COPD

1. Presented By-
Haranjan Kaur
MSc Nursing 2nd Year
Roll No.- 4
Critical Care Nursing
CON, DMCH
Submitted To-
Mrs.Shivani Kalra
Asst.Prof.
Critical Care Nursing
CON, DMCH

3.  COPD is a broad, non specific term that
describe a group of pulmonary disorder with
symptoms of chronic cough and
expectoration, dyspnea, and impaired
expiratory air flow.
 COPD is a condition in which air flow is
obstructed by emphysema, chronic bronchitis
or both.

5.  The airflow obstruction is usually progressive
and irreversible, and it may be associated
with airway hyperactivity.
 Asthma used to be considered with in disease
group of COPD, but now it is considered as a
separate disorder.
 People with COPD commonly become
symptomatic during the middle adult years
and the incidence of COPD increases with
age.

6. COPD commonly occurs either as a result of-
 bronchial mucosal edema
 Smooth muscle cell contraction
 As a result of decrease elastic recoil

11. •Chronic obstructive
lung diseaseCOLD
•Chronic obstructive
airflow diseaseCOAD
•Chronic airflow
obstructionCAO

17.  Cigarette smoking
 Exposure to smoke from biomass
 Exposure to dusty of polluted air
 Alpha antitrypsin deficiency can cause
emphysema in non smokers
 An association of low birth weight

19. Smoking, cigar or pipes
Irritates the goblet cells Depress the activity
and mucus glands of scavenger cells
Causes increased accu-
Mulation of mucus Affects respiratory
tract’s cleaning
mechanism which keeps
breathing passage free of
inhaled irritants, bacteria etc.
Produces more irritation,
infection and damage
to the lungs

20. Airflow is obstructed
Air becomes trapped behind the obstruction
Alveoli gets distended
Diminishes lung capacity

21. Deficiency of alpha 1 antitrypsin
Predisposes young patients to rapid
development of lobular emphysema

22. Noxious gases inhalation
Abnormal inflammatory response in airways,
parenchyma, pulmonary vasculature
Body attempts to repair the chronic
inflammation

23. Narrowing in the air ways
Over time injury and repair process causes
scar tissue formation
Permanent narrowing of airway lumen

24. Parenchymal destruction ( emphysema)
Airflow obstruction resulting in
 muscular weakness
 Increased circulatory inflammatory markers

25.  COPD to be suspected in any patient over the
age of 40 years who presents with symptom
of-
 Persistent cough and sputum production
 Breathlessness

31.  Chronic bronchitis is
a prolonged (or
extended)
inflammation of
bronchi,
accompanied by a
chronic cough and
excessive production
of mucus for at least
3 months each year
for 2 consecutive
year.

32. Cigarette smoking is
the most leading
cause of COPD (90%).
Second hand smoking
inhalation.
Long term inhalation
of irritants into lungs
such as air pollution,
chemical fumes or
dust.

33.  It is chronic ongoing, progressive disease of
lower respiratory tract in the lung. It is one
type of COPD.

34.  Occupational exposure to
hazardous airborne substance.
 Viral, Bacterial and mycoplasmal
infection can produce acute
episodes of bronchitis.

36. Causes like smoke or another environmental
pollutants irritates the airways.
Hyper secretion of mucus and inflammation
Constant irritation increase the number of
mucus secreting glands and goblet cells

37. Ciliary function is reduced more mucus
production
Bronchial wall get thickened, the bronchial
lumen is narrowed and may plug the airway
Alveoli adjacent to bronchioles may become
damaged and fibrosed, resulting in altered
function of alveolar macrophages

38. Bronchial narrowing follows as a result of
fibrotic changes that occur in airway
Irreversible lung changes eventually may
occur possibly resulting in emphysema
Accumulation of secretion in bronchioles
reduced the alveolar ventilation

39. Hypoxia
Respiratory acidosis

42.  Earliest symptom is a chronic
cough, production of thick,
white mucus especially when
rising in the morning and in
the evening.
 Chronic productive cough
most commonly in winter
season and may persists for
several weeks.
 Bronchospasm may occur
during severe bouts of
coughing.

43.  As disease progress, sputum
may become yellow, purulent
and copious.
 Expiration is prolonged
secondary to obstructed air
passage.
 Cyanosis secondary to
hypoxemia may be noted,
especially after severe
coughing.

44.  Dyspnea begins with
exertion, but progress to
occurring with minimal
activity and later occur at
rest.
 Right sided heart failure
results from tachycardia in
response to hypoxemia,
which causes edema in the
extremities.

46. Type A
 These fighter are pink and puffing.
 Although the person is breathless, arterial
perfusion of oxygen and carbondiooxide are
normal.
 There is no cor pulmonale.

47. Type B
 On the other hand these non fighter is blue
and bloated.
 The person does not appear to be breathless,
but has marked arterial hypoxemia, CO2
retention.

49. o A complete history including
family, environmental
exposure to irritating
substance, occupation and
smoking habits.
o Physical examination of the
patient includes-
 Palpation reveals a hyper
inflated chest with
reduced expansion.
 Percussion reveals increased
resonance.

50. o Chest X-ray of the patient
reveals an enlarged heart.
o Pulse oximetry may show
desaturation.
o ABG may reveals hypoxemia
with beginning hypercapnia.
o CBC:-Hematocrit and
hemoglobin level may be
slightly increased. This may
be caused by body’s response
to chronic hypoxemia.

51.  Pulmonary function test
demonstrate decreased
vital capacity, forced
expiratory volume and
increased residual
volume and total lung
capacity.
 Bronchoscopy
 Microscopic examination
of sputum for malignant
cells.

52.  Avoidance of respiratory
irritants (particularly
tobacco smoke)
 Vaccination against
influenza and
S.pneumoniae.
 All patient with acute
URTI should receive proper
treatment, including
antimicrobial therapies at
first signs of purulent
sputum.

55.  Quitting smoking:-is most important, yet
most commonly overlooked part of treatment
for chronic bronchitis.

56.  Bronchodilators:-helps to remove bronchial
secretions, while relieving bronchospasm and
reducing airway obstruction. In doing so,
more oxygen is distributed throughout the
lungs and breathing is improved.

57.  Fluids:-are given by mouth
or I/V and are an important
part of chronic bronchitis
treatment.
 Proper hydration helps
loosen secretion, making
them easier to expel from
the airway through
coughing.

58.  Postural drainage:-is a technique that uses
gravity to assist in the removal of secretions
from airways. It is often coupled with chest
physiotherapy.

59.  Chest Physiotherapy:-also referred to as
chest percussion, is a technique that involve
clapping on the chest and or back to help
loosen thick secretion in order to make them
easier to expel, or cough up.
 It is often used with postural drainage and
can be performed using cupped hands or an
airway clearance device.

62.  Glucocorticoids:- When a patient does not
respond to more conservative measures,
glucocorticoids may be prescribed as a part
of treatment plan for chronic bronchitis.
 Change in occupation if work involves
exposure to dust and chemical irritants.

63. Emphysema

64. Emphysema

65.  Emphysema is defined as an abnormal
distention of air spaces beyond the terminal
bronchioles, with destruction of the wall of
the alveoli. It is end stage of a process that
has progressed slowly for many years.
 By the time, the patient develops symptoms,
pulmonary function is often irreversibly
impaired. Along with chronic obstructive
bronchitis, it is a major cause of disability.

68.  Smoking is the main cause of emphysema.
 However there is a familial predisposition to
emphysema associated with a plasma protein
abnormality.
 A deficiency of Alpha1 antitrypsin, an enzyme
inhibitor. Without it certain enzyme like
protease and elastase can attack and destroy
the connective tissue of the lungs.
 Genetically susceptible person is sensitive to
environmental factors (smoking, air pollution,
infectious agents, allergens) and develops
chronic obstructive symptoms.

70. Several factors causes airway obstruction
like inflammation of bronchial mucosa,
excessive mucus production, loss of elastic
recoil of the airway collapse of bronchioles
and redistribution of air to functional alveoli.
As the wall of alveoli are destroyed, pockets
of air form between the alveolar spaces
(blebs) and with in lungs parenchyma
(bullae).

71. This leads to increased ventilatory dead space
from the area that do not participate in the
gas exchange.
Work of breathing is increased, because there
is less functional lung tissue too exchange
oxygen and carbon dioxide.
Impaired oxygen diffusion cause hypoxemia.

72. As stage of disease progresses, the CO2
elimination decreases and Increase CO2
tension in arterial blood
Respiratory Acidosis
Continuous breakdown of alveolar wall leads to
destruction of pulmonary capillaries, further
decreasing perfusion and ventilation.

73. Pulmonary blood flow increased
Increase right ventricle pressure
Increase in pulmonary artery pressure
Right sided heart failure
( Cor pulmonale)

74.  Centrilobar (Centroacinar) :-is the most
common types, produces destruction in
bronchioles, usually in upper lung region.
Inflammation develops in the bronchioles,
but usually the alveolar sac remains intact.
 Pathological changes occurs in the centre of
secondary lobule, peripheral portion of the
acinus are preserved.
 It leads to hypoxemia, hypercapnia,
polycythemia and right sided heart failure.

76. Pan lobular (Panacinar):- Affects both
the bronchioles and the alveoli and most
commonly involves the lower lungs. These
forms of emphysema occur most often in
smokers.
 There are destruction of respiratory
bronchioles, alveolar duct, and alveoli).
 All air spaces with in lobule are enlarged, but
there is little inflammatory response.
 It leads to hyper inflated chest, Dyspnea on
exertion and weight loss.

78. Para septal:-It destroy the alveoli in lower
lobes of lungs resulting in isolated blebs
along the lung periphery. It occurs in older
clients and the client with an inherited
deficiency of AAT.(Alpha1 antitrypsin)

81.  Symptom commonly occurs
in 5th decade (after about
20 years of smoking)
 Increasing dyspnea on
exertion.
 Dyspnea develops insidiously
and become the major
symptom in emphysema.
 The difficulty in breathing
progress and occur with
even the simplest activity of
daily living, such as eating,
bathing and walking.

82.  Exertional dyspnea
 Anorexia, weight loss, weakness and inactivity
 Pursed lip breathing and use of accessory
muscles (sternocleido mastoid muscle) are
common.
 Inspiration is difficult because of rigid chest
cage.
 Retraction of supra clavicular fossae occurs on
inspiration causing the shoulder to heave
upward.
 Expiration is prolonged, difficult and often
accompanied by wheezing.

83.  Instead of being an involuntary passive act,
expiration becomes active and require
muscular effort.
 Patient becomes increasingly short of breath,
the chest becomes rigid and ribs are fixed at
their joints.
 Chronic hyperinflation of patient with
emphysema leads to barrel chest.

85.  Increased cough, purulent sputum, wheezing,
dyspnea, occasionally fever.
 When sitting up, they often lean slightly
forward and are markedly short of breath.
 Distended neck veins.

86. In advanced stage of emphysema-
 Memory loss, drowsiness, confusion, loss of
judgment.
 If disorder goes untreatment, the CO2
content in blood may reach toxic levels,
resulting in lethargy stupor and eventually
coma.
 This condition is called CO2 narcosis.

87.  History of the patient.
 Physical examination of the patient include:-
 Visual inspection shows a barrel chested
person.
 When chest is examined, hyper resonance
are found though out lung field.
 Persistent shortness of breath with gradual
progressive Exertional dyspnea.
 Auscultation reveals distant heart sounds,
lungs auscultation reveals diminished breath
sound, wheezing and crackles.

88.  Chest radiography shows hyper inflated lung
fields.
 No cardiac involvement
 PFT shows decrease in overall function
including total lung capacities, residual
volume and vital capacity and forced
expiratory volume.
 ABG shows hypoxemia and respiratory
acidosis.

89. Grade Degree of breathlessness related
to activities
0 No breathlessness except with
strenuous exercise
1 Breathlessness when hurrying on
the level of walking up a slight hill
2 Walk slower than the people of
same age on the level because of
breathlessness, or stop for breath
when walking at my own pace on
the level

90. Grade Degree of breathlessness
related to activity
3 Stop for breath after walking about
100 yards or after a few minutes on
the level.
4 Too breathlessness to leave house
or while dressing or undressing.

91.  Chest X Ray:- Presence of large bullae
 Blood Count:- Polycythemia
Alpha 1 antiproteinase assayed
 Spirometery:- Severity FEV1
Mild 50-80%
Moderate 30-49%
Severe <30%

92. Diagnosis of COPD when:-
Post broncho dilator FEV1 <80% of predicted
value
 CT Scan:- To quantify emphysema and to
detect bullae.
 Pulse Oximetry:- Oxygen saturation <93%
 ABG

94. Stage Characteristics
0 Normal Spirometery, Chronic
symptom of cough, sputum
production
1 (Mild) FEV1/FVC <70%
FEV1 more or equal to 80%
predicted
May or may not have chronic
symptom of cough, sputum
production

95. 2 ( Moderate):- FEV1/FVC <70%
FEV1 50-80%
May or may not have chronic
symptom of cough, sputum
production, people usually
experience some shortness of
breath with exertion
3 ( Severe):- FEV1/FVC <70%
FEV1 30-50%In this stage, people usually
are often tired and short of breath. They may
have frequent exacerbation flares (or "flare-
ups") requiring extra treatment or even
hospitalization.

96. 4 ( Very severe) FEV1 is less than 30 percent
of normal; or FEV1 is less than
50 percent of normal and
chronic respiratory failure is
present (meaning the person
needs chronic oxygen
therapy). In this stage, people
are often short of breath even
at rest.

100. Oxygen Therapy:-is the only therapy for
COPD.
 In severe hypoxemia, oxygen is administered
at least 16 hours per day, with 24 hours
preferable.

101. Bronchodilators:-are prescribed to
reverse bronchospasm, thereby reducing
obstruction and improving air flow.
 The preferred route is via MDI.
 This allows for direct administration to the
affected area, minimizing side effects and
systemic infection.

102. Beta2-adregenic agonist:- produce less
broncho dilation in COPD than in Asthma but
are helpful in rapid reversal of bronchospasm
on an as needed basis.
 The choice of drug are-
 Albuterol
 Terbutaline
 Isoetherine

104. Anti cholinergic agents:- may be more
effective than beta adrenergic agonist in
COPD.
 The only currently available preparation are-
 Ipratropium bromide (Atrovent):- The regular
use of Ipratropium is recommended, if the
patient has daily symptom.

106. Methylxanthines:- (Theophylline and
Aminophylline) have experienced a decline in
popularity due to the potentially for toxicity.
 It has incompatibility with many other
medication, and multiple systemic side
effect

111.  Short acting bronchodilator (Beta2-
adregenic agonist )
 If still symptomatic, use combined therapy
with short acting B2 agonist and short acting
anti cholinergic.
 In moderate or severe cases, use long acting
bronchodilators with inhaled corticosteroids.
 If no improvement is seen, consider adding
Theophylline.

112.  Antimicrobial Therapy:-Patient with
emphysema are susceptible to lung infection.
 S. pneumoniae, H.influenzae are the most
common organism involved.
 Antimicrobial therapy is usually prescribed.
 An antimicrobial regimen is used at the first
sign of respiratory infection, as evidenced by
purulent sputum, increased cough.
 Patient should receive the pneumococcal
vaccine every 5 to 10 years.

114.  Anti inflammatory therapy:-Approximately
one third of the patients with COPD improve
with chronic oral corticosteroid therapy.
 Inhaled as an aerosol spray, steroid can help
relieve symptom of emphysema.
 Dexamethasone, beclomethasone are the
example of corticosteroids.

115.  Patients with
emphysema caused
by an alpha 1
antitrypsin (AAT)
may be given
infusion of AAT to
help slow the
progression of lung
damage.

116.  Lung Volume Reduction Surgery:-It involves
the removal of portion of the diseased lung
parenchyma that is not contributing to the
ventilation but occupies a space in the
thorax.
 This allows the functional tissue to expand,
resulting in improved elastic recoil of the
lung and improved chest wall and
diaphragmatic mechanics.

117.  This type of surgery does not cure the
emphysema, but it may decrease dyspnea,
improve lung function and improve the
patient’s overall quality of life.

118.  BULLECTOMY:- Bullae are the enlarged air
spaces that do not contribute to the
ventilation but occupy space in thorax. These
areas are need to be excised.
 Bullectomy helps to reduce dyspnea and
improve lung function.

119.  Lung Transplantation:-Single lung
transplantation is a viable alternative for
definite surgical treatment of end stage
emphysema .
 It is usually reversed for younger patients
with alpha 1 antitrypsin deficiency.
 Generally, the patients must be younger
than 60 years of age and in relatively good
health.

121. An important part of chronic bronchitis
treatment is pulmonary rehabilitation which
includes-
 Education
 Nutritional counseling
 Learning breathing technique
 Help the patient in quitting smoking
 Starting an exercise regimen
 Avoiding cold air and wind exposure that can
cause bronchospasm

122.  Monitor sputum for signs of infection
 Learn, how to use MDI.
 Teach the client about measures to improve
overall health, such as eating a well
balanced diet, getting plenty of rest and
engaging in moderate activity.

123.  Identify patient and check instruction of
physician and nursing care plan.
 Explain procedure to the patient and check
when meals were last taken.
 Wash hands and dry.
 Instruct the patient to perform
diaphragmatic breathing.
 Position the patient in prescribed postural
drainage position after consulting with the
physician.

124.  Cover area and towel.
 Percussion:- Clap with cupped hands over
chest wall for 1 to 2 minutes in each lung
area. Percuss from-
 Lower ribs to shoulder in back.
 Lower ribs to top of the chest in front.
Avoid clapping over spine, liver, kidney, spleen,
clavicle or sternum.

126.  Vibration:- Remove towel or place hand,
palm down on chest area to be drained with
one hand over the other and fingers together
or place hands side by side.
 Instruct the patient to inhale deeply and
exhale slowly through pursed lip.
 Tense all the muscles of the hands and arm
and vibrate the hands specially heels with
moderate pressure during exhalation.

127.  Stop vibration and relieve pressure on
inspiration.
 Vibrate for 5 exhalation over each lung area
which is affected.
 After 3-4 vibrations, encourage the patient
to cough and expectorate sputum in the
sputum cup.
 Allow the patient to rest for several minute.
 Repeat percussion and vibration cycles to
patient tolerance.

128.  Wash hands.
 Assists the patient to comfortable position.
 Assist with oral hygiene.
 Record procedure.

129. Nursing Diagnosis:-Impaired gas exchange
related to ventilation-perfusion inequality.
Goal:-Improvement in gas exchange
Intervention:-Administer bronchodilators as
prescribed by inhalation.
 Assess for correct technique of metered dose
inhaler (MDI) administration.
 Evaluate effectiveness of nebulizer or MDI
treatments.
 Instruct and encourage patient in
diaphragmatic breathing and effective
coughing.

130.  Administer oxygen to the patient.
 Observe the patient for signs of hypoxemia,
cyanosis and tachycardia.

131. Nursing Diagnosis:-Ineffective airway
clearance related to broncho constriction,
increased mucus production, ineffective
cough, and broncho pulmonary infection.
Goal:-Achievement of airway clearance.
Intervention:-Adequately hydrate the
patient.
 Teach and encourage the use of
diaphragmatic breathing and coughing
technique.
 Assist in administering nebulizer or MDI.

132.  If indicated, perform postural drainage with
percussion and vibration in the morning and
at night as prescribed.
 Instruct the patient to avoid bronchial
irritants such as cigarette, smoke, aerosols
extremes of temperature and fumes.
 Teach early signs of infection that are to be
reported to the clinician immediately.
 Administer antibiotics as prescribed.

133. Nursing Diagnosis:-Ineffective breathing
pattern related to shortness of breath,
mucus, broncho constriction, and airway
irritants.
Goal:-Improvement in breathing pattern
Intervention:-Teach the patient
diaphragmatic breathing and pursed lip
breathing.
 Encourage the use of an inspiratory muscle
trainer if prescribed.

134.  Encourage the patient to be immunized
against influenza and streptococcus
pneumoniae.

135.  Encourage alternating activity with rest
periods. Allow patient to make some
decisions ( bath, shaving) about care based
on tolerance.

136. Nursing Diagnosis:-Self care deficits related
to fatigue secondary to increased work of
breathing and insufficient ventilation and
oxygenation.
Goal:-Independence in self care activities
Intervention:-Teach patient to coordinate
diaphragmatic breathing with activity (e.g.
walking, bending)
 Encourage patient to begin to bathe self,
dress self, walk and drink fluids.
 Teach postural drainage.

137. Nursing Diagnosis:-Activity intolerance
due to fatigue, hypoxemia and ineffective
breathing pattern.
Goal:- Improvement in activity tolerance
Intervention:-Support the patient in
establishing a regular regimen of exercise
such as walking or other appropriate
exercises.
 Assess the patient’s current level of
functioning and develop exercise plan based
on baseline functional status.

138.  Suggest consultation with a physical therapist
or pulmonary rehabilitation program to
determine an exercise program specific to
the patient’s capability.