Respiratory system

1. COPD
CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE

2. SYNONYMS
• Chronic obstructive pulmonary disease(COPD)
is also called as chronic obstructive lung
disease(COLD), chronic obstructive airway
disease(COAD),chronic airflow
obstruction(CAO).

3. DEFINITION
• Chronic obstructive pulmonary disease is a
progressive disease that makes it hard to breath.
“progressive” means the disease get worse over
time.
In COPD, less air flows in and out of the airways
because of one or more of the following:
• The airways and air sacs lose their elastic quality.
• The walls between many of the air sacs are
destroyed.
• The walls of the airways become thick and
inflamed.
• The airways make more mucus than usual, which
can clog them.

5. RISK FACTORS
Exposures:
• Cigarette smoking, pipe & cigar smoking is the
most important risk factor.
• Breathing in second hand smoke, Air
pollution, or chemical fumes or dust from the
environment or workplace.
• Previous Infectious diseases like HIV,
tuberculosis
• Poverty & malnutrition

6. Host factors:
• Genetic condition called alpha-1 antitrypsin
deficiency.(alpha-1 anti protease
deficiency)
• age:>40yrs
• Airway hyperactivity as in asthma

7. Chronic bronchitis Emphysema
Incidence:
• middle & late adult life
• More in male than females
• More in smokers than non smokers
• More in urban than in rural dwellers

8. CHRONIC BRONCHITIS
• Chronic bronchitis is defined as condition
associated with excessive tracheobronchial
mucus production to cause productive cough
for at least 3 months of the year for more than
2 consecutive years.
• Chronic bronchitis is characterized by
inflammation of airways extended from
trachea to small airways, alveoli.

9. EMPHYSEMA
• Emphysema is defined as abnormal
permanent distension of air spaces distal to
the terminal bronchiole with destruction of
alveolar septa.

10. PATHOLOGY OF COPD
• Chronic bronchitis & Emphysema occurs as a
result of inflammatory process involving the
airways and distal air spaces.
• Smoking & other airway irritants cause
neutrophils, macrophages, T-
lymphocytes(CD8+) & other inflammatory
cells accumulate in airways.
• Once they activated, they trigger
inflammatory response in which inflammatory
mediators navigate to site to destroy &
remove foreign debris

11. • Repeated exposure to airway irritants cause
ongoing inflammatory response which causes
permanent inflammation of airways, chronic
bronchitis.
• In emphysema, oxidants produced by smoking
& proteases produced by inflammatory
macrophages, epithelial cell cause protease &
anti protease imbalance which is responsible
for breakdown of lungs fragile elastic lamina,
destruction of alveolar septa.
• Mediators: LTb4( attracts neutrophils,
lymphocytes),TNFα, IL1β, IL6(amplify
inflammatory response) & TGFβ(induce
fibrosis in small airways)

13. s

14. PATHOLOGICAL CHANGES
In chronic bronchitis:
• Hypertrophy & hyperplasia of mucous
producing glands.
• Goblet cell hyperplasi
• Reduction in ciliated cells
• Mucosal edema & intra luminal mucous
plug
• Reduction in caliber of airways

15. Normal reid index 0.44±0.09
Chronic bronchitis>0.51

16. In Emphysema:
• Severe destruction of small airways, alveoli.
• Destruction of alveolar septa.
• Formation of large pockets called bullae.

18. CLASSIFICATION OF EMPHYSEMA
Centriacinar:
Destruction and distension are
limited to respiratory bronchiole and alveoli
closely related to them(with sparing of the
periphery).
Predominantly found in upper
lobe & superior segments of lower lobe,
most frequently associated with cigarette
smoking.

19. • Panacinar:
Generalized destruction of both
central & peripheral portion of acinus.
Predominant in lower half of the lungs,
mostly associated with alpha 1 antitrypsin
deficiency.
• Paraseptal:
Involves only distal acinus. It involves
distal airway structures, alveolar ducts &
sacs. Localized around septa of the lungs.

21. SYMPTOMS
Chronic bronchitis Emphysema
•Ongoing cough with mucus
production(called smoker’s cough)
•Copious purulent sputum
•Breathlessness relatively late in onset
•Mucopurulent relapses more frequent
•Wheezing
•Chest tightness
•Minimal cough with expectoration
•Scanty mucoid sputum
•Breathlessness insidious in onset initially
on Exertional, gradually even at rest
•Mucopurelent relapses less frequent
• Generalised Weakness
•lethargy

23. On examination:
Inspection:
• Pt looks dyspnic
• Use of accessory muscles
• Barrel shaped chest (due to hyper inflation)
• Prolonged expiration
• Tripod positioning to facilitate action of accessory muscles.
• advanced disease patients have paradoxical inward movement
of the rib cage with inspiration (Hoover's sign),
• Patients with advanced disease have paradoxical inward
movement of the rib cage with inspiration (Hoover's sign).
• Emphysema patients, termed "pink puffers" are thin and non
cyanotic at rest and have prominent use of accessory muscles
• Chronic bronchitis patients are more likely to be heavy and
cyanotic & termed as “blue bloaters”.

26. Palpation:
-decreased chest expansion
Percussion:
- hyper resonance on lung fields
Auscultation:
–Decreased breath sounds
–Normal vesicular breathing but
prolonged expiration
–Expiratory ronchi
–Coarse crepitatons on both phases

27. INVESTIGATIONS
Chest X-Ray:
– Not sensitive for Dx
– To exclude other diseases
– Hyper-inflation signs
– Low set flat diaphragm
ABG:
 important for assessing patients with severe COPD.
Detect acute & chronic hypercapnia
 Respiratory acidosis(pco2 raised, hypercarbia)
Pao2 is markedly reduced (hypoxemia)
Measurement of serum α1AT level, normal level 2-4 g/l.

28. • ECG: May show features of right atrial
&ventricular hypertrophy.(tall P waves)
Pulmonary function testing (spirometry):
– Main method for diagnosing COPD.
low FEV1/FVC (< 70%)
– Used for classification of COPD severity.
Obstructive pattern
FEV1-reduced (<80%)
FEV1/FVC-reduced (<70%)
PEF-reduced
TLC-increased
RV-increased
CT Chest:can detect emphysema

29. COMPLICATIONS OF COPD
• Carbon dioxide narcosis: Persistant Co2
retention causes increase Paco2; hypercarbia,
causes drowsiness, altered sensorium,
headache.
• Respiratory failure:
Type Ι respiratory failure(low Pao2,
normal Paco2) occurs in mild to moderate
COPD.
Acute or Chronic Type ΙΙ respiratory
failure occurs in severe COPD.
• Secondary polycythemia: Results from
hypoxemia stimulating erythropoiesis.

30. COPD
Hypoxaemia
Hypercarbia
Pulmonary vasoconstriction
Pulmonary HTN
Chronic after load to R ventricle
RVH
RVF
Corpulmonale:

31. • Clinical findings: peripheral edema
raised JVP
tender hepatomegaly

33. MANAGEMENT
General measures:
• Cessation of smoking
• Avoid lung irritants
• Improve nutrition
• Regular exercises
• Chest physiotherapy.

34. Specific management:
• Mild COPD: Add short acting β2 agonists like
salbutamol 2-4mg or terbutaline 2.5-5mg 6 hourly.
• Moderate COPD: Add long acting β-stimulants like
salmetrol,2puffs of 25 mcg each 2-3 times a day,
formetrol 2 puffs of 6 mcg each 1-3 times a day with
short acting anti cholinergic like ipratropium
bromide 40-80μg 6 hourly or long acting anti
cholinergic like tiotropium bromide 18μg once a
day.
• Severe COPD: Add inhaled glucocorticosteroids like
beclomethasone/budesonide/fluticasone. If
response is not satisfactory add systemic
glucocorticosteroids like prednisolone/methyl
prednisolone.

35. • Very severe COPD: Long term O2, ventilatory
support, management of cardiac failure, may
consider surgical management.
Methylxanthines like aminophylline or
theophylline can be administered when
necessary.
Long term domiciliary oxygen therapy should
be administered to patients with PaO2<55 mm
hg, >16 hrs/day, 2-3ltr/min to maintain
SaO2>90%. This reduces pulmonary
hypertension, polycythemia, dyspnoea,
hypoxemia.
Antibiotics like tetracycline or ampicillin is
needed when respiratory infection present, if
no response sputum culture sensitivity to be

36. For out patients management doxycycline,
amoxicilline-clavulanate can be given.
Patients older than 65 years fluoroquinolones
like levofloxacin, gemifloxacin, moxifloxacin
can be given.
For hospitalized patients IV antibiotics like
azithromycin or fluoroquinolones or third
generation cephalosporins like ceftriaxone or
cefotaxime should be administered.

37. Severe acute exacerbation of COPD:
Oxygen: Initial therapy should be maintaining
SaO2 >90%, can be ).
Bronchodilators: Nebulisation of β2 agonists like
salbutamol 2.5mg every 20 min & anti
cholinergic agents like ipratropium bromide to
be administered.
Antibiotics: Indicated if sputum volume &
purulence is increased.
Most common organisms incluce
S.pneumoniae, H.influenzae, M,catarrhalis.
patients with severe exacerbation third
generation cephalosporins & fluoroquinolones
or an aminoglycoside to be given.

38. Corticosteroids: IV or oral corticosteroids to
be administered as they improve lung
function & hypoxemia.
Aminophylline: should be administered if
patient fails to respond to initial treatment
with Nebulization of β2 agonists. . Given as a
loading dose of 5mg/kg/hr as an infusion.
Diuretics: should be administered to patients
with gross cardiac failure.
Respiratory stimulants: Like Doxapram can
be if patient is not responding to
conventional agents. Dose 1.5-4mg/min as
infusion.

39. Non-invasive positive pressure
Ventilation(NIPPV): Ventilation should be
tried with tight fitting face mask.
This is used in patient with normal mental
status, stable cardiovascular function.
Indications- severe dyspnoea, use of
accessory muscles, paradoxical abdominal
motion, PH<7.35 mmhg, PaCo2> 45 mmhg,
Respiratory rate>25/min.

40. Invasive mechanical ventilation: When NIV fails
patient should be intubated for mechanical
ventilation.
Indications- severe dyspnoea, use of accessory
muscles, paradoxical abdominal motion,
Respiratory rate>35/min
Severe acidosis-PH<7.25
Hypercapnia>60 mmhg
Hypoxia<40 mmhg
Altered sensorium
Respiratory arrest, unstable cardiovascular
function, sepsis, hypotension, shock.

41. Surgical management:
• Bullectomy
• Lung volume reduction surgery(LVRS)-
resection of damaged portion of lung,
improves exercise tolerance but doesn’t
improve life expectancy.
• Lung transplantation- If FEV1<35% (PaO2<
60 mmhg), & PaCo2>50 mmhg.

42. GOLD
Stage
Severity Spirometry Management
0 At Risk Normal Avoid risk factors
I Mild FEV1/FVC <0.7 and FEV1 80%
predicted
Short acting β- 2
agonist
II Moderate FEV1/FVC <0.7 and 50% FEV1
<80% predicted
Long acting β- 2
agonist/short or long
acting anti cholinergics
III Severe FEV1/FVC <0.7 and 30% FEV1
<50% predicted
Add inhaled
steroids/methylxanthin
es
IV Very Severe FEV1/FVC <0.7 and FEV1 <30%
predicted
or
FEV1 <50% predicted with
respiratory failure or signs of
right heart failure
Add oxygen,
ventilatory support,
management of RHF

44. THANK YOU