema, a key form of COPD.
Here’s a breakdown of how this happens
1. Lack of Protection
 In AAT deficiency, the lungs lack protection
from neutrophil elastase, leading to
uncontrolled damage.
2. Loss of Elasticity
As the elastase destroys elastic fibers, the
alveoli lose their ability to expand and contract
properly.
This makes it difficult for the lungs to exchange
gases (oxygen and carbon dioxide) efficiently.
3.Development of Emphysema
The damaged alveoli collapse or form
large, irregular air spaces, reducing the
surface area available for gas exchange.
This condition is known as emphysema.
4.Airflow Limitation
As lung tissue continues to be destroyed,
the airways become narrower and
obstructed, causing the hallmark
symptoms of COPD, such as shortness of
breath and chronic cough.
Risk Factors for Developing COPD in AAT
Deficiency
1. Smoking In people with AAT deficiency, smoking
dramatically accelerates lung damage and the
onset of COPD. Even passive smoke exposure can
increase risk.
2. Environmental Factors Exposure to dust, fumes, or
pollution can also hasten the development of COPD
in individuals with AAT deficiency.
3. Genetic Factors AAT deficiency is inherited in an
autosomal codominant pattern. Having two copies
of the abnormal gene (from both parents) typically
leads to severe deficiency and a higher risk of early
Management of COPD in AAT Deficiency
1. Treatment focuses on both managing COPD symptoms
and addressing the underlying AAT deficiency:
2. Augmentation therapy This involves infusions of
purified AAT protein to restore its protective function in
the lungs.
3. Bronchodilators and corticosteroids Help alleviate
COPD symptoms.
4. Oxygen therapy For those with severe lung damage.
5. Pulmonary rehabilitation Exercise and education
programs to improve lung function.
6. Smoking cessation Essential to slow disease
progression.
PATHOPHYSIOLOGY

• In COPD, the airflow limitation is both

progressive and associated with lung’s abnormal
inflammatory response (gas or noxious particles)
• Inflammatory response occurs throughout the
proximal and peripheral airways, lung
parenchyma, and pulmonary vasculature
• Changes and narrowing occur in airways due to
chronic inflammation on body’s attempt to repair
PATHOPHYSIOLOGY
• A. In proximal airways (trachea/bronchi):
changes include increased number in goblet cells
and enlarged submucosal glands leading to
hypersecretion of mucus.
• B. In peripheral airways (bronchioles)-
inflammation causes thickening of the airway wall,
peri-bronchial fibrosis, exudate in the airway, and
overall airway narrowing (obstructive bronchiolitis).
• ongoing injury-and-repair process causes scar tissue
formation and narrowing of the airway lumen
PATHOPHYSIOLOGY

C. In lung parenchyma (respiratory

bronchioles/ alveoli)
• Alveolar wall destruction leads to loss of alveolar
attachments and decrease elastic recoil.

D. In pulmonary vasculature
• causes thickening of the lining of the vessel and
hypertrophy of smooth muscles that leads to
pulmonary hypertension
PATHOPHYSIOLOGY

The pathophysiology of COPD involves

chronic inflammation, structural changes,
and airflow limitation in the lungs.
COPD encompasses two major conditions:
chronic bronchitis and emphysema, which
often occur together.
Key Processes Involved
1.Chronic Inflammation
COPD is primarily caused by long-term
exposure to lung irritants, with smoking being
the most common trigger.
These irritants lead to an abnormal
inflammatory response in the lungs:
Irritants (e.g., smoke, pollution, dust) trigger
inflammation in the airways, lung
parenchyma (the functional tissue of the
lungs), and pulmonary vasculature.
Inflammation causes the release of
inflammatory cells (e.g., neutrophils,
macrophages, and T lymphocytes) and
inflammatory mediators (e.g., cytokines,
proteases, and reactive oxygen
species).
The persistent inflammatory response
leads to tissue injury and the
recruitment of more inflammatory cells,
perpetuating the cycle.
2. Airflow Limitation and
Obstruction
Airflow limitation is the hallmark of
COPD and is primarily due to the
following factors:
a.Bronchial Inflammation (Chronic
Bronchitis)
Chronic bronchitis involves long-
term inflammation of the bronchi
(the larger airways).
This leads to mucus gland hypertrophy
and hyperplasia, causing excessive
mucus production.
The airway walls thicken due to
inflammation, fibrosis, and smooth
muscle hypertrophy.
Excessive mucus and thickened airway
walls narrow the bronchial tubes,
obstructing airflow and causing the
characteristic chronic cough and
sputum production in COPD.
b. Emphysema (Alveolar Damage)
In emphysema, the inflammation
damages the alveoli (tiny air sacs),
leading to the destruction of the
alveolar walls and capillary beds.
The elastin fibers that provide
structural support to the alveoli are
degraded, causing a loss of lung
elasticity.
As a result, the alveoli become
overinflated, and air is trapped in the
lungs (this is known as air trapping),
making it difficult to fully exhale and
creating a sensation of breathlessness.
The surface area for gas exchange is
reduced due to alveolar destruction,
impairing the lungs’ ability to transfer
oxygen and remove carbon dioxide.
c. Small Airway Obstruction
In the small airways (bronchioles),
inflammation leads to fibrosis
(scarring) and narrowing, further
contributing to airflow limitation.
Loss of elastic recoil in the alveoli
causes these airways to collapse
during exhalation, exacerbating
the obstruction.
3. Mucociliary Dysfunction
Inflammation in COPD also impairs the
function of the mucociliary escalator, the
mechanism that clears mucus and debris
from the lungs
Ciliary dysfunction results in the buildup of
mucus, further obstructing airflow and
creating a breeding ground for infections.
Frequent infections and exacerbations
accelerate lung damage and disease
progression.
4. Gas Exchange Abnormalities
The combination of airflow limitation, alveolar
destruction, and small airway obstruction leads to:
1. Hypoxemia (low oxygen levels in the blood)
Reduced surface area for gas exchange and
ventilation-perfusion mismatch (where areas of
the lung are ventilated but not adequately
perfused with blood) result in less oxygen
entering the bloodstream.
2. Hypercapnia (elevated carbon dioxide levels)
 Due to impaired exhalation, carbon dioxide
builds up in the blood, especially in more
advanced stages of COPD.
5. Pulmonary Hypertension
Chronic hypoxemia causes vasoconstriction
of the pulmonary arteries (blood vessels in
the lungs), leading to pulmonary
hypertension (high blood pressure in the
lung arteries).
Over time, this can cause the right side
of the heart to become enlarged and
weakened, a condition called cor
pulmonale, leading to right-sided heart
failure.
6.Systemic Effects
COPD is not confined to the lungs; it has systemic
effects that include:
Skeletal muscle dysfunction Chronic hypoxemia,
inflammation, and reduced physical activity lead to
muscle wasting and weakness.
Osteoporosis Due to chronic steroid use and
inactivity.
Weight loss and cachexia (muscle wasting) in
advanced stages, partly due to increased energy
expenditure from labored breathing.
Increased risk of cardiovascular diseases due to
chronic inflammation and systemic oxidative stress.
 1. CHRONIC BRONCHITIS
a long-term inflammation of the bronchi (the
major airways of the lungs) that results in
excessive mucus production and chronic
coughing
Inflammation of bronchial tubules
It is defined by clinical features
Major cause: smoking, other environmental
pollutants
Constant irritation causes the mucus-
secreting gland and goblet cells to increase
in number leading to increased mucus
production
Mucus plugging reduces ciliary function
Bronchial walls become thickened,
narrowing the bronchial lumen
Patients are more susceptible to respiratory
infection due to altered alveolar
macrophages brought by alveoli/bronchiole
damage and become fibrosed
Causes and Risk Factors
1.Smoking
The most common cause. Over 90% of cases
are associated with long-term cigarette
smoking. Smoking irritates the airways and
destroys the cilia, leading to chronic
inflammation.
2.Air pollution and occupational exposure
Long-term exposure to environmental
pollutants, such as dust, chemical fumes, or
toxic gases, can also trigger chronic
bronchitis.
3.Respiratory infections
Repeated lung infections can increase the risk of
developing chronic bronchitis, particularly in
people with weak immune systems or underlying
conditions.
4.Genetic factors
People with a family history of lung disease may
be more susceptible to developing chronic
bronchitis.
5.Age
Chronic bronchitis typically affects people over
the age of 40, especially those with a history of
smoking or long-term exposure to lung irritants.
Key Features of Chronic
Bronchitis
1.Chronic cough
Often referred to as a "smoker's cough," it is
typically productive (meaning it produces mucus)
2.Excess mucus production
This is due to hyperplasia (increased number) of
the mucus-secreting glands in the airways
3.Airway obstruction
The increased mucus and inflammation can
narrow the airways, making it harder to breathe.
Diagnosis of Chronic Bronchitis
1. History and physical examination
Diagnosis often starts with a patient's history of
persistent cough and mucus production.
2. Spirometry
This lung function test measures airflow and is essential
for diagnosing COPD (including chronic bronchitis). It
shows decreased airflow due to airway obstruction.
3. Chest X-rays or CT scans
Help rule out other lung conditions like pneumonia or lung
cancer.
4. Sputum analysis
This may be done to check for infections or other lung
diseases.
Diagnostic Criteria
Chronic bronchitis is diagnosed when a
person has:
Cough and sputum production occurs
on most days for at least 3 months a
year, over at least 2 consecutive years.
This condition is not just an acute
episode of bronchitis, but a persistent,
long-term illness.
Pathophysiology of Chronic Bronchitis
1.Irritation of the Bronchi
Chronic exposure to irritants such as
smoking, air pollution, dust, or chemical
fumes triggers inflammation in the
bronchial tubes.
Smoking is the most common cause, as it
directly damages the airway lining,
leading to inflammation and excessive
mucus production.
2.Mucus Hypersecretion
In response to ongoing irritation, the mucus
glands in the bronchi enlarge (hypertrophy)
and increase in number (hyperplasia).
These glands produce more mucus than
normal, leading to excessive production that
obstructs the airways.
Goblet cells, which are mucus-producing in
the lining of the airways, also increase,
contributing further to the thick mucus.
3.Chronic Inflammation
The persistent irritation causes chronic
inflammation in the airways, involving
neutrophils, macrophages, and lymphocytes.
This inflammation causes the bronchial walls
to thicken due to scarring (fibrosis) and
swelling.
As inflammation continues, the bronchial
smooth muscle can also hypertrophy (thicken),
further contributing to airway narrowing.
4.Ciliary Dysfunction
The cilia are tiny hair-like structures that
normally help move mucus and trapped
particles out of the lungs.
In chronic bronchitis, the cilia are damaged or
destroyed by inflammation and irritants,
particularly cigarette smoke, which impair their
function.
Without properly functioning cilia, mucus
clearance is reduced, leading to mucus build-
up in the airways.
5.Airway Obstruction
The combination of thickened airway
walls, increased mucus production, and
reduced ciliary clearance leads to airflow
obstruction.
This results in narrowing of the bronchial
tubes, making it difficult to move air in
and out of the lungs.
Patients often experience wheezing and
shortness of breath due to this
obstruction.
6.Frequent Infections
The excess mucus and impaired
clearance provide a fertile ground for
bacterial growth.
Patients with chronic bronchitis are prone
to frequent respiratory infections, which
can worsen symptoms and accelerate
lung damage.
Each respiratory infection causes more
inflammation and scarring in the airways,
further reducing lung function.
Symptoms of Chronic Bronchitis
1. Chronic productive cough
A hallmark of chronic bronchitis, the cough typically
brings up thick, sticky mucus (phlegm).
The amount and color of the mucus can change
during infections.
2. Shortness of breath
Difficulty breathing, especially during physical
activity, due to airway narrowing and mucus
obstruction.
3. Wheezing
A high-pitched sound when breathing out, is caused
by narrowed airways.
4.Chest tightness
A feeling of pressure or heaviness in the
chest
5.Fatigue
Due to the effort required to breathe
6.Frequent respiratory infections
Patients may experience more frequent
episodes of bronchitis, colds, or pneumonia
 Why CHRONIC
BRONCHITIS is
also known “BLUE
BLOATERS”?
The term "blue bloaters" is an older term
historically used to describe patients with
chronic bronchitis
Though this terminology is less commonly used
in modern medicine, it helps illustrate the clinical
characteristics associated with chronic bronchitis

Why "Blue Bloaters"?

1. "Blue”
Refers to cyanosis, or a bluish discoloration of
the skin, lips, and nails due to low oxygen levels
in the blood (hypoxemia).
In chronic bronchitis, the airways are narrowed by
inflammation, mucus, and airway obstruction. This
leads to poor ventilation (oxygen exchange), which can
result in low oxygen levels in the blood.
The body responds by increasing blood flow through
the lungs to pick up more oxygen, but because the
airways are obstructed, this doesn’t fully compensate,
leading to chronic low oxygen (hypoxemia) and an
increased amount of carbon dioxide (hypercapnia).
As a result, patients develop cyanosis, a blue tinge to
the skin and mucous membranes, especially visible
around the lips and fingers.
2."Bloaters”
Refers to fluid retention and a body shape
characterized by bloating or swelling.
Chronic bronchitis patients may develop
pulmonary hypertension (high blood
pressure in the pulmonary arteries), which
occurs because the blood vessels in the
lungs constrict in response to low oxygen
levels.
Over time, this increased pressure can strain the
right side of the heart, leading to a condition
called cor pulmonale (right-sided heart failure).
When the right side of the heart weakens, it has
difficulty pumping blood efficiently, leading to
fluid retention (edema) in the body, especially in
the legs and abdomen. This gives the patient a
bloated or swollen appearance.
This "bloated" appearance is what contributed to
the term "bloaters."
Pathophysiology Behind "Blue Bloaters”

1. Ventilation-Perfusion Mismatch

In chronic bronchitis, the lungs are poorly

ventilated due to mucus obstruction and airway
narrowing.
This causes a mismatch between areas of the
lung that are ventilated (getting air) and areas
that are perfused (getting blood flow).
As a result, not enough oxygen is exchanged,
leading to hypoxemia.
2.Hypercapnia
Because ventilation is impaired, carbon dioxide
(CO₂) builds up in the bloodstream (a condition
known as hypercapnia). Unlike emphysema patients,
who tend to "puff" out air to compensate for trapped
air, chronic bronchitis patients retain CO₂ due to the
more significant airway obstruction.
3.Right-Sided Heart Failure (Cor Pulmonale)
As the right side of the heart works harder to pump
blood through the lungs, it eventually becomes
weakened. This results in fluid buildup in tissues,
leading to peripheral edema (swelling in the legs)
and abdominal bloating.
Treatment of Chronic Bronchitis
Though there is no cure, treatment focuses on
managing symptoms and slowing disease
progression:
1. Smoking cessation The most important step in
preventing further lung damage.
2. Medications:
a. Bronchodilators Help open the airways and
make breathing easier.
b. Inhaled corticosteroids Reduce
inflammation in the airways.
c. Antibiotics May be prescribed during
infections.
3. Oxygen therapy For people with severe
chronic bronchitis and low oxygen levels
in the blood.
4. Pulmonary rehabilitation A combination of
exercise training, nutritional advice, and
education to improve breathing.
5. Vaccinations Regular flu and pneumonia
vaccines are recommended to prevent
respiratory infections.
Complications
1. COPD
Chronic bronchitis is a major cause of COPD, and the
disease often progresses to more severe forms of COPD,
involving emphysema.
2. Frequent lung infections
The buildup of mucus and impaired cilia function
increases the risk of infections, which can worsen the
condition.
3. Respiratory failure
In advanced cases, the lungs may not be able to supply
enough oxygen or remove enough carbon dioxide from
the blood.
Prognosis
The course of chronic bronchitis varies.
While some people may have mild
disease with infrequent exacerbations,
others may develop severe COPD with
progressive lung damage.
The best way to improve outcomes is
by quitting smoking and adhering to a
treatment plan that includes
medications and lifestyle changes.
 2. EMPHYSEMA
a type of Chronic Obstructive Pulmonary
Disease (COPD) that primarily affects the alveoli
(tiny air sacs in the lungs), leading to their
destruction
This results in reduced elasticity of the lungs
and impaired gas exchange, making it harder to
breathe.
The main characteristic of emphysema is air
trapping—the inability to fully exhale, leading to
overinflated lungs
It means “Inflate or swell”
Alveoli are destroyed and damaged causing a
permanent enlarge and loss elasticity
impaired oxygen and carbon dioxide exchange
results from overdistended alveoli
Difficulty exhaling since it depends on the lung's
ability to recoil
Defined by structural changes (enlargement of
the air spaces)
Key Features of Emphysema
1. Alveolar damage
The walls between the alveoli are destroyed,
reducing the surface area available for
oxygen and carbon dioxide exchange.
2. Loss of lung elasticity
The lung tissue loses its ability to recoil,
making exhalation difficult.
3. Air trapping
Air becomes trapped in the lungs, leading to
overinflation and shortness of breath.
Causes and Risk Factors
1. Smoking
The most significant risk factor for emphysema.
Cigarette smoke causes inflammation and
damage to the lung tissue, particularly the
alveoli.
2. Alpha-1 Antitrypsin Deficiency
A genetic condition that leads to early-onset
emphysema, even in non-smokers.
 People with this deficiency lack the protein that
normally protects the lungs from the enzyme
elastase, which can break down lung tissue.
3. Environmental/occupational exposure
Long-term exposure to pollutants, chemical
fumes, or dust can contribute to the development
of emphysema.
4. Age
Emphysema is more common in people over the
age of 40, particularly those with a history of
smoking.
5. Secondhand smoke exposure
Being exposed to smoke from others can
increase the risk of emphysema.
Diagnosis of Emphysema
1. Spirometry
A lung function test that measures airflow
and lung volumes. It shows reduced forced
expiratory volume (FEV1) and increased
lung volumes due to air trapping.
2. Chest X-rays or CT scans
These imaging tests can reveal
hyperinflation of the lungs and the presence
of bullae or other structural changes in the
lungs.
3.Arterial blood gas (ABG) analysis
Measures the levels of oxygen and
carbon dioxide in the blood, which can
show hypoxemia and hypercapnia in
advanced cases.
4.Alpha-1 antitrypsin testing
This may be done to rule out genetic
causes of emphysema in younger patients
or those with a family history of lung
disease.
Pathophysiology of Emphysema
1.Destruction of Alveoli
In emphysema, chronic exposure to irritants (such
as cigarette smoke, air pollution, or industrial fumes)
leads to the recruitment of inflammatory cells,
including macrophages and neutrophils, into the
lungs.
These cells release proteolytic enzymes (especially
elastase), which break down the structural proteins
(e.g., elastin) in the alveolar walls.
Over time, the destruction of alveolar walls leads to
the formation of larger, less efficient air spaces
called bullae. This results in a reduction in the total
surface area available for gas exchange.
2.Loss of Elastic Recoil
The elastic fibers in the lungs are responsible
for helping the alveoli contract and expel air
during exhalation. In emphysema, these fibers
are damaged or destroyed.
Without adequate elastic recoil, the alveoli
cannot fully empty during exhalation, leading to
air trapping and lung hyperinflation
(overinflation of the lungs).
This trapped air increases the work of
breathing, causing patients to experience
shortness of breath (dyspnea), especially during
3.Small Airway Collapse
The bronchioles (small airways) lack cartilage
and depend on the surrounding alveolar
structures to keep them open during
exhalation.
As the alveoli are destroyed, the bronchioles
collapse prematurely during exhalation, further
contributing to air trapping.
This collapse leads to increased resistance to
airflow and worsening shortness of breath.
4.Gas Exchange Impairment
The destruction of the alveolar walls
leads to the loss of pulmonary capillaries,
reducing the efficiency of oxygen entering
the blood and carbon dioxide being
removed.
This results in impaired oxygenation of
the blood and can lead to hypoxemia (low
oxygen levels in the blood) and, in severe
cases, hypercapnia (high carbon dioxide
levels).
5.Increased Lung Compliance
Paradoxically, while the lungs are stiffer in
diseases like fibrosis, in emphysema, the
lungs become more compliant (easier to
inflate) due to the loss of elastic tissue.
However, this increased compliance
means that the lungs are less able to
recoil and push air out, contributing to air
trapping and hyperinflation.
Types of Emphysema
There are different types of emphysema based
on the pattern of lung tissue destruction:
1.Centrilobular (Centracinar) Emphysema
Affects the central parts of the acinus
(functional units of the lungs) primarily in the
upper lobes.
Most commonly associated with smoking and
is the most prevalent type of emphysema in
smokers.
2.Panlobular (Panacinar) Emphysema
Affects the entire acinus, and is more
commonly seen in the lower lobes of the
lungs.
Associated with alpha-1 antitrypsin
deficiency, a genetic disorder that causes
an imbalance between proteases (like
elastase) and antiproteases (like alpha-1
antitrypsin) in the lungs.
3.Paraseptal Emphysema
Involves the distal alveoli near the pleura
(outer surface of the lungs).
Can lead to spontaneous pneumothorax
(collapsed lung) in younger individuals, as
the bullae formed near the lung surface
can rupture.
Symptoms of Emphysema
1. Shortness of breath (dyspnea)
This is the most prominent symptom and typically
worsens over time. It may initially occur only during
physical exertion but can progress to dyspnea at
rest.
2. Chronic cough
While less common than in chronic bronchitis,
some patients may have a mild chronic cough.
3. Pursed-lip breathing
Patients may breathe with pursed lips, which helps
them exhale more effectively by maintaining
airway pressure and preventing airway collapse.
4. Barrel chest
Hyperinflation of the lungs leads to a characteristic
rounding of the chest (increased anterior-posterior
diameter).
5. Wheezing
A high-pitched whistling sound during breathing
due to narrowed airways.
6. Weight loss
Patients with severe emphysema may experience
significant weight loss due to increased energy
expenditure from labored breathing.
7. Fatigue
Why is it called
PINK PUFFERS?
The term "pink puffers" is an older term
used to describe patients with emphysema
This label highlights some of the
characteristic features of emphysema
patients, particularly in comparison to
those with chronic bronchitis (who were
historically called "blue bloaters")
Why "Pink Puffers"?
1."Pink”
Refers to the relatively normal or pink skin complexion
that patients with emphysema tend to have, despite their
underlying lung disease.
Unlike chronic bronchitis patients, people with
emphysema maintain near-normal levels of oxygen in
the early stages of the disease by increasing their
breathing efforts.
Pink complexion suggests that their oxygen levels
are often sufficient to avoid cyanosis, even though
they are still experiencing significant respiratory
problems.
2."Puffer"
Refers to the way emphysema patients
tend to breathe
People with emphysema often use a
technique called pursed-lip breathing to
help manage their airflow.
This breathing pattern involves slow, deep
breaths with lips pursed (like puffing) on
exhalation.
Pursed-lip breathing helps to keep the
airways open for longer during exhalation,
reducing the collapse of small airways and
allowing better expulsion of trapped air
from the lungs. This strategy compensates
for the loss of elastic recoil in the lungs.
This breathing effort, combined with the
increased work of breathing to overcome
air trapping, results in the "puffing"
appearance, as they work harder to exhale
trapped air.
Pathophysiology Behind "Pink Puffers"
1. Air Trapping and Hyperinflation
In emphysema, the destruction of the alveolar
walls and loss of lung elasticity result in air
trapping and lung hyperinflation.
Patients have to work harder to breathe,
especially when exhaling because the lungs do
not easily empty due to loss of elastic recoil.
This increased work of breathing gives the
"puffing" appearance.
2.Maintaining Oxygenation
In the early stages, emphysema patients
can maintain relatively normal oxygen
levels in their blood by increasing their
breathing rate and depth.
Although they experience dyspnea
(shortness of breath), they can avoid
cyanosis (blue skin discoloration) in the
early to mid stages of the disease, which
contributes to the "pink" label.
3.Cachexia and Weight Loss
The increased work of breathing consumes a lot
of energy, which can lead to weight loss and
muscle wasting (cachexia).
These patients often appear thin and frail
because they burn more calories just to
breathe.
This thin, wasted appearance is in contrast to
the more bloated look seen in chronic bronchitis
patients, who tend to retain fluid (hence the
term "blue bloaters").
4.Pursed-Lip Breathing
Pursed-lip breathing is a common adaptive
behavior in emphysema patients.
By breathing out slowly through tightly pressed
lips, they increase the pressure in their airways,
preventing premature airway collapse during
exhalation.
This technique allows them to maintain better
airflow, reduce air trapping, and improve gas
exchange.
It’s a conscious effort to "puff" out the air,
hence the term "puffer."
Treatment of Emphysema
Although there is no cure for emphysema,
treatment focuses on managing symptoms,
slowing disease progression, and improving quality
of life:
1. Smoking cessation
The most important intervention to prevent
further lung damage.
2. Bronchodilators
Medications that relax the muscles around the
airways, help to open them up and improve
airflow.
3. Inhaled corticosteroids
4. Oxygen therapy
For patients with severe emphysema and low oxygen
levels in the blood.
5. Pulmonary rehabilitation
A program that combines exercise, education, and
breathing strategies to improve lung function and overall
well-being.
6. Lung volume reduction surgery
 In some cases, removing the most damaged
portions of the lung can improve breathing.
4. Lung transplantation
In severe cases where other treatments have failed, a
lung transplant may be considered.
Complications of Emphysema
1. Respiratory failure
As the disease progresses, the lungs may not be
able to provide sufficient oxygen to the body or
remove carbon dioxide.
2. Pneumothorax
The presence of large bullae in the lungs increases
the risk of lung collapse.
3. Pulmonary hypertension
Chronic low oxygen levels can lead to increased
pressure in the pulmonary arteries, potentially
leading to right-sided heart failure (cor pulmonale).
Prognosis
Emphysema is a progressive disease,
meaning it worsens over time.
However, with appropriate management
(especially smoking cessation), the
progression of the disease can be slowed,
and symptoms can be managed to improve
the quality of life.
In advanced cases, life expectancy is
reduced, particularly in those who continue
to smoke.
 WHY IS IN CHRONIC BRONCHITIS THERE IS
HYPOXEMIA BUT IT WILL ALSO MANIFEST
ELEVATED HEMOGLOBIN?
In chronic bronchitis, hypoxemia (low blood oxygen)
occurs due to inflammation and mucus production that
obstructs airways, reducing oxygen exchange in the lungs.
To compensate for the lack of oxygen, the body increases
the production of red blood cells in a process called
secondary polycythemia, which raises hemoglobin levels.
Elevated hemoglobin helps carry more oxygen, but it
doesn’t fully correct the underlying oxygen deficiency,
leading to persistent hypoxemia despite the increased red
blood cell count.
Comparison: "Pink Puffers" vs. "Blue
Bloaters"
A."Pink Puffers" (Emphysema)
Pink complexion due to relatively normal oxygen
levels early in the disease
Thin, frail appearance due to weight loss and muscle
wasting
Pursed-lip breathing as a compensatory mechanism
to improve exhalation.
Barrel chest (increased anterior-posterior diameter)
due to hyperinflated lungs.
Less mucus production compared to chronic
bronchitis.
Progressive dyspnea (shortness of breath),
B."Blue Bloaters" (Chronic Bronchitis)
Cyanosis (blue tint) due to low oxygen levels
in the blood (hypoxemia)
Overweight or bloated appearance due to fluid
retention and cor pulmonale (right-sided heart
failure)
Chronic productive cough with excessive
mucus production
Frequent respiratory infections
Wheezing and breathlessness due to airway
obstruction from mucus
Medical Management
1.Promoting smoking cessation
2.Prescribe medications
3.Managing exacerbations
4.Providing supplemental oxygen therapy as
indicated
A. Risk Reduction: Smoking Cessation

• Smoking cessation: single most cost-

effective intervention to reduce developing
COPD
Difficult if chronic smokers:
strength of nicotine addiction, continues
exposure to environment, stress,
depression and habit
• promote cessation by explaining the risks of
smoking and personalizing the “at-risk”
message to the patient
• should work with the patient to set a
definite “quit date.”
• Referral to a smoking cessation program
• Continued reinforcement with a modality
that is individualized to the patient and
their lifestyle
• Nicotine replacement—a first- line
pharmacotherapy that reliably increases long-
term smoking abstinence rates—(gum, inhaler,
nasal spray, transdermal patch, sublingual
tablet, or lozenge)
• Bupropion SR and nortriptyline - both
antidepressants, may also increase long- term
quit rates.
• Clonidine (Catapres) – antihypertensive drug
also used
• Varenicline (Chantix) – nicotinic acetylcholine
receptor partial agonist ; primarily used as a
B. PHARMACOLOGIC THERAPY
- Medications are given based on disease severity

1. Grade I (mild) – short- acting bronchodilators

2. Grade II or III (moderate) short-acting and
regular treatment of one or more long-acting
bronchodilators
3. Grade III or IV (severe or very severe) –
regular treatment with one or more
bronchodilators and inhaled corticosteroids for
repeated exacerbations
1. BRONCHODILATORS

- Key for symptoms management

- Inhaled therapy is preferred
- relieve bronchospasm by improving expiratory
flow through widening of the airways and promoting
lung emptying with each breath
- reduce airway obstruction by allowing increased
oxygen distribution throughout the lungs and
improving alveolar ventilation
- It can be given MDI or nebulization or oral route
a. Beta-Adrenergic Agonists
1. SABA (short-acting)
2. LABA (Long-acting)

Short-acting beta-agonists (SABAs) and long-

acting beta-agonists (LABAs) are both classes of
bronchodilators used in the management of
Chronic Obstructive Pulmonary Disease
(COPD).
They work by relaxing the muscles around the
airways, leading to improved airflow and
reduced symptoms such as breathlessness.
1. Short-acting beta-agonists (SABAs)
SABAs are primarily used for quick relief of acute
symptoms and are often referred to as rescue
medications.
Common SABAs:
Albuterol (Salbutamol)
 Commonly used for relief of bronchospasm.
Levalbuterol
 An isomer of albuterol, often used in similar
situations.
Mechanism of Action
SABAs stimulate beta-2 adrenergic receptors in the
smooth muscle of the airways, leading to
bronchodilation.
Indications
Immediate relief of bronchospasm
 Used during exacerbations or when experiencing
sudden shortness of breath.
Pre-exercise use
 For individuals who experience exercise-induced
bronchospasm
Dosage and Administration
Typically delivered via metered-dose inhalers
(MDIs), nebulizers, or dry powder inhalers (DPIs).
Dosing is generally as needed for symptom relief.
Side Effects
•Common side effects may include:
• Tachycardia (increased heart
rate)
• Tremors
• Nervousness
• Headaches
•These effects are generally mild
and short-lived.
2.Long-Acting Beta-Agonists (LABAs)
LABAs are used for maintenance therapy in
COPD and provide prolonged bronchodilation.
Common LABAs:
Salmeterol
 Typically administered twice daily.
Formoterol
 Can be taken twice daily, but the onset of
action is quicker than salmeterol.
Mechanism of Action
Like SABAs, LABAs stimulate beta-2 adrenergic
receptors but provide longer-lasting
bronchodilation, lasting 12 hours or more.
Indications
Daily maintenance therapy
 LABAs are used to help control chronic
symptoms and prevent exacerbations.
They are not used for acute relief; rather, they
help provide a baseline level of
bronchodilation.
Dosage and Administration
Administered via MDIs, DPIs, or nebulizers.
Dosing is typically twice daily or once daily,
depending on the specific LABA used.
Side Effects
• Side effects can be similar to those of SABAs,
including:
• Tachycardia
• Tremors
• Palpitations
• There is a potential risk of increased asthma-
related deaths if LABAs are used as
monotherapy in asthma, so they are often
prescribed in combination with inhaled
corticosteroids (ICS).
Combination Therapy
In many cases, LABAs are prescribed in combination
with inhaled corticosteroids (ICS) or long-acting
muscarinic antagonists (LAMAs) for COPD
management to improve symptom control and reduce
exacerbations.
Example Combination Inhalers:
Breztri Aerosphere (budesonide/formoterol)
Advair (fluticasone/salmeterol)
Symbicort (budesonide/formoterol)
Dulera (mometasone/formoterol)
b. Muscarinic (anticholinergics)
Antagonists
1. SAMA (short-acting)
2. LAMA (long-acting)
Short-acting muscarinic antagonists (SAMAs) and
long-acting muscarinic antagonists (LAMAs) are
classes of medications used in the management of
Chronic Obstructive Pulmonary Disease (COPD).
They work by blocking the action of acetylcholine
on muscarinic receptors in the airways, leading to
bronchodilation and improved airflow.
1. Short-Acting Muscarinic Antagonists (SAMAs)
SAMAs are primarily used for quick relief and can
be considered as rescue medications.
Common SAMAs:
Ipratropium Bromide
 The most commonly used SAMA in COPD
management.
Mechanism of Action:
SAMAs block the muscarinic receptors in the
bronchial smooth muscle, leading to
bronchodilation.
This mechanism reduces bronchoconstriction
induced by vagal stimulation.
Indications
Acute symptom relief
 SAMAs can be used during exacerbations or for
sudden shortness of breath.
Often used in combination with short-acting beta-
agonists (SABAs) for synergistic effects during acute
exacerbations.
Dosage and Administration
Administered via metered-dose inhalers (MDIs) or
nebulizers.
Dosing is typically as needed for symptom relief.
Side Effects
• Common side effects may include:
• Dry mouth
• Cough
• Dizziness
• Nausea
• Generally well tolerated, with fewer
cardiovascular side effects compared to
beta-agonists.
2. Long-Acting Muscarinic Antagonists
(LAMAs)
LAMAs are used for maintenance therapy in COPD and
provide prolonged bronchodilation.
Common LAMAs:
Tiotropium
 The most widely used LAMA in COPD
Glycopyrrolate
Aclidinium
Umeclidinium
Mechanism of Action:
LAMAs also block muscarinic receptors in the airway
smooth muscle, leading to sustained bronchodilation
for a longer duration (typically 24 hours).
Indications
Daily maintenance therapy
 LAMAs are used to control chronic symptoms
and prevent exacerbations in patients with
COPD.
Dosage and Administration
Administered via inhalation devices such as
dry powder inhalers (DPIs) or soft mist inhalers
(SMIs).
Dosing is generally once daily or twice daily,
depending on the specific LAMA used.
Side Effects
• Side effects can include:
• Dry mouth
• Constipation
• Urinary retention
• Increased heart rate (less common than with
beta-agonists)
• Side effects are generally mild and related to
anticholinergic activity.
Combination Therapy
For optimal management of COPD, LAMAs are
often used in combination with long-acting
beta-agonists (LABAs) to provide
complementary bronchodilation and better
symptom control.
Example Combination Inhalers:
Stiolto Respimat (tiotropium/olodaterol)
Inspiolto Respimat (tiotropium/olodaterol)
Anoro Ellipta (umeclidinium/vilanterol)
2. CORTICOSTEROIDS
• may improve the symptoms of COPD, they do
not slow the decline in lung function
• Long-term treatment with oral corticosteroids is
not recommended in COPD and can cause
steroid myopathy, leading to muscle weakness,
decreased ability to function
• Inhaled corticosteroids are frequently prescribed
in COPD
3. Other Medications
• Augmentation therapy, also known as
replacement therapy, is a treatment for patients
with severe alpha-1 antitrypsin (AAT) deficiency
who have emphysema.
• Antibiotic agents
• Mucolytic
• Anti-tussive
• Vaccination: influenza, pneumococcal
4. Management of
Exacerbation

• Primary causes of exacerbation

are tracheobronchial infection
and air pollution

• Roflumilast (Daliresp)-
given to reduce flare-ups of
COPD
5. General Principle of Oxygen Therapy

• Oxygen therapy can be given as long-term continuous

therapy
• main objective in treating patients with hypoxemia and
hypercapnia
• hypoxic drive is often cited as a concern in administering
supplemental oxygen to patients with COPD
• Administering too much oxygen can result in the
retention of carbon dioxide
• Patients with alveolar hypoventilation cannot increase
ventilation to adjust for this increased load, and increasing
hypercapnia occurs.
SURGICAL MANAGEMENT
1. Bullectomy
• a surgical option for select patients with bullous
emphysema
• Bullae are enlarged airspaces that do not contribute
to ventilation but occupy space in the thorax
• These bullae compress areas of the lung and may
impair gas exchange.
• Bullectomy may help reduce dyspnea and improve
lung function. It can be performed via a video-assisted
thoracoscope or a limited thoracotomy incision
SURGICAL MANAGEMENT
2. Lung Volume Reduction Surgery
• the removal of a portion of the diseased lung
parenchyma
• reduces hyperinflation and allows the functional tissue
to expand, resulting in improved elastic recoil of the
lung and improved chest wall and diaphragmatic
mechanics
• type of surgery does not cure the disease but may
improve life expectancy
3. Lung transplantation
Nursing Intervention
• Urge the patient to stop smoking and to avoid
other respiratory irritants.
• Explain that bronchodilators alleviate
bronchospasm and enhance mucociliary
clearance of secretions. Familiarize the patient
with prescribed bronchodilators. Teach or
reinforce the correct method of using an inhaler.
Nursing Intervention
• To strengthen the muscles of respiration, teach the
patient for:
a.diaphragmatic breathing- which reduces the
respiratory rate, increases alveolar ventilation, and
sometimes helps expel as much air as possible
during expiration
b. Pursed-lip breathing helps slow expiration,
prevents collapse of small airways, and helps the
patient control the rate and depth of respiration. It
also promotes relaxation, enabling the patient to
gain control of dyspnea and reduce feelings of
Nursing Intervention
• Teach the patient how to cough effectively to
help mobilize secretions. If secretions are thick,
urge the patient to maintain adequate hydration.
• If the patient will continue oxygen therapy at
home, teach him how to use the equipment
correctly.
• administer 1 to 2 liters of low-flow oxygen
because of carbon dioxide retention.
• give high-flow oxygen via nonrebreather only if
patient is in severe respiratory distress.
Nursing Intervention
• Planning activity of the day
• Self-care activities
• Chest-Physiotherapy
• Nutritional Therapy
• Coping measures