The slideset will help faculties in teaching medical students and also for medical students in understanding the topic better.

1. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE.
Saswat…

2. DEFINITION…
• Chronic Obstructive Pulmonary Disease (COPD) is a common,
preventable and treatable disease that is
- characterized by persistent respiratory symptoms and
- airflow limitation that is due to airway and/or alveolar
abnormalities
- usually caused by significant exposure to noxious particles or
gases.

3. EPIDEMIOLOGY…
• The prevalence of COPD increases steeply with age, with the
highest prevalence among those > 60 years.
• Surveys have been completed in 29 countries. BOLD reported
worse lung function than earlier studies, with a prevalence of
COPD grade 2 or higher of 10.1% overall, 11.8% for men and
8.5% for women and a substantial prevalence of COPD of 3-11%
among never-smokers.

4. • In ICD-10, deaths from COPD or chronic airways obstruction are
included in the broad category of “COPD and allied conditions”
(ICD-10 codes J42-46).
• In 2005 COPD was the eighth leading cause of DALYs lost across
the world but by 2013 COPD was ranked as the fifth leading
cause of DALYs lost.

6. RISK FACTORS…
1. Genetic:
• The genetic risk factor that is best documented is a severe
hereditary deficiency of alpha-1 antitrypsin (AATD),48 a major
circulating inhibitor of serine proteases
• A significant familial risk of airflow limitation has been observed
in people who smoke and are siblings of patients with severe
COPD, suggesting that genetics together with environmental
factors could influence this susceptibility.

7. • Single genes, such as the gene encoding matrix
metalloproteinase 12 (MMP-12) and glutathione S-transferase
have been related to a decline in lung function50 or risk of
COPD.
• Several genome-wide association studies have linked genetic loci
with COPD including markers near the alpha-nicotinic
acetylcholine receptor, hedgehog interacting protein (HHIP), and
several others. Nevertheless, it remains uncertain whether these
genes are directly responsible for COPD.

8. 2. Age and Sex
• Age is often listed as a risk factor for COPD. It is unclear if
healthy aging as such leads to COPD or if age reflects the sum
of cumulative exposures throughout life. Aging of the airways
and parenchyma mimic some of the structural changes
associated with COPD.
• Recent data from developed countries has reported that the
prevalence of COPD is now almost equal in men and women,
probably reflecting the changing patterns of tobacco smoking.

9. • Although controversial, some studies have even suggested
that women are more susceptible to the effects of tobacco
smoke than men, leading to more severe disease for the
equivalent quantity of cigarettes consumed.

10. 3. Lung Growth and Development
• Any factor that affects lung growth during gestation and
childhood has the potential for increasing an individual’s
risk of developing COPD.
• A large study and meta-analysis confirmed a positive
association between birthweight and FEV1 in adulthood
and several studies have found an effect of early childhood
lung infections.

11. 4. Exposure to particles
• Cigarette smoking is the most commonly encountered risk
factor for COPD. Cigarette smokers have a higher prevalence
of respiratory symptoms and lung function abnormalities, a
greater annual rate of decline in FEV1, and a greater COPD
mortality rate than non-smokers.
• Other types of tobacco (e.g., pipe, cigar, water pipe) are also
risk factors for COPD.

12. • Smoking:
- During years of lung growth reduces maximally attained
lung function.
- The plateau phase is decreased in duration.
- The rate of decline of lung function is increased.
• Trivia: The average smoker loses about 2l of FEV1 over
50yrs.

13. DECLINE OF LUNG FUNCTION..

14. • Passive exposure to cigarette smoke, also known as
environmental tobacco smoke (ETS), may also contribute to
respiratory symptoms and COPD.
• Smoking during pregnancy may pose a risk for the fetus, by
affecting lung growth and development in utero, and possibly the
priming of the immune system.
• Occupational exposures, including organic and inorganic dusts,
chemical agents and fumes, are under-appreciated risk factors.

15. 5. Indoor and Outdoor Pollutants
• There is growing evidence that indoor biomass exposure to
modern and traditional fuels used during cooking may
predispose women to develop COPD. Almost three billion people
worldwide use biomass and coal as their main source of energy.
• The role of outdoor air pollution as a risk factor for COPD is
unclear, but its role appears to be relatively small in adults
compared to the role of cigarette smoking.

16. • The Children’s Health Study found that children from
communities with the highest levels of outdoor nitrogen
dioxide (NO2) and particulate matter < 2.5 μm in
aerodynamic diameter (PM2.5) were nearly 5 times more
likely to have reduced lung function.

17. 6. Socio-economic Status:
• Poverty is consistently associated with airflow obstruction
and lower socioeconomic status is associated with an
increased risk of developing COPD.

18. 7. Asthma and airway hyper-reactivity.
• Asthma may be a risk factor for the development of chronic
airflow limitation and COPD. In a report from the Tucson
Epidemiological Study of Airway Obstructive Disease, adults
with asthma were found to have a 12-fold higher risk of
acquiring COPD.
• Airway hyper-responsiveness can exist without a clinical
diagnosis of asthma and has been shown to be an independent
predictor of COPD.

19. 8. Chronic Bronchitis:
• An association between mucus hypersecretion and increased
FEV1 decline and in younger adults who smoke, the presence of
chronic bronchitis has been associated with an increased
likelihood of developing COPD.
• Chronic bronchitis has also been associated with an increased
risk in the total number as well as severity of exacerbations.

20. 9. Childhood infections:
• A history of severe childhood respiratory infection has been
associated with reduced lung function and increased
respiratory symptoms in adulthood.

21. PATHOLOGY OF COPD…

22. • Cigarette smoke exposure may affect the large airways, small
airways (≤2 mm diameter), and alveoli.
• Changes in large airways cause cough and sputum production, while
changes in small airways and alveoli are responsible for physiologic
alterations.
• The early stages of COPD, based on the severity of airflow obstruction
appear to be primarily associated with medium and small airway
disease.
• Advanced stages of COPD are typically characterized by extensive
emphysema.

23. • Mucus secreting cells in the airways are known as
…………………………???.
• Which of the following monoclonal antibodies causes decreased
expression of goblet cells?
a. Lebrikizumab
b. Infliximab
c. Gemtuzumab
d. Omalizumab

24. Lebrikizumab Anti-IL13 BA
Infliximab Anti- TNF alpha RA, CD, AS
Gemtuzumab CD 33 AML
Omalizumab Anti-IL5 BA

25. LARGE AIRWAYS.
• The thickness or area of mucus glands in subjects with COPD in
general, or chronic bronchitis in particular, is increased.
• Mild goblet cell or squamous cell metaplasia.
• A mild, usually mixed, inflammatory infiltrate.
• Bronchus associated lymphoid tissues (BALT) appears to be
considerably higher in smokers than nonsmokers.

26. • Desquamation of the epithelium is a common feature in asthma.
• Sloughing of cohesive epithelial clusters produces the …………. found
in cytology specimens.
Creola bodies

27. • Normal Reid Index is???
• 0.4
• Ratio of > ………. Is suggestive of COPD
(chronic bronchitis)??
• 0.5

28. Chronic smoking causes submucosal gland hypertrophy an
hyperplasia, leading to a Reid Index of >0.5 indicating
chronic bronchitis.

29. • A certain type of cells are present in the bronchioles which are mainly secretory in
function (lysozymes, surfactant-like protein). These are known as
a. Clara cells
b. Club cells.
c. Goblet cells.
d. None of the above.

30. • Max Clara in 1937.
• Tissue was taken from executed victims.
• In May 2012, the editorial boards of most of the major respiratory journals
concluded that the continued use of Clara's eponym would be equivalent to
honoring him.
• "Clara cell" and "Clara cell secretory protein" were conclusively replaced with "club
cell" and "club cell secretory protein", respectively.

31. 2. ALTERATION OF SMALL AIRWAYS…
• Increased airflow resistance in COPD is associated with the alteration,
remodeling, and obliteration of the small bronchioles (less than 2 mm
internal diameter).
• Respiratory bronchioles are the primary site of involvement.
• Smokers’ bronchiolitis or respiratory bronchiolitis, is recognized
pathologically as an increase of macrophages.

32. • Name of this classification of
airways???

33. • Goblet cell metaplasia, with these mucus-secreting cells
replacing surfactant-secreting Club cells.
• Smooth-muscle hypertrophy may also be present.
• Luminal narrowing can occur by fibrosis, excess mucus, edema,
and cellular infiltration.
• Reduced surfactant may increase surface tension at the air-tissue
interface, predisposing to airway narrowing or collapse.

34. • Respiratory bronchiolitis with mononuclear inflammatory cells
collecting in distal airway tissues may cause proteolytic destruction
of elastic fibers in the respiratory bronchioles and alveolar ducts.
• Narrowing and drop-out of small airways precede the onset of
emphysematous destruction.

35. • These changes result in an overall decrease in the internal
bronchiolar diameter.

36. 3. EMPHYSEMA:
• Emphysema is defined as ‘‘a condition of the lung characterized by
permanent, abnormal enlargement of the respiratory airspaces,
accompanied by destruction of their walls without obvious fibrosis.’’
• The fibrosis refers to gross fibrosis, not microscopic fibrosis, and thus
differentiates emphysematous destruction of airspaces from the
airspace remodeling seen in interstitial lung diseases.

37. • The inclusion of ‘‘destruction’’ in the definition serves to differentiate
emphysema from the simple airspace enlargements seen in aging,
compensatory emphysema and congenital lobar hyperinflation.

38. • There are 3 main types of emphysema:
1. Centriacinar/ Proximal acinar emphysema:
• Seen characteristically in cigarette smokers
• Mainly seen in upper lobes.
2. Panacinar emphysema:
• characteristically found in a1-antitrypsin deficiencies.
• Mainly seen in lower lobes.
3. Distal acinar (paraseptal) emphysema:
• Localises near the septa.

40. • All are true about acinus except:
- TB+RB+alveolar ducts+alveoli.
- RB+alveolar ducts+alveoli.
- Structural unit of lung.
- Means “berry”.

41. 3. ALTERATION OF VASCULATURE…
• The increased thickness of the intima in the arterial vasculature in
COPD has been shown to be caused by smooth muscle proliferation,
with increased deposition of both elastin and collagen.
• In the very small arteries and large arterioles, the longitudinal
smooth muscle remodeling results in the formation of a definite
muscularis media.

42. • Endothelial dysfunction is defined as a physiologic alteration of the
normal biochemical processes carried out by the endothelium.
• The characteristic feature of dysfunction is the inability of the arteries
to dilate fully in response to exercise, acetylcholine, or increases in
flow.

44. PATHOGENESIS OF COPD…

45. THE PROTEASE-ANTIPROTEASE THEORY…
• Various proteinases are
implicated in the pathogenesis
of emphysema.
• Serine proteinases, especially
neutrophil elastase, and several
matrix metalloproteinases, have
the maximum data.

46. • α1-AT has the highest concentration of all of the plasma proteinase
inhibitors.
• α1-AT is a member of a family of serine proteinase inhibitors called
serpins (SERPINA1).
• SERPINA1, that encodes α1-AT is on the proteinase inhibitor (PI) locus
on chromosome 14.
• What else???

47. • α1-AT is an acute-phase reactant.
• Plasma levels rise with trauma, estrogen therapy, use of birth-control
pills, and during pregnancy.
• α1-AT has a higher affinity for neutrophil elastase than trypsin or
other serine proteinases.

48. • If I need to supplement alpha 1 AT in a patient with severe
deficiency, the route of administration will be:
1. IV weekly once.
2. IM weekly once.
3. Oral tablets.
4. Inhalational once a week.

50. • α1-AT disease is AD/AR?????
• The original letters were chosen to
reflect…………….
• MC variant of alpha-1 AT is…………..
• Homozygosity for the Z allele, Pi ZZ, is
associated with
• Autosomal Recessive
• Electrophoretic mobility: F = fast, M =
medium, S = slow, and Z = ultraslow.
• PiMM.
• Severe deficiency of α1-AT.

51. THE OXIDANT-ANTIOXIDANT MODEL.
• Up to 20 mg of tar may be deposited in a smoker’s lung per cigarette smoked!!!!!!

52. Tobacco
smoke
“Prime” neutrophils and
alveolar macrophages to
generate elevated
amounts of reactive
oxygen species.
Oxidants modify and
inactivate proteins,
such as protease and
histone deacetylase 2
(HDAC2).
•HDAC2 is a/w
glucocorticoid
related anti-
inflammatory
process

53. • There is a constant or episodic release of proteinases into the lung
parenchyma.
• These proteinases come principally from inflammatory cells.
• Under normal conditions circulating proteinase inhibitors, permeate
lung tissue and prevent these proteinases from digesting the
structural proteins of the lungs.

54. • Emphysema results when the balance between proteinases and
antiproteinases in lung tissue tilts in favor of proteinases due to
increased proteinase release into the tissue and/or a reduction in the
antiproteinase content in the tissue.

55. Inflammatory
mediators

56. PATHOPHYSIOLOGY OF COPD…

57. AIRFLOW OBSTRUCTION…
• The FEV1 is the result of the balance between the elastic recoil of the
lungs promoting expiratory flow and the resistance of the airways
that limits flow.
• In normal lungs and in c/o COPD, maximal expiratory flow
diminishes as the lungs empty because the lung parenchyma
provides progressively less elastic recoil and the cross-sectional area
of the airways falls causing an increase in airway resistance.

58. • In mild COPD the abnormality in airflow is evident only at lung
volumes at or below functional residual capacity, appearing as a
“scooped out” lower part of the descending limb of the flow-volume
curve.
• In advanced COPD, the entire curve demonstrates decreased
expiratory flow.

60. HYPERINFLATION…
• “Air trapping” leads to increases in total lung capacity, functional
residual capacity (FRC), residual volume, and the residual volume to
total lung capacity ratio (RV/TLC).
• These abnormalities may be beneficial in that they help to preserve
expiratory airflow by increasing lung elastic recoil and the cross-
sectional areas of airway lumens.
• However, they displace the diaphragm into a flattened position
causing a number of adverse effects.

61. 1. Decreases the zone of apposition between the diaphragm and the abdominal
wall, hindering rib cage movement.
2. Shortens diaphragmatic muscle fiber length, decreasing the force that can be
generated by the diaphragm.
3. Increases the radius of curvature of the diaphragm, thereby decreasing
transpulmonary pressure.
4. Directs diaphragmatic muscle fibers medially, impairing inflation with
diaphragmatic contraction.

62. • These abnormalities of increased lung volume may increase further
with exertion because reductions in airflow in diseased lungs reduce
expiratory volume during rapid breathing.
• This phenomenon, called dynamic hyperinflation, adds to the
workload on the inspiratory muscles while further reducing their
mechanical advantage.

63. DYSPNEA…
• Dyspnea is seldom a complaint until the FEV1 has fallen below about
60% of predicted.
• An increased sense of effort relating to the pressures needed from
the respiratory muscles relative to their maximum pressure-
generating capacity is thought to be an important factor in causing
the dyspnea associated with COPD.

64. • Signals of “length-tension inappropriateness” from the respiratory
muscles due to hyperinflation are another factor.
• Dynamic hyperinflation exaggerates these problems for respiratory
muscles.

65. DIAGNOSIS OF COPD Saswat

66. • Normal nonsmoking adults lose FEV1 at a rate of
• 30 mL/yr
• Studies of patients with COPD show an average annual decline in
FEV1 of
• 45 to 69 mL/yr

67. • Dyspnea. - Major cause of the disability and anxiety.
- Described as a sense of increased effort to breathe, chest heaviness, air hunger, or gasping.
• Cough. - Often the first symptom of COPD and is frequently discounted by the patient as an
expected consequence of smoking.
- Initially, the cough may be intermittent, but subsequently may be present every day, often
throughout the day.
- May be productive or unproductive.

68. MMRC
GRADING
OF
DYSPNEA.

69. • Sputum production. -Small quantities of tenacious sputum with coughing.
- Chronic bronchitis????
- Producing large volumes of sputum may have underlying
- Bronchiectasis.
- The presence of purulent sputum reflects???
- An increase in inflammatory mediators and its development may identify the
onset of a bacterial exacerbation, though the association is relatively weak.

70. • Wheezing and chest tightness: Wheezing
and chest tightness are symptoms that
may vary between days, and over the
course of a single day.
- Audible wheeze may arise at the
laryngeal level ????
- How do we differentiate???

71. - Alternatively, widespread inspiratory or expiratory wheezes can be
present on auscultation.
- Chest tightness often follows exertion, is poorly localized, is muscular
in character, and may arise from isometric contraction of the
intercostal muscles.
• Fatigue, weight loss and anorexia are common problems.

72. SIGNS:
• Barrel-shaped chest.
• Reduced lung expansion.
• Hyper-resonant note on both sides of
chest.
• Reduced vesicular breath sounds.
• Added sounds.
• Signs s/o cor-pulmonale like loud P2, right
ventricular heave, tricuspid regurgitation
murmur, hepatojugular reflux, ascites and
edema.

73. DOCUMENTING
A DIAGNOSIS
OF COPD.
• History and physical examination.
• Spirometry: - Most reproducible and objective
measurement of airflow limitation.
- Measure the volume of air forcibly exhaled from
the point of maximal inspiration (FVC) and the
volume of air exhaled during the first second of
this maneuver (FEV1), and the ratio of these two
measurements (FEV1/FVC).
- Criterion for airflow limitation: FEV1/FVC < 0.70.

75. CASE 1…
• A 60year old male,
smoker since the last 25
years presented with
complaints of cough and
SOB since 3months.

76. CASE 2…
• A 65year old male, smoker since 25years
presented with complaints of cough and
sputum production, mostly during winters
since the last 3 years.
• Spirometry reveals:
• FEV1: 1l
• FVC: 2l

77. CASE 3… • A 55 year old male,
occasional smoker
presented with complaints
of SOB since the last
3months, gradually
progressive.
• On examination, basal
crepitations present.
• FEV1: 1.3ltrs (52%
predicted).
• FVC: 1.5ltrs ( 54%
predicted).

78. • A Chest X-ray is not useful to
establish a diagnosis in COPD but it
is valuable in excluding alternative
diagnosis (Pulmonary fibrosis,
bronchiectasis, pleural disease and
cardiac disease).

79. RADIOLOGY…
• Hyperlucency of lung fields.
• Flattened dome of
diaphragms.
• Decreased vascularity in
the lung periphery.
• Bullae.
• Widening of intercostal
spaces.
• Small heart/ hanging heart.

80. BULLA…

81. • ?????

82. DIAPHRAGMATIC INDEX

83. • CT scan is not routinely recommended when there is any doubt about
the diagnosis of COPD, CT scanning might help in the differential
diagnosis where concomitant diseases are present

84. • The intrathoracic narrowing of the trachea with internal coronal diameter
two thirds or less than the sagittal diameter at the same level without any
mediastinal pathology causing extrinsic compression. This sign is known
as???
• Saber-sheath trachea.
• Usually measurements are taken 1 cm above the aortic arch.
• Ratio of the coronal and sagittal diameters is known as????
• Tracheal index.

85. Treatment of COPD

86. • Which of the following classes of drugs are used in the management of
COPD?
- SABA.
- LABA.
- SAMA.
- BABA.
- ICS.
- ALL OF THE ABOVE.

87. • The mainstay in the treatment of COPD is:
- Bronchodilators.
- Inhaled corticosteroids.
- Mucolytics.

89. Β2-AGONISTS.
• The β2AR is a member of the G-protein coupled receptor (GPCR) family
and was in fact the first GPCR to be cloned (Dixon et al., 1986).
• SABAs provide almost instant symptomatic relief and are the frontline
therapy to combat bronchoconstriction and acute exacerbations.
• Their bronchoprotective effect is evident in minutes and remains for 4-6
hours.

90. • These drugs are also available for oral administration; however this
method is of less therapeutic value with the patient being more prone to
systemic side effects.

93. Side effects include:
• Sinus tachycardia.
• Precipitate cardiac rhythm disturbances in susceptible patients.
• Exaggerated somatic tremor in some older patients.
• Hypokalemia.

94. ANTI-MUSCARINIC AGENTS…
• The binding of acetylcholine to the M1 receptors in the nerve ganglia stimulates its
release from post-ganglionic endings which in turn bind to the M3 receptors of the airway
smooth muscle and submucosal glands, causing bronchoconstriction and increased
bronchial secretion.
• In the ganglia, however, acetylcholine also binds to M2 receptors, causing a decrease in
its production.
• Blocking M1 and M3 receptors reduces or reverses bronchoconstriction.

95. CLASSIFICATIO
N OF AMA

96. METHYLXANTHINES…
The likely mechanisms involve elevations of cyclic adenosine
monophosphate (cAMP) in airway smooth muscle due to
phosphodiesterase inhibition, antagonism of adenosine
receptors, and/or systemic release of catecholamines.
Mild improvement in bronchodilation when compared to
placebo groups.

97. INHALED CORTICOSTEROIDS…
Their effect on airway obstruction is due in part to their
contraction of engorged vessels in the bronchial mucosa and
their potentiation of the effects of β-receptor agonists, but
their most important action is inhibition of the infiltration of
asthmatic airways by lymphocytes, eosinophils, and mast
cells.
Beclomethasone, budesonide, ciclesonide, flunisolide,
fluticasone, mometasone, and triamcinolone.

98. PDE-4 INHIBITORS.
Reduce inflammation by inhibiting the breakdown of
intracellular cyclic AMP.
Roflumilast is a once daily oral medication with no direct
bronchodilator activity.
Roflumilast reduces moderate and severe exacerbations
treated with systemic corticosteroids.

99. A/e: diarrhea, nausea, reduced appetite, weight loss,
abdominal pain, sleep disturbance, and headache.

100. DIFFERENTIAL DIAGNOSIS…
Asthma Early onset in life
Variation of symptoms.
H/o eczema/ allergy present.
Family history
CCF Orthopnea, PND
CXR s/o cardiomegaly, PE.
Bronchiectasis Large volumes of purulent
sputum.
CXR shows bronchial dilation/
wall thickening.
Tuberculosis
Obliterative bronchiolitis Young age
H/o RA, exposure to fumes.

101. KEY NOTES IN TREATMENT…
LABAs and LAMAs are preferred over short acting agents
except for patients with occasional dyspnea and for
immediate relief of symptoms.
Inhaled bronchodilators are preferred over oral ones.
Theophyllines are indicated only if LABAs or LAMAs are
unavailable or unaffordable.

102. Long term therapy only with inhaled steroids is not
recommended.
In patients with exacerbations of COPD even with maximal
treatment, the addition of PDE4 may be considered.
Anti-tussives cannot be recommended.

104. Influenza vaccine is recommended in all COPD patients.
Pneumococcal vaccines PPSV13 and PCV23 are recommended
for all patients >65 years of age.
PPSV 23 is recommended in young patients with chronic co-
morbid conditions.

105. OTHER SUPPORTIVE MODALITIES…
Smoking cessation.
LTOT.
Non-invasive ventilation.
Surgery.

106. • Nicotine dependence is determined by Fagerstorm’s
scoring system.
Nicotine
replacement
therapy
Lozenge
s
Transdermal
Patch
Inhaler
Nasal
spray

107. • Bupropion.
• Anti-depressant.
• Varenicline
• Partial agonist at α4, β2 nicotinic receptors.
• Clonidine.
• Α-agonist, anti-hypertensive.
• Nor-tryptilline
• TCA.

109. SURGICAL PROCEDURES…
Endo-bronchial one way valve placements.
Bullectomy.
LVRS.
Lung transplant.

110. ACUTE EXACERBATION OF COPD.
 An exacerbation of COPD is defined as an acute
worsening of respiratory symptoms that results in
additional therapy.
Mild Treated with short acting
bronchodilators only, SABDs
Moderate Treated with SABDs plus
antibiotics and/or oral
corticosteroids
Severe Patient requires
hospitalization or visits the
emergency room

111. Exacerbations are mainly triggered by respiratory
viral infections.
Bacterial infections and environmental factors such
as pollution and ambient temperature may also
initiate and/or amplify these events.
The most common virus isolated is human
rhinovirus.

112. WHEN TO ADMIT A CASE OF AE COPD?

113. DRUGS USED IN AN ACUTE
EXACERBATION…
Bronchodilators: Short-acting inhaled beta2-agonists, with or without
short-acting anticholinergics, are the initial bronchodilators.
• One puff every hour for two or three doses and then every 2-4 hours
based on the patient’s response.
• Intravenous methylxanthines (theophylline or aminophylline) are not
recommended to use in these patients due to significant side effects.

114. Glucocorticoids: Systemic glucocorticoids in COPD
exacerbations shorten recovery time and improve
lung function (FEV1).
• A dose of 40 mg prednisone per day for 5 days is
recommended.
• Therapy with oral prednisolone is equally effective to
intravenous administration.
• Nebulized budesonide alone may be a suitable
alternative for treatment.

115. Antibiotics: The use of antibiotics in exacerbations remains
controversial.
• Antibiotics should be given to patients with exacerbations of
COPD who have three cardinal symptoms:
1.Increase in dyspnea,
2.Sputum volume, and
3.Sputum purulence;
4.Have two of the cardinal symptoms, if increased purulence of
sputum is one of the two symptoms; or
5.Require mechanical ventilation (invasive or noninvasive).

116. • The recommended length of antibiotic therapy is
5-7 days
• The choice of the antibiotic should be based on
the local bacterial resistance pattern.
Respiratory support: Oxygen therapy.
• NIV/ Invasive ventilation as and when needed.

117. • Adjunct Therapies: Diuretics when clinically indicated,
• Anticoagulants,
• Treatment of comorbidities and
• Nutritional aspects should be considered.

118. INDICATIONS FOR NIV…
Respiratory acidosis (PaCO2 ≥ 45mm Hg and pH ≤ 7.35.
Severe dyspnea with signs of respiratory muscle fatigue/
work of breathing.
Persistent hypoxemia despite oxygen therapy.

119. INDICATIONS FOR INVASIVE
VENTILATION…
• NIV failure.
• Post-respiratory or cardiac arrest.
• Reduced consciousness/ agitation.
• Massive aspiration/ persistent vomiting.
• Inability to clear secretions.
• Severe hemodynamic instability.
• Arrythmias.