COPD

 This illustration shows the respiratory system

and images of healthy alveoli and alveoli
damaged by COPD.
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD) IS ALSO KNOWN AS:

 chronic obstructive lung disease (COLD),

 chronic obstructive airway disease (COAD),
chronic airflow limitation (CAL)
 chronic obstructive respiratory
disease.(CORD)
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE

(COPD) is the overall term for a

group of chronic lung conditions
that obstruct the airways in the
lungs. It usually refers to
obstruction caused by chronic
bronchitis an emphysema, but it
can also refer to damage caused
by asthmatic bronchitis.
DEFINITION
 Chronic obstructive pulmonary disease
(COPD) is a disease state characterized by
airflow limitation that is not fully reversible. This
newest definition of COPD, provided by the
Global Initiative for Chronic Obstructive Lung
Disease, (National Institutes of Health [NTH],
2001).
 COPD may include diseases that cause airflow
obstruction (eg, emphysema, chronic bronchitis)
or a combination of these disorders.
 Other diseases such as cystic fibrosis,
bronchiectasis, and asthma were previously
classified as types of chronic obstructive lung
disease. However, asthma is now considered a
separate disorder and is classified as an
abnormal airway condition characterized
primarily by reversible inflammation. COPD can
coexist with asthma. (Lippincott Williams & Wilkins )
 Bronchiectasis is a disease state defined by
localized, irreversible dilation of part of the
bronchial tree caused by destruction of the
muscle and elastic tissue. It is most often
secondary to an infectious process and is
manifested by airways that are inflamed and
easily collapsible.
COPD is a
progressive disease
which means the
disease gets worse
over time.
CAUSES
tobacco smoking (the most
common cause).
Pneumoconiosis ( an
industrial disease of lungs
due to inhalation of dust
particles)
long-term fume inhalation
PATHOPHYSIOLOGY

 In COPD, the airflow limitation is both

progressive and associated with an
abnormal inflammatory response of the
lungs to noxious particles or gases. The
inflammatory response occurs throughout the
airways, parenchyma, and pulmonary
vasculature. Early in the course of COPD, the
inflammatory response causes pulmonary
vasculature changes that are characterized by
thickening of the vessel wall.
PATHOPHYSIOLOGY CONT’D

 The body attempts to repair the chronic

inflammation and this causes narrowing in the
small peripheral airways. Over time this injury-
and-repair process causes scar tissue formation
and narrowing of the airway lumen.
 Airflow obstruction may also be due to
parenchymal destruction as seen with
emphysema (a disease of the alveoli). Chronic
inflammation activates proteinases and other
substances to be released, and they damage the
parenchyma of the lung. The parenchymal
changes may also be consequences of
inflammation, environmental, or genetic factors
(eg, alpha, antitrypsin deficiency).
RISK FACTORS FOR COPD

environmental exposures
and host factors
cigarette smoking: Pipe,
cigar, and other types of
tobacco smoking & passive
smoking .
RISK FACTORS
CONT’D

 Smoking depresses the activity of scavenger cells and

affects the respiratory tract's ciliary cleansing
mechanism. When this happens airflow is obstructed
and air becomes trapped behind the obstruction. The
alveoli greatly distend, diminishing lung capacity.
 Smoking also irritates the goblet cells and mucus
glands, causing an increased accumulation of mucus,
which in turn produces more irritation, infection, and
damage to the lung. In addition, carbon monoxide (a
byproduct of smoking) combines with hemoglobin to
form carboxyhemoglobin. Hemoglobin that is bound
by carboxyhemoglobin cannot carry oxygen efficiently.
RISK FACTORS
CONT’D

 prolonged and intense exposure to occupational

dusts and chemicals,
 indoor air pollution, and outdoor air pollution,

 a deficiency of alpha antitrypsin (an enzyme

inhibitor that protects the lung parenchyma from
injury). This deficiency predisposes young
patients to rapid development of lobular
emphysema even in the absence of smoking.
 Caucasians are genetically susceptible.
CLINICAL MANIFESTATIONS

 COPD is characterized by three primary

symptoms: cough, sputum production, and
dyspnea on exertion (NIH, 2001).
 Chronic cough and sputum production often
precede the development of airflow limitation by
many years then often worsen over time.
Dyspnea may be severe and often interferes with
the patient's activities.
 Weight loss is common because dyspnea
interferes with eating, and breathing depletes
energy.
CLINICAL MANIFESTATIONS
CONT’D

 Acute and chronic respiratory failure.

 chronic hyperinflation leads to the "barrel chest"
thorax configuration. This results from fixation of
the ribs in the inspiratory position (due to
hyperinflation) and from loss of lung elasticity.
 Retraction of the supraclavicular fossae occurs on
inspiration, causing the shoulders to heave
upward.
 In advanced emphysema, the abdominal muscles
also contract on inspiration.
OTHER MANIFESTIONS/SIGNS/SYMPTOMS
 shortness of breath, dyspnea during vigorous
exercise when the demands on the lungs are
greatest. Over time progressing to occurring
during milder, everyday activities such as
housework and in advanced stages of COPD, it
occurs during rest and is constantly present.
 persistent cough, sputum or mucus production,
wheezing, chest tightness, and tiredness,
cyanosis, respiratory failure(advanced).
OTHER MANIFESTIONS/SIGNS/SYMPTOMS
 cor pulmonale,
 peripheral edema, swelling of the ankles,

 tachypnea, wheezing sounds or crackles

 enlargement of the chest, particularly the front-

to-back distance (hyperinflation)
 active use of muscles in the neck to help with
breathing
 breathing through pursed lips, barrel chest
THE GOALS OF COPD MANAGEMENT
(INTERNATIONAL GOLD GUIDELINES)

 Prevent disease progression.

 Relieve symptoms.

 Improve exercise and activity tolerance.

 Improve health status.

 Prevent and treat complications.

 Prevent and treat exacerbations.

 Reduce mortality.
DIAGNOSIS
 A physical examination
 Pulmonary Function Tests (PFT) or spirometry).

 FEV1 / FVC ratio also called Tiffeneau index, is a

calculated ratio used in the diagnosis of
obstructive and restrictive lung disease. It
represents the proportion of the forced vital
capacity exhaled in the first second.
 A Chest Xray : this will reveal hyperinflation

 Sputum Culture: shows the type of pathogenic

microorganism such as Streptococcus, and WBCs
DIAGNOSIS CONT’D
 Blood investigations : would indicate
inflammation
 Neutrophils presence in the lungs : Damage
caused by irritation of the airways leads to
inflammation and leads to neutrophils being
present . Mucosal hyper-secretion is promoted by
a substance released by neutrophils
 Check for the presence of goblet cells in the small
airways: since this is typical of chronic bronchitis.
DIAGNOSIS CONT’D
 Pulmonary function studies are used to help
confirm the diagnosis of COPD determine disease
severity, and follow disease progression.
 Spirometry is used to evaluate airflow
obstruction, which is determined by the ratio of
FEV, (volume of air that the patient can forcibly
exhale in 1 second) to forced vital capacity (FVC)
With obstruction, the patient either has difficulty
exhaling or cannot forcibly exhale air from the
lungs, reducing the FEV,. Obstructive lung
disease is defined as a FEV,/FVC ratio of less
than 70%.
DIAGNOSIS CONT’D
 bronchodilator reversibility testing may be
performed to rule out the diagnosis of asthma.
 Arterial blood gas measurements may also be
obtained to assess baseline oxygenation and gas
exchange.
 alpha, antitrypsin deficiency screening may be
performed for patients under age 45 or for those
with a strong family history of COPD.
MEDICAL TREATMENT
 Antibiotics : for acute exacerbations of chronic
bronchitis, amoxicillin or doxycycline is
recommended.

 Corticosteroids. Inhaled and systemic

corticosteroids (oral or intravenous) may also be
used in COPD but are used more frequently in
asthma these medications may improve
symptoms. E.g. beclomethasone Beclovent,
Pulmicort, Flovent, and Azmacort.

 Smoking cessation: is a must

MEDICAL TREATMENT CONT’D
 Bronchodilators : may be helpful. E.g.
Ipratropium in chronic bronchitis.
Bronchodilators to relieve bronchospasm they
are delivered through a metered-dose inhaler, by
nebulization, or via the oral route in pill or liquid
form.
 They may also be used prophylactically to
prevent breathlessness by having the patient use
them before an activity, such as eating or
walking.
MEDICAL TREATMENT CONT’D
 Patients should receive a yearly influenza
vaccine and the pneumococcal vaccine every 5 to
7 years as preventive measures.
 alpha, antitrypsin augmentation therapy,

 antibiotic agents

 mucolytic agents

 antitussive agents.
Lets look
specifically at
emphysema and
Chronic bronchitis
separately.
EMPHYSEMA
Emphysema can be
classified into primary
and secondary.
However, it is more
commonly classified by
location.
BOTH EMPHYSEMA AND CHRONIC BRONCHITIS.
EMPHYSEMA CAN BE SUBDIVIDED INTO:
 panacinary and centroacinary or
 panacinar and centriacinar or

 panlobular and centrilobular

IN EMPHYSEMA
 impaired gas exchange (oxygen, carbon dioxide)
results from destruction of the walls of over-
distended alveoli.
 "Emphysema" is a pathological term that
describes an abnormal distention of the air
spaces beyond the terminal bronchioles, with
destruction of the walls of the alveoli. It is the
end stage of a process that has progressed slowly
for many years.
IN EMPHYSEMA CONT’D
 As the walls of the alveoli are destroyed (a
process accelerated by recurrent infections), the
alveolar surface area in direct contact with the
pulmonary capillaries continually decreases,
causing an increase in dead space (lung area
where no gas exchange can occur) and impaired
oxygen diffusion, which leads to hypoxemia.
 In the later stages of the disease, carbon dioxide
elimination is impaired, resulting in increased
carbon dioxide tension in arterial blood
(hypercapnia) and causing respiratory acidosis.
IN EMPHYSEMA CONT’D
 As the alveolar walls continue to break down, the
pulmonary capillary bed is reduced.
Consequently, pulmonary blood flow is increased,
forcing the right ventricle to maintain a higher
blood pressure in the pulmonary artery.
Hypoxemia may further increase pulmonary
artery pressure. Thus, right-sided heart failure
(cor pulmonale) is one of the complications of
emphysema. Congestion, dependent edema,
distended neck veins, or pain in the region of the
liver suggests the development of cardiac failure.
IN EMPHYSEMA CONT’D
 There are two main types of emphysema, based
on the changes taking place in the lung:
panlobular (panacinar) and centrilobular
(centroacinar). Both types may occur in the same
patient
IN EMPHYSEMA CONT’D
 In the panlobular (panacinar) type, there is
destruction of the respiratory bronchiole, alveolar
duct, and alveoli. All air spaces within the lobule are
essentially enlarged, but there is little inflammatory
disease. The patient with this type of emphysema
typically has a hyperinflated (hyperexpanded) chest
(barrel chest on physical examination), marked
dyspnea on exertion, and weight loss. To move air into
and out of the lungs, negative pressure is required
during inspiration, and an adequate level of positive
pressure must be attained and maintained during
expiration. The resting position is one of inflation.
Instead of being an involuntary passive act,
expiration becomes active and requires muscular
effort.
IN EMPHYSEMA CONT’D
 The patient becomes increasingly short of breath,
the chest becomes rigid, and the ribs are fixed at
their joints.
 Centrilobular (centroacinar) form, pathologic
changes mainly in the center of the secondary
lobule, preserving the peripheral portions of the
acinus. Frequently, there is a derangement of
ventilation—perfusion ratios, producing chronic
hypoxemia, hypercapnia (increased CO2 in the
arterial blood),polycythemia, and episodes of
right-sided heart failure. This leads to central
cyanosis, peripheral edema, and respiratory
failure patient may receive diuretic therapy for
edema.
 Panacinary (or panlobular) emphysema is related
to the destruction of alveoli, because of an
inflammation or deficiency of alpha 1-antitrypsin.
It is found more in young adults who do not have
chronic bronchitis.
 Centroacinary (or centrilobular) emphysema is
due to destruction of terminal bronchioli
muchosis, due to chronic bronchitis. This is found
mostly in elderly people with a long history of
smoking or extreme cases of passive smoking.
OTHER TYPES; CONGENITAL LOBAR,
DISTALACINAR, AND IRREGULAR EMPHYSEMA.

 Congenital lobar emphysema (CLE) is a

developmental anomaly of the lower respiratory
tract that is characterized by hyperinflation of
one or more of the pulmonary lobes.
PARASEPTAL EMPHYSEMA / DISTAL
ACINAR EMPHYSEMA

 The alveoli around the proximal parts of the

respiratory bronchioles are unaffected. Most of
the damage is around the distal alveoli, aveolar
ducts and septa.
 The enlarged alveoli form cyst-like bullae, which
may compress surrounding tissue. There is
almost no airway obstruction and may be
clinically insignificant until complications arise.
(It is one of the more common causes of a
spontaneous pneumothorax among young
adults).
IRREGULAR EMPHYSEMA

 In this type of emphysema, there may be

widespread damage although the distribution is
irregular. Fibrosis of the lung tissue may be
observed and usually it does not cause any
symptoms.
 Irregular emphysema may have been associated
with the other types of emphysema initially,
which was localized and healing occurred thereby
preventing the progression of the disease in that
area. It is clinically insignificant and therefore
not often considered among the other types of
emphysema.
CENTRIACINAR/CENTRILOBULAR
EMPHYSEMA

 So named because the central parts of the acini

are affected which lie nearest or closer to the
terminal bronchioles. The distal alveoli are
usually unaffected.
 Centriacinar emphysema is the more common
type of emphysema and it is frequently seen in
long-term smokers. It is often associated with
chronic bronchitis. Usually the upper half of
the lungs are affected.
PANACINAR / PANLOBULAR EMPHYSEMA
 The alveoli along the entire length of the
respiratory bronchioles are enlarged and affected
uniformly. The lower half of the lungs are
predominantly affected, particularly the anterior
parts of the lung and especially the base of the
lung. The entire lobule may be affected, but not
the entire lobe of the lung.
PATHOPHYSIOLOGY (EMPHYSEMA)
 Normally air is drawn in through the bronchi and into the
alveoli , which are tiny sacs surrounded by capillaries the
alveoli absorb oxygen and then transfer it into the blood.
 When toxicants, such as cigarette smoke, are breathed into
the lungs, the harmful particles become trapped in the
alveoli, causing a localized inflammatory response.
Chemicals released during the inflammatory response (e.g.,
elastase) can eventually cause the alveolar septum to
disintegrate. This condition, known as septal rupture, leads
to significant deformation of the lung architecture. These
deformations result in a large decrease of alveoli surface
area used for gas exchange. To accommodate the decreased
surface area, thoracic cage expansion (barrel chest) and
diaphragm contraction (flattening) take place. Expiration
increasingly depends on the thoracic cage and abdominal
muscle action, particularly in the end expiratory phase.
Due to decreased ventilation, the ability to exude carbon
dioxide is significantly impaired. In the more serious cases,
oxygen uptake is also impaired.
PATHOPHYSIOLOGY (EMPHYSEMA)
 As the alveoli continue to break down,
hyperventilation is unable to compensate for the
progressively shrinking surface area, and the body is
not able to maintain high enough oxygen levels in the
blood. The body's last resort is vasoconstricting
appropriate vessels. This leads to pulmonary
hypertension, which places increased strain on the
right side of the heart, the side responsible for
pumping deoxygenated blood to the lungs. The heart
muscle thickens in order to pump more blood. This
condition is often accompanied by the appearance of
jugular venous distension. Eventually, as the heart
continues to fail, it becomes larger and blood backs up
in the liver.
PATHOPHYSIOLOGY (EMPHYSEMA)
 Patients with alpha 1-antitrypsin deficiency (A1AD) are
more likely to suffer from emphysema. A1AD allows
inflammatory enzymes (such as elastase) to destroy the
alveolar tissue. Most A1AD patients do not develop
clinically significant emphysema, but smoking and severely
decreased A1AT levels (10-15%) can cause emphysema at a
young age. The type of emphysema caused by A1AD is
known as panacinar emphysema (involving the entire
acinus) as opposed to centrilobular emphysema, which is
caused by smoking. Panacinar emphysema typically affects
the lower lungs, while centrilobular emphysema affects the
upper lungs. A1AD causes about 2% of all emphysema.
Smokers with A1AD are at the greatest risk for
emphysema. Mild emphysema can often develop into a
severe case over a short period of time (1–2 weeks).
(a serine protease found in neutrophils, as a primary
contributor to the connective tissue damage seen in the
disease. )
TREATMENT OF EMPHYSEMA
 Emphysema is also treated by supporting the
breathing with anticholinergics, bronchodilators,
steroid medication (inhaled or oral), and
supplemental oxygen as required.
 Treating the patient's other conditions including
gastric reflux and allergies may improve lung
function. Supplemental oxygen used as
prescribed (usually more than 20 hours per day)
is the only non-surgical treatment which has
been shown to prolong life in emphysema
patients. There are lightweight portable oxygen
systems which allow patients increased mobility.
TREATMENT OF EMPHYSEMA
 The only known "cure" for emphysema is lung
transplant, but few patients are strong enough
physically to survive the surgery. The
combination of a patient's age, oxygen
deprivation and the side-effects of the
medications used to treat emphysema cause
damage to the kidneys, heart and other organs.
 Transplants also require the patient to take an
anti-rejection drug regimen which suppresses the
immune system, and so can lead to microbial
infection of the patient.
MANAGEMENT OF EMPHYSEMA
 Bronchodilators
 Corticosteroids

 Smoking cessation

 Mucolytics
SIGNS & SYMPTOMS
 expectorating cough (also known as a productive
cough, i.e. one that produces sputum),
 shortness of breath (dyspnea)

 wheezing.

 chest pains,

 fever,

 fatigue

 malaise may also occur.

 Mucus is often green or yellowish green and also

may be orange or pink, depending on the
pathogen causing the inflammation.
 In emphysema, the walls between many of the
air sacs are damaged, causing them to lose their
shape and become floppy. This damage also can
destroy the walls of the air sacs, leading to fewer
and larger air sacs instead of many tiny ones.
 In chronic obstructive bronchitis, the lining of the
airways is constantly irritated and inflamed. This
causes the lining to thicken. Lots of thick mucus
forms in the airways, making it hard to breathe.
 Most people who have COPD have both
emphysema and chronic obstructive bronchitis.
Thus, the general term "COPD" is more accurate.
EPIDIMIOLOGY
 COPD is a major cause of disability, and it's the
fourth leading cause of death in the United
States. More than 12 million people are currently
diagnosed with COPD. An additional 12 million
likely have the disease and don't even know it.
 COPD develops slowly. Symptoms often worsen
over time and can limit your ability to do routine
activities. Severe COPD may prevent you from
doing even basic activities like walking, cooking,
or taking care of yourself.
 Most of the time, COPD is diagnosed in middle-
aged or older people
 Worldwide, COPD ranked sixth as the cause of
death in 1990. It is projected to be the third
leading cause of death worldwide by 2020 due to
an increase in smoking rates and demographic
changes in many countries. COPD is the 4th
leading cause of death in the U.S., and the
economic burden of COPD in the U.S. in 2007
was $42.6 billion in health care costs and lost
productivity.
 COPD has no cure
 doctors don't know how to reverse the damage to
the airways and lungs.
 However, treatments and lifestyle changes can
help you feel better, stay more active, and slow
the progress of the disease.
EMPHYSEMA
NOT A COPD
 Acute bronchitis is an inflammation of the
large bronchi (medium-size airways) in the lungs
that is usually caused by viruses or bacteria and
may last several days or weeks. Characteristic
symptoms include cough, sputum (phlegm)
production, and shortness of breath and
wheezing related to the obstruction of the
inflamed airways.
CHRONIC BRONCHITIS
 Chronic bronchitis, a disease of the airways, is
defined as the presence of cough and sputum
production for at least 3 months in each of 2
consecutive years.
CHRONIC BRONCHITIS PATHOPHYSIOLOGY
 Smoke and other environmental pollutants
irritates the airways and cause hyper-secretion of
mucus and inflammation. Because this irritation
is constant it causes mucus-secreting glands and
goblet cells to increase in amount, the ciliary
function to be reduced and more mucus to be
produced. Also bronchial walls thicken and its
lumen is narrowed. So mucus may plug the
airways. Also the alveoli next to the bronchioles
may become damaged and fibrosed. This results
on altered function of the alveolar macrophage.
DIAGNOSIS OF CHRONIC BRONCHITIS

 Pulmonary function tests

 Arterial blood gas

 Chest x-ray

 Pulse oximetry (oxygen saturation testing)

 Complete blood count (CBC)

 Exercise testing

 Chest CT scan
MANAGEMENT OF CHRONIC BRONCHITIS
 Antibiotics/antimicrobials
 Bronchodilators

 Corticosteroids

 Smoking cessation

 Antitussive / ecpectorants

 Mucolytics

 Analgesics/antipyretics
NURSING ALERT
 Since hypoxemia stimulates respiration in the
patient with severe COPD, increasing the oxygen
flow to a high rate may greatly raise the patient's
blood oxygen level but at the same time, this will
suppress the respiratory drive, causing increased
retention of carbon dioxide and CO2 narcosis. The
nurse should closely monitor the patient's
respiratory response to oxygen administration
via physical assessment, pulse oximetry, and/or
arterial blood gases.
NURSING DIAGNOSES FOR
PATIENTS WITH COPD

 Impaired gas exchange and airway clearance related

to chronic inhalation of toxins
 Ineffective airway clearance related to broncho-
constriction increased mucus production, ineffective
cough, bronco- pulmonary infection, and other
complications
 Ineffective breathing pattern related to shortness of
breath, mucus, broncho-constriction, and airway
irritants
 Activity intolerance due to fatigue, ineffective breath
patterns, and hypoxemia
 Knowledge deficit of disease
 Ineffective coping related to reduced socialization,
anxiety depression, lower activity level, and the
inability to work
 Lung parenchyma in its strictest sense refers
solely to alveolar tissue with respiratory
bronchioles, alveolar ducts and terminal
bronchioles. However, the term is often used
loosely to refer to any form of lung tissue, also
including bronchioles, bronchi, blood vessels and
lung interstitium.
THE END
ASTHMA/ BRONCHIAL ASTHMA
 Asthma is a common chronic inflammatory
disease of the airways characterized by variable
and recurring symptoms, reversible airflow
obstruction, and bronchospasm. Symptoms
include wheezing, coughing, chest tightness, and
shortness of breath.
 Asthma is thought to be caused by a combination
of genetic and environmental factors, and many
patients show signs of both.
DEFINITION 2
 Bronchial Asthma is a persistent, inflammatory
disorder of the airways with a lasting history of
hypersensitivity. There is bronchial
hyperreactivity or hyperresponsiveness. There is
airway narrowing brought on by elevated
secretion of mucus, spasm of the bronchi and
formation of edema of the bronchial mucosa. It
is reversible. A variety of stimuli lead to the boost
of the sensitivity of the airways and the
associated irritation.
 Asthma may be classified as atopic
(hypersensitivity response to an extrinsic
antigen) or non-atopic (intrinsic) response to
diverse nonimmune mechanisms e.g. exercise, RI
infections, ingestion of aspirin, emotional upset,
irritants cigarrette smoke.
 An acute asthma exacerbation is commonly
referred to as an asthma attack. The classic
symptoms are shortness of breath, wheezing, and
chest tightness.
 The pathophysiology of asthma involves the
presence of known triggering elements and an
error in the body’s response to external matters.
Hereditary factors also play a big role.
 Asthmatics react strongly to things that they are
allergic to or find irritating.
 Airway hyperresponsiveness or bronchial
hyperreactivity in asthma is an exaggerated
response to numerous exogenous and endogenous
stimuli. The mechanisms involved include direct
stimulation of airway smooth muscle and indirect
stimulation by pharmacologically active
substances from mediator-secreting cells such as
mast cells or nonmyelinated sensory neurons.
 So, there is excessive responsiveness of the
airways to different stimuli like viruses,
allergens or strenuous physical exercise.
SOME TYPES OF ASTHMA
 Type 1 brittle asthma refers to disease with
wide peak flow variability, despite intense
medication.
 Type 2 brittle asthma describes background
well-controlled asthma, with sudden severe
exacerbations.
 Status asthmaticus is an acute exacerbation of
asthma that does not respond to standard
treatments of bronchodilators and steroids. Half
of cases are due to infections with others caused
by allergen, air pollution, or insufficient or
inappropriate medication use.
 Exercise-induced asthma is a medical condition
that occurs when the airways narrow as a result
of exercise.
 Cardiac asthma is a medical symptom, of
wheezing, coughing or shortness of breath which
may be due to congestive heart failure. It is
known as cardiac asthma because the symptoms
may mimic asthma.
NB
 The autonomic nervous system innervates and
therefore controls contraction and relaxation of
smooth muscles layers in the airways. It
therefore controls the diameter of the bronchi
and resistance to airflow.
 The vagus nerve and the cholinergic
receptors under parasympathetic control
produce broncho-constriction
 and the sympathetic NS through beta
adrenergic receptors produce broncho-
dilation.
Sensitization
 Sensitization is the initial exposure to an
allergen. The initial exposure causes the immune
system to react by producing histamine and
mediators, which are inflammatory substances.
THERE ARE TWO RESPONSE PHASES IN ASTHMA.

Early Phase / acute-phase response

 The early phase response typically occurs within 20
mins to an hour of initial exposure to an allergen. (but
can result in immediate bronchoconstriction ) the
reaction occurs when antigen binds to sensitized mast
cells on the mucosal surface of the airways .The
trigger causes release of chemical mediators from IgE
coated mast cells. The histamines and mediators
cause allergy symptoms such as sneezing, itchy eyes
and runny nose. They also cause asthma symptoms
such as wheezing, coughing and shortness of breath.
There is bronchoconstriction due to direct stimulation
of parasympathetic receptors, mucosal edema due to
increased vascular permeability, and increased mucus
secretions.
LATE PHASE

 The late phase response begins from three to 10 hours

after the initial reaction / trigger . The trigger causes
release of inflammatory mediators from mast cells,
macrophages, and epithelial cells. This in turn causes
activation of other inflammatory cells like basophils,
esinophils, neutrophils. They themselves produce
epithelial injury and edema, changes in mucociliary
function and reduced clearance of respiratory tract
secretions plus increased airway responsiveness. This
response can last for days or even weeks, it prolongs
the asthma attack and includes more severe
congestion and inflammation than is seen in the
initial response. Chronic inflammation can lead to
airway remodeling, in which case airflow limitations
may be only partially reversible.
PATHOPHYSIOLOGY
 The pathophysiology of asthma involves the
trigger or triggering event, then inflammatory
cell infiltration by Neutrophils, basophils,
Eosinophils, Lymphocytes that respond to
invasion of infectious agents and there is
epithelial cell injury.
 Mast cell activation and cytokins makes
inflammation worse. Allergens cause mast cells
to degranulate, releasing histamine,
leukotrienes, and other mediators that
perpetuate the airway inflammation.
 Airway inflammation contributes to airway
hyperresponsiveness, airflow limitation,
respiratory symptoms, and disease chronicity.
 (IgE)-mediated response to aeroallergens.
 There is lung hyperinflation, smooth muscle
hypertrophy, lamina reticularis thickening,
mucosal edema, epithelial cell sloughing, cilia cell
disruption, and mucus gland hypersecretion
excess secretion of mucus, bronchial spasm and
inflammation of the airways.
 In some patients, persistent changes in airway
structure occur, including sub-basement fibrosis,
mucus hypersecretion, injury to epithelial cells,
smooth muscle hypertrophy, and angiogenesis.
 The bronchial tubes react severely in response to
allergens; this exaggerated reaction can lead to
suffocation and coughing due to hypersensitivity
of the airways. There is secretion of excessive
mucus that floods and even blocks the airways.
Broncho-spasm occurs spasms of the muscle
layers in the bronchial walls. The early and late
phases of an allergic response together contribute
to inflammation of the airways and increased
mucus production. There is increased vascular
permeability and edema. Plasma cells leak into
the bronchial tissues.
 The mechanism underlying airway angiogenesis
in asthma and its precise clinical relevance have
not yet been completely determined. Reports
suggest that a pro-angiogenic milieu is not a
consequence of, but rather dictates the chronic
inflammation of asthma.
CAUSES OF ASTHMA ATTACKS
 Airborne allergens, such as pollen, animal
dander, mold, cockroaches and dust mites
 Respiratory infections, such as the common cold

 Physical activity (exercise-induced asthma)

 Extremes in temperature such as Cold air

 Air pollutants and irritants, such as smoke

 Certain medications, including beta blockers,

aspirin and other nonsteroidal anti-inflammatory
drugs
 Strong emotions and stress
 Sulfites, preservatives added to some types of
foods and beverages
 Gastroesophageal reflux disease (GERD), a
condition in which stomach acids back up into
your throat
 Menstrual cycle in some women changes in
hormone levels
 Allergic reactions to some foods, such as peanuts
or shellfish
FOODS ASSOCIATED WITH ALLERGIC
SYMPTOMS ARE

 Eggs
 Cow's milk

 Peanuts

 Soy

 Wheat

 Fish

 Shrimp and other shellfish

 Salads & fresh fruits

RISK FACTORS

 Having a blood relative with asthma

 Having an allergic condition, such as atopic
dermatitis or allergic rhinitis (hay fever)
 Being overweight
 Being a smoker
 Exposure to secondhand smoke
 Having a mother who smoked while pregnant
 Exposure to exhaust fumes or other types of pollution
 Exposure to occupational triggers, such as chemicals
used in farming, hairdressing and manufacturing
 Low birth weight
 Factors that contribute to exercise-induced
bronchospasm symptoms (in both people with
asthma and athletes) include the following:
 Exposure to cold or dry air

 Environmental pollutants (eg, sulfur, ozone)

 level of bronchial hyperreactivity

 Chronicity of asthma and symptomatic control

 Duration and intensity of exercise

 Allergen exposure in atopic individuals

 Coexisting respiratory infection

ADDITIONAL INFORMATION
 In some patients with chronic asthma, airflow
limitation may be only partially reversible because of
airway remodeling (hypertrophy and hyperplasia of
smooth muscle, angiogenesis, and subepithelial
fibrosis) that occurs with chronic untreated disease.
 Airway inflammation in asthma may represent a loss
of normal balance between two "opposing"
populations of Th lymphocytes. Two types of Th
lymphocytes have been characterized: Th1 and Th2.
Th1 cells produce interleukin (IL)-2 and IFN-α, which
are critical in cellular defense mechanisms in
response to infection. Th2, in contrast, generates a
family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13)
that can mediate allergic inflammation.
 Airway obstruction causes increased resistance to
airflow and decreased expiratory flow rates.
 There is decreased ability to expel air and this
may result in hyperinflation. The resulting over-
distention helps maintain airway patency,
thereby improving expiratory flow; however, it
also alters pulmonary mechanics and increases
the work of breathing.
 Vasoconstriction occurs due to alveolar hypoxia.
Vasoconstriction is considered an adaptive
response to ventilation/perfusion mismatch.
 In the early stages, when ventilation-perfusion
mismatch results in hypoxia, hypercarbia is
prevented by the ready diffusion of carbon
dioxide across alveolar capillary membranes.
Thus, patients with asthma who are in the early
stages of an acute episode have hypoxemia in the
absence of carbon dioxide retention.
Hyperventilation triggered by the hypoxic drive
also causes a decrease in PaCO2.
 An increase in alveolar ventilation in the early
stages of an acute exacerbation prevents
hypercarbia. With worsening obstruction and
increasing ventilation-perfusion mismatch,
carbon dioxide retention occurs. In the early
stages of an acute episode, respiratory alkalosis
results from hyperventilation. Later, the
increased work of breathing, increased oxygen
consumption, and increased cardiac output result
in metabolic acidosis. Respiratory failure leads to
respiratory acidosis. Death can result.
DIAGNOSIS
 A physical examination
 bronchodilator reversibility testing.

 Pulmonary Function Tests (PFT) or spirometry).

 FEV1 / FVC ratio

 A Chest Xray

 skin testing

 Blood levels of IgE and esinophils

NB
 Chronic obstructive pulmonary disease can
coexist with asthma and can occur as a
complication of chronic asthma. After the age of
65, most people with obstructive airway disease
will have asthma and COPD.
 COPD can be differentiated by increased airway
neutrophils, abnormally increased wall
thickness, and increased smooth muscle in the
bronchi.
 COPD and asthma sharing similar principles of
management: corticosteroids, long-acting beta-
agonists, and smoking cessation.
 The end
PEAK FLOW METER
TREATMENT / MANAGEMENT OF ASTHMA
 Bronchodilators
 Mucolitics

 Cortico steroids

 Beta adrenergics agonists(promote

bronchodilation)
 Anti cholernergics (prevent bronchoconstriction)

 Antihistamines, antibiotics, patient teaching,

Expectorants
SUBCUTANEOUS EMPHYSEMA
 Occurs when gas or air is present in the subcutaneous
layer of the skin. It usually occurs on the chest, neck
and face, where it is able to travel from the chest
cavity along the fascia. It can result from puncture of
parts of the respiratory or gastrointestinal systems.
Air may become trapped as a result of penetrating
trauma (e.g., gunshot wounds or stab wounds) or
blunt trauma. Infection (e.g., gas gangrene) can cause
gas to be trapped in the subcutaneous tissues.
 Subcutaneous emphysema can be caused by medical
procedures and medical conditions that cause the
pressure in the alveoli of the lung to be higher than
that in the tissues outside of them. Its most common
causes are pneumothorax and a chest tube that has
become occluded by a blood clot or fibrinous material.
 When the condition is caused by surgery it is
called surgical emphysema. The term
spontaneous subcutaneous emphysema is used
when the cause is not clear. Subcutaneous
emphysema is not typically dangerous itself, but
the underlying condition like a pneumothorax
can be. Subcutaneous emphysema usually does
not require treatment as small amounts of air are
reabsorbed by the body. When necessary it is
treated by removing air from the tissues using
large bore needles, skin incisions or
subcutaneous catheterization. Chest tubes would
only be used if there is a definite pneumothorax.
COPD
 Asthma costs the United States approximately
$56 billion each year in medical costs, lost school
and work days, and early deaths.
 The environment, allergens, and genetics interact
with the body's immune system to cause the
disease and aggravate the symptoms.
 The airway obstruction in asthma is usually
reversible; however, if left untreated, the chronic
inflammation from asthma can lead the lungs to
become irreversibly obstructed due to airway
remodelling.
 Asthma is the result of chronic inflammation of
bronchi and bronchioles, which subsequently results
in increased contractability of the surrounding
smooth muscles. The narrowing is typically reversible
with or without treatment. Occasionally the airways
themselves change. Typical changes in the airways
include an increase in eosinophils and thickening of
the lamina reticularis. Chronically the airways'
smooth muscle may increase in size along with an
increase in the numbers of mucous glands. Other cell
types involved include: T lymphocytes, macrophages,
and neutrophils. There may also be involvement of
other components of the immune system including:
cytokines, chemokines, histamine, and leukotrienes.
 goblet cell metaplasia, and epithelial basement
membrane thickening.
 The wheezing is most often when breathing out.
While there are the primary symptoms of
asthma, some people present primarily with
coughing, and in severe cases, air motion
may be significantly impaired such that no
wheezing is heard.
 In a mild exacerbation the peak expiratory flow
rate (PEFR) is ≥200 L/min, or ≥50% of the
predicted best. Moderate is defined as between 80
and 200 L/min, or 25% and 50% of the predicted
best, while severe is defined as ≤ 80 L/min, or
≤25% of the predicted best.