Chronic Obstructive Pulmonary Disease (COPD) is a common preventable respiratory disease characterized by persistent airflow limitation caused by airway and alveolar abnormalities due to significant exposure to noxious particles or gases. The document discusses the definition, epidemiology including risk factors, pathophysiology, clinical features, complications, staging, and management of COPD according to the GOLD guidelines. It also provides case scenarios and discusses approaches to diagnosing and differentiating COPD from other conditions.

1. Chronic
Obstructive
Pulmonary
Disease (COPD)
2020
Dr. Kishore Kumar Ubrangala,MD
Professor, Dept. of Medicine,
Yenepoya Medical college,
Yenepoya (Deemed to be)
University, Mangalore, India.
sankish@gmail.com
21.04.2020 & 28.04.2020

2. Objectives
1. Definition
2. Epidemiology – Risk factors
3. Pathophysiology
4. Clinical Features
5. Complications
6. GOLD staging
7. Management – as per GOLD staging
8. In hospital Management
9. Drugs used in COPD, contraindications, drug
interactions
10.Prognosis
1. Clinical case scenarios x 3, management
2

3. Learning Objectives
1. Define COPD & Enumerate the Clinical Features
2. Order investigations
3. Manage a case of COPD based on severity
4. Demonstrate the use of Inhalers, Rotahalers and Nebulisers
5. Instruct a patient clearly on the use of Inhalers
6. Read X-Ray of a COPD patient
7. Read ABG reports of different types of COPD
8. Recognise and Diagnose Cor-Pulmonale – based on clinical
features, ECG & Echocardiography findings
9. Educate the patient on quitting of Smoking
10.Teaching COPD patient simple respiratory execises
PRACTICAL:
Demonstration of signs of Emphysema
Elicitation of history of Chronic Bronchitis
Rhonchi, Recognition of Cyanosis, Types of Respiratory failure,
Signs oh Hypoxia and Hypercapnia
3
2 Sessions

4. Case scenario
� 45 Yr old male, chronic smoker.
� Admitted with: h/o cough & expectoration many
months in a year x 5 years, progressive shortness of
breath x 1 year, worsened 1 week.
� H/o fever, cough with yellowish sputum,
headache.
� P/E: BMI 28%, Temp 38C, RR 28, PR 112/mnt, high
vol, BP 110/66, Drowsy, Central cyanosis +, Pedal
edema b/l, Flapping tremor +, JVP �, RS – B/l
wheezes & creps,
� What is the likely diagnosis?
� What investigations you will order to arrive at
diagnosis?
� What findings you expect in ABG ?
� What is the emergency management?
4

5. Case scenario
� 60 yr old male, seen in OPD.
� H/o progressive breathlessness x 6 years.
� Smoking: 20 cigarette packs/yr x 35 years.
� H/o Systemic HTN – on Metoprolol 50mg OD.
� P/E: Dyspneic, not cyanosed, no pedal edema,
BMI 20%, BP 160/80, RR 24, PR 100, Temp - N
� RS: Barrel shaped chest, Trachea central,
Accessory muscles used, Campbell sign +ve.
� What is your suspicion ?
� What other findings on RS exam you expect ?
� How will you confirm your suspicion ?
� What advice you will offer ?
5

6. COPD: Background
� Currently, the 4th leading cause of death
world, but projected to be 3rd by the end
of 2020.
� Imp. Public health challenge –
treatable/preventable
� Projected to increase in coming decades
– contd. exposure to COPD risk factors,
aging of the population
GOLD Report,
6

7. 7

8. COPD: Definition
A common, preventable & treatable disease –
characterised 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, influenced by
host factors including abnormal lung development.
Comorbidities may have an impact on mortality and
morbidity.
GOLD Report, 2020
8

9. Note: This is a simplified diagram of FEV1 progression over time. In reality, there is tremendous heterogeneity in the rate
of decline in FEV1 owing to the complex interactions of genes with environmental exposures and risk factors over an
individual’s lifetime
[adapted from Lange et al. NEJM 2015;373:111-22].
GOLD Report,
9

10. COPD: Pulmonary + Systemic
features
PULMONARY:
� Emphysema
� Chronic Bronchitis
� Traditionally taught as 2 entities, but currently are
discussed together (as features merge) – but, for
understanding the basics – may be defined &
discussed separately
SYSTEMIC:
ASTHMA – COPD OVERLAP (?)
10

11. Davidson’s
11

12. 12

13. COPD
Davidson’s
13

14. Harrison’s
Pathogenesis14

15. 15

16. 16

17. 17

18. 18

19. Chronic Cough
At BED-SIDE:
Chronic Bronchitis:
History of Cough & Expectoration for at least 3 months in a year x
2 consecutive years, provided
Other causes of chronic expectoration (like Bronchiectasis)
are excluded.
Hence, a history based diagnosis.
Emphysema:
An anatomical & pathological diagnosis,
History may give hint
Hyperinflation ha to be proved by clinical examination.
* (GOLD now doesn’t differentiate between these now – spectrum)
19

20. Other Causes of Chronic Cough
Intrathoracic
� Ashma
� Lung Cancer
� TB
� Bronchiectasis
� Left Heart Failure
� ILD
� Cystic Fibrosis
� Idiopathic Cough
Extrathoracic
� Chronic Allergic
rhinitis
� Post Nasal Drip
Syndrome (PNDS)
� Upper Airway Cough
Syndrome (UACS)
� GERD
� Medications (Eg:
ACEI)
GOLD 2020
20

21. GOLD 2020
21

22. Key Indicators to Consider diagnosis of
COPD: Age > 40 (Spirometry Indicated)
Dyspnea Progressive over time
Worsens on Exercise
Persistent
Chronic Cough May be intermittent & Unproductive
Recurrent Wheeze
Chronic Sputum
Production
Any sputum of Chronic sputum production
may indicate COPD
Recurrent Rep
Infections
History of Risk factors Host Factors, Tobacco, Smoke – Cooking,
Occupational dust, fumes, vapours, gases,
Chemicals
Family H/o COPD &/or
Childhood factors
Low birth weight, Childhood respiratory
infections (‘Childhood disadvantage
factors’)
GOLD 2020
22

23. 23

24. Etiology(risk factors)
Cigarette smoking:
� 15-20 % smokers develop clinically significant COPD,
suggesting genetic predisposition and environmental
factors play a a role in the pathogenesis of disease.
� Pipe and cigar smokers have increased risk of COPD.
� Risk of developing COPD relates to both the amount and
the duration of smoking.
� It is unusual to develop COPD with less than 10 pack years
(1 pack year = 20 cigarettes/day/year).
Cigarette Smoking24

25. Smoking & Other gases
� Passive/2nd hand smoking.
� Children of smoking parents.
� Natural, wood based fuel used for
cooking.
� Occupational causes- furnace blowers,
goldsmiths, exposure to cadmium
25

26. Cigarette smoking causes:
� Sluggish ciliary movements.
� Bronchoconstriction (through smooth
muscle constriction).
� Hypertrophy and hyperplasia of mucus
secreting glands.
� Release of proteolytic enzymes from
polymorphonuclear leucocytes.
� Release of inflammatory mediators to the
lungs.
� Inhibition of function of alveolar
macrophages.
Cigarette Smoking26

27. Familial and genetic factors:
Influence the development of chronic bronchitis.
Alpha 1 antitrypsin deficiency:
� If present: for Emphysema. Incidence: 25/100,000 in Asia, 8%
of children with liver disease in N. India.(AIIMS - 2009)
� (Autosomal co-dominant disorder. Gene that encodes AAT
is called SERPINA1 & is located in the long arm of
chromosome 14.
� AAT is a member of serpin family of protease inhibitors. It
protects the lower airways from damage caused by
proteolytic enzymes, such as elastase. Hepatocytes - Primary
source,
� The normal AAT allele is M allele, the most common severely
deficient variant is the Z allele.
� Pathologically severe pan-acinar emphysema,
predominantly at lung bases.
� Occurs in young adults. Progressive dyspnea and minimal
cough).
27

28. 28
AAT1 Deficiency
UpToDate 2020

29. 29
AAT1 Deficiency
UpToDate 2020

30. Other Risk Factors
� Previous tuberculosis
� Low socio economic status
� Pre –existing Asthma
� Infections with rhinovirus, Strep.
pneomonia, H. influenzae and Moroxella
catarrhalis causes exacebration of
chronic bronchitis.
� Exposure to dampness, fog and sudden
changes in temperaure can cause
exacebrations.
30

31. 31

32. Davidson’s
RISK Factors32

34. Pathology
� The chronic airflow limitation that is characteristic of COPD is
caused by a mixture of small airways disease and parenchymal
destruction (emphysema), the relative contributions of which
vary from person to person.
� These changes do not always occur together, but evolve at
different rates over time.
� Chronic inflammation causes structural changes, narrowing of
the small airways and destruction of the lung parenchyma that
leads to the loss of alveolar attachments to the small airways and
decreases lung elastic recoil.
� In turn, these changes diminish the ability of the airways to
remain open during expiration.
� A loss of small airways may also contribute to airflow limitation
and muco-ciliary dysfunction is characteristic feature of the
disease.
GOLD 2020
34

35. Pathology
� Premature airway closure, leads to gas trapping
and hyperinflation, reducing pulmonary and chest
wall compliance.
� Pulmonary hyperinflation also flattens the
diaphragmatic muscles and leads to an
increasingly horizontal alignment of the intercostal
muscles placing the respiratory muscles at a
mechanical disadvantage.
� The work of breathing is therefore markedly
increased, first on exercise, when the time for
expiration is further shortened, but then, as the
disease advances, at rest.
Davidson’s
35

36. � Centrilobular emphysema, the type most frequently
associated with cigarette smoking, is chrtd. by enlarged air
spaces found (initially) in assn. with respiratory bronchioles.
� Is usually most prominent in the upper lobes and superior
segments of lower lobes and is often quite focal.
� Panlobular emphysema - abnormally large air spaces evenly
distributed within and across acinar units.
� Is commonly observed in patients with α1AT deficiency,
which has a predilection for the lower lobes.
� Paraseptal emphysema occurs in 10–15% of cases and is
distributed along the pleural margins with relative sparing of
the lung core or central regions.
� It is commonly associated with significant airway
inflammation and with centrilobular emphysema.
Emphysema
Harrison’s
36

37. Emphysema
Smokingα1-AT def
37

38. Emphysema
Harrison’s
38

39. 39
UpToDate 2020

40. Davidson’s
EMPHYSEMA
40

41. COPD Phenotypes41

42. COPD Phenotypes42

43. COPD Phenotypes43

44. 44

45. COPD Comorbidities
KEY POINTS:
1. COPD often coexists with other diseases that may
have significant impact on the disease.
2. In general, presence of Comorbidities should not
alter COPD treatment &
Comorbidities should be treated as per usual
standards regardless of the presence of COPD.
3. Lung cancer is frequently seen in patients with
COPD & is a main cause of death.
4. CVDs are common & imp comorbidities in COPD.
GOLD 2020
45

46. COPD Comorbidities
KEY POINTS:
5. Osteoporosis and Depression/Anxiety are
frequent, imp comorbidities are often under-
diagnosed and are associated with poor
health status & prognosis.
6. GERD is assoc. with increased risk of
exacerbations and poorer health status.
7. When COPD is part of a multi-morbidity care
plan,
attention should be directed to ensure
simplicity of treatment & also to minimise poly-
pharmacy.
GOLD 2020
46

47. Diagnosis & Initial Assessment
KEY POINTS:
� COPD should be considered in any patient with
Dyspnea, C/c cough or Sputum production, a H/o
recurrent LRTI &/or a H/o exposure to a risk factor for the
disease.
� Spirometry is reqd. for diagnosis; post-bronchodilator
FEV1/FEC < 0.70 confirms the presence of persistent
airflow limitation.
� The goals of COPD assessment are to determine the
level of airflow limitation, impact of disease on patient’s
health status, and the risk of future events (such as
Exacerbations, Hospital admissions, or Death), in order to
guide therapy.
� Concomitant comorbidities
GOLD 2020
47

48. 48

49. 49

50. 50

51. 51

52. 52

53. D. D. of COPD
D. D. COPD
� COPD
� Asthma
� CHF
� Bronchiectasis
� TB
� Obliterative Bronchiolitis
� Diffuse Panbronchiolitis
GOLD 2020
53

54. D. D. of COPD
GOLD 2020
54

55. 55

56. � We no longer refer to Asthma & COPD
Overlap (ACO),
Instead,
� We emphasise that Asthma & COPD are
different disorders,
although, they may share some common traits
and clinical features (eg., eosinophilia, some
degree of reversibility).
Gold report, 2020
56

57. D. D. of COPD
GOLD 2020
57

58. SYMPTOMS
(Dyspnea, C/c cough,
Sputum)
RISK FACORS
(Host factors,
Tobacco,
Occupation, Indoor/
outdoor pollution)
Spirometry
(Reqd. for
diagnosis)
Pathways to diagnosis
GOLD 2020
58

59. 59

60. GOLD 2020
60

61. Davidson’s
PULMONARY FUNCTION TESTS
61

62. Davidson’s
PULMONARY FUNCTION TESTS
62

63. Davidson’s
63

64. GOLD 2020
64

65. PULMONARY FUNCTION TESTS
Davidson’s
65

66. GOLD Staging
Classification of Airflow limitation
severity in COPD
(based on post-bronchodilator FEV1)
In patients with FEV1/FVC < 0.70
GOLD 1 Mild FEV1 ≥ 80% predicted
GOLD 2 Moderate 50% ≤ FEV1 < 80% predicted
GOLD 3 Severe 30% ≤ FEV1 < 50% predicted
GOLD 4 Very Severe FEV1 < 30% predicted
GOLD 2020
66

67. Davidson’s
67

68. Davidson’s
68

69. Normal Chest X-ray PA view
Davidson’s
69

70. COPD: Emphysema70

71. Emphysematous Bullae71

72. HRCT Chest - Emphysema
Davidson’s
72

73. Chronic Bronchitis73

74. Cor Pulmonale74

75. P Pulmonale75

76. Cor pulmonale, also referred
to as pulmonary heart disease
is broadly defined by:
� Altered RV structure (dilation with or without
hypertrophy) and/or function in the context of
chronic lung disease and is triggered by the
presence of pulmonary hypertension.
� Develops in response to chronic pulmonary
hypertension resulting from parenchymal lung
disorders, primary pulmonary vascular diseases, or
conditions leading to alveolar hypoxia.
Cor Pulmonale
Harrison’s
76

77. Harrison’s
77

78. � Normally, mean pulmonary artery pressure is only ~15
mmHg and does not increase significantly even with
increasing multiples of cardiac output, because of
pulmonary vasodilation and blood vessel recruitment in
the pulmonary circulatory bed.
� But, in the setting of parenchymal lung diseases,
primary pulmonary vascular disorders, or chronic
(alveolar) hypoxia, the circulatory bed undergoes
vascular remodeling, vasoconstriction, and destruction.
� As a result, pulmonary artery pressures and RV afterload
increases, setting the stage for cor pulmonale.
� The systemic consequences of cor pulmonale relate to
alterations in cardiac output as well as salt and water
homeostasis.
Cor Pulmonale
Harrison’s
78

79. Cor Pulmonale
ECHO
� Is used to measure RV wall thickness and
chamber dimensions.
� The IVS may move paradoxically during systole in
the presence of RV pressure overload,
highlighting a deleterious interaction between
the RV and the LV.
� Doppler echocardiography can be used to
assess pulmonary artery pressures
BNP LEVELS:
� Elevated in patients with cor pulmonale
secondary to RV myocardial stretch
Harrison’s
79

80. ABG80

81. ABG
pH = Overall Acid Base status of blood
paCO2 = Reflects Ventilation
paO2 = Reflects Oxygenation
Base Excess = +/- 2 mEq/L calculated
Anion Gap = Na++K+- (Cl-)+HCO3-) = 10-15 mEq/L
(Major Cations –Major Anions)
81

82. 82
How to do an ABG

83. 83 ABG

84. Primary & Compensatory changes
Primary change Compensation
Respiratory
Acidosis
PaCO2 (HCO3)
Respiratory
Alkalosis
PaCO2 (HCO3)
Metabolic Acidosis (HCO3) PaCO2
Metabolic Alkalosis (HCO3) PaCO2
ABG84

85. 85 ABG

86. 86 ABG

87. 87 ABG

88. Uncompensated ABG Values
ABG88

89. Davidson’s
ABG89

90. ABG90

91. ABG91

92. A VBG measures the venous oxygen tension (PvO2), carbon
dioxide tension (PvCO2), acidity (pH), oxyhemoglobin
saturation (SvO2), and serum bicarbonate (HCO3)
concentration:
●PvCO2, venous pH, and venous serum HCO3 concentration
are used to assess ventilation and/or acid-base status.
●SvO2 may be used to guide resuscitation during severe
sepsis or septic shock - early goal-directed therapy.
PvO2 has no practical value at this time.
( It is not useful in assessing oxygenation because oxygen has
already been extracted by the tissues by the time the blood
reaches the venous circulation).
VBG
UpToDate 2020
92

93. The inability of a VBG to measure oxygenation is the
major drawback compared with an ABG.
To overcome this limitation, VBGs are often considered
in combination with pulse oximetry.
Correlation with arterial blood gases:
VBG
UpToDate 2020
93

94. VBG94

95. 95

96. 96

97. Case Scenario:
� A 45 Yr old female – admitted with severe attack of breathlessness. She
has been experiencing increasing SOB since admission 3 hours ago.
� Past history: Non-smoker, H/o cough & expectoration since 4 years, uses
wood-based cooking at home.
� Her ABG: pH – 7.22, PaCO2 – 55, HCO3 – 25
Follow the steps:
pH – low – acidosis
PaCO2 – high – in the opposite direction of pH
HCO3 – normal
Respiratory Acidosis - Uncompensated
Management:
Need to improve ventilation by oxygen therapy, bronchodilators,
mechanical ventilation, Antibiotics - infection
ABG – What is Wrong ?97

98. ABG98

99. Interpret the ABG
• Mr. X (72)
• Dx: CHF
• Hx: HTN, CHF, CKD
• Found this AM in full
cardiopulmonary arrest
• pH 6.98
• pCO2 62
• HCO3- 14
• pO2 80
• SPO2 89%
• BE -11
• AG 18
99

100. D.D. of COPD Exacerbations
� Pneumonia: (Chest X-ray, CRP +/or Procalcitonin)
� Pneumothorax: (Chest X-ray or Ultrasound)
� Pleural Effusion: (Chest X-Ray or Ultrasound)
� Pulmonary Embolism: (D-Dimer &/or Doppler
sonogram of LL, Chest Tomography – PE protocol)
� Pulmonary Odema: Due to cardiac related
conditions (ECG, Echo, Cardiac Enzymes)
� Cardiac Arrhythmias: Atrial fibrillation/flutter (ECG)
GOLD 2020
100

101. Potential indications for Hospitalisation
� Severe symptoms: sudden worsening of resting
dyspnea, high RR, SPO2, confusion, drowsiness.
� A/c Resp. Failure.
� Onset of new Physical signs (cyanosis,
peripheral edema).
� Failure of an exacerbation to respond to initial
medical management.
� Presence of serious co-morbidities (HF, New
Arrhythmias, etc.)
� Insufficient home support.
� Local resources need to be considered.
GOLD 2020
101

102. Indications to RICU/MICU
� Severe dyspnea that responds to inadequately
to initial emergency measures.
� Changes in mental status (confusion, lethargy,
coma).
� Persistent or worsening Hypoxemia (PaO2 < 40
mmHg) &/or severe/worsening respiratory
acidosis (pH < 7.25) despite supplemental O2
& NIV.
� Need for Invasive ventilation.
� Hemodynamic instability.
� Local resources need to be considered.
GOLD 2020
102

103. GOLD 2020
103

104. 104

105. 105

106. GOLD 2020
106

107. 107

108. 108

109. 109

110. 110

111. DRUGS in COPD
GOLD 2020
111

112. DRUGS in COPD
GOLD 2020
112

113. DRUGS in COPD
GOLD 2020
113

114. DRUGS in COPD
GOLD 2020
114

115. Harrison’s
Management
Revised ABCD Assessment Tool
115

116. 116

117. GOLD 2020
117

118. GOLD 2020
118

119. GOLD 2020
Management119

120. Harrison’s
Management120

121. Davidson’s
Management121

122. MDI & DPI122

123. GOLD 2020
123

124. Davidson’s
MDI124

125. 125
Use of MDI

126. Use of Spacer with MDI
126

127. How to use a Rotahaler
127

128. How to use a Revolizer
128

129. How to use a Lupihaler
129

130. How to use a Diskhaler - Accuhaler
130

131. How to use a Turbuhaler
131

132. * Tiotropium improves effectiveness of Pulmonary rehabilitation in
Increasing exercise performance (Evidence B)
* Theophylline exerts a small bronchodilator effect in stable COPD
(Evidence A) and that is associated with modest symptom benefits
(Evidence B)
GOLD 2020
132

133. GOLD 2020
133

134. � PD4 Inhibitors: In a patient with severe to very severe COPD & H/o
exacerbations:
• PD4 Inhibitor improves lung fn & reduces moderate & severe exacerbations
(Evidence A)
• For those on fixed dose LABA/ICS – PD4 Inhibitors improves lung fn &
decreases exacerbations (Evidence A)
GOLD 2020
134
Moderate Increased risk of TB

135. Roflumilast tab. 250 mcg, 500 mcg ( cost Rs 15/Tab of 500 mcg): Start OD
135

136. GOLD 2020
136

137. GOLD 2020
137

138. 138
AAT Supplementation
Cost: USD 1 lacs/yr
UpToDate 2020

139. 139

140. UpToDate 2020
Antibiotics140

141. UpToDate 2020
Antibiotics141

142. Antibiotics:
� Long-term azithromycin / erythromycin
therapy reduces exacerbations over 1 year
(Evidence A)
� Treatment with azithromycin is associated
with increased incidence of bacterial
resistance (Evidence A) & hearing test
impairment (Evidence B)
Mucoregulators & Antioxidant agents:
▪ Regular treatment with mucolytic agents
such as Erdosteine, Carbocysteine & NAC
reduces risk of exacerbations in select
populations (Evidence B)
Leukotriene modifiers:
▪ Have not been tested adequately in COPD
GOLD 2020
142

143. GOLD 2020
143

144. GOLD 2020
144

145. GOLD 2020
145

146. FOLLOW-UP
GOLD 2020
146

147. OXYGEN
Oxygen – Hb Dissociation Curve
147

148. Davidson’s
ABG148

149. OXYGEN
Chronic Type 2 RF
� The most common cause: Severe COPD.
� Although PaCO2 may be persistently raised,
there is no persisting acidaemia because the
kidneys retain bicarbonate, correcting arterial
pH to normal.
� This ‘compensated’ pattern is maintained until
there is a further acute illness, such as an
exacerbation of COPD - which precipitates an
episode of ‘acute on chronic’ respiratory failure,
with acidaemia and initial respiratory distress
followed by drowsiness and eventually coma.
Davidson’s
149

150. Davidson’s
OXYGEN
Chronic Type 2 RF; A/c on C/c
� These patients have lost their chemo-
sensitivity to elevated PaCO2, and so they
may paradoxically depend on hypoxia
for respiratory drive, and are at risk of
respiratory depression if given high
concentrations of oxygen – for example,
during ambulance transfers or emergency
departments.
150

151. Chronic Type 2 RF; A/c on C/c
� The principal aims of treatment in A/c on C/c type
II RF are to achieve a safe PaO2 (>52 mmHg)
without PaCO2 and acidosis, while identifying
and treating the precipitating condition.
� In these patients, it is not necessary to achieve a
normal PaO2; even a small will often have a
greatly beneficial effect on tissue oxygen delivery,
since their PaO2 values are often on the steep part
of the oxygen saturation curve.
� The risks of worsening hypercapnia and coma must
be balanced against those of severe hypoxaemia,
which include potentially fatal arrhythmias or
severe cerebral complications
Davidson’s
OXYGEN151

152. Masks – for Oxygen
UpToDate 2020
152

153. Davidson’s
A/c on C/c Type 2 RF153

154. Davidson’s
A/c on C/c Type 2 RF154

155. Arterial Hypoxemia (PaO2 < 55 mmHg or SaO2 < 88%)
Or
PaO2 > 55 but <60 with Rt HF or Erythrocytosis
Prescribe supplemental O2 and titrate to keep SaO2 ≥ 90%
Recheck in 60 to 90 days to assess:
* If supplemental O2 is still needed
* If prescribed supplemental O2 is effective
Prescription for supplemental O2
GOLD 2020
OXYGEN155

156. OXYGEN156

157. Davidson’s
OXYGEN157

158. Management of exacerbations
� Inhaled SABA, with or without SAMA, are
recommended as the initial bronchodilators (Evidence
C)
� Systemic corticosteroids can improve lung function
(FEV1), oxygenation & shorten recovery time &
hospitalisation duration. Duration of therapy should be
5-7 days. (Evidence A)
� Antibiotics, when indicated, can shorten recovery time,
reduce risk of early relapse, treatment failure, &
hospitalisation duration. Duration of therapy should be
5-7 days (Evidence B)
� Methylxanthines are not recommended due to
increased side effect profile (Evidence B)
� NIV should be the 1st mode of ventilation used in COPD
patients with acute respiratory failure who have no
absolute CI because it improves as exchange, reduce
work of breathing & need for intubation, hospitalisation
duration & improves survival. (Evidence A)
KEY POINTS
GOLD 2020
158

159. 159

160. 160

161. 161

162. GOLD 2020
162
NAC : Tab 600mg - TN: Mucinac, Mucomix, Nafcil, Easynac, Mucotroy - Rs 20) Nebuliser
solution 10%, 20%
Carbocisteine Cap 150mg (Rs 15), 250mg (Rs 47), 375mg (Rs 50), Sy 250mg /100ml Rs 70):
TN: Mucodyne (Elder)
Erdosteine: Cap 300mg(Rs 8) / Sy.175mg - 60ml (Rs 70) - TN: Erdomac, Erdozet

163. GOLD 2020
NIV163

164. Indications for Invasive Mechanical Ventilation
� Unable to tolerate NIV or NIV failure
� Status post-respiratory or cardiac arrest
� Consciousness, psychomotor agitation inadequately controlled by
sedation
� Massive aspiration or persistent vomiting
� Persistent inability to remove respiratory secretions
� Severe hemodynamic instability without response to fluids and
vasoactive drugs
� Severe ventricular or Supraventricular arrhythmias
� Life-threatening hypoxemia in patients unable to tolerate NIV
GOLD 2020
164

165. Smoking Cessation
Tobacco Dependence
� Effective, long-term treatment exists & should be
offered to all
� Every visit – brief counseling sessions: strong
dose-response relationship between counseling
& effectiveness
� 3 types of counseling: practical counseling,
social support of family & friends as part of
treatment, & social support arranged outside of
treatment
� 1st line drugs: Varenicline (0.5 mg, 1 mg - Rs 25),
Bupropion sustained release (150 mg - Rs 9), Nicotine
gum, inhaler, nasal spray & patch – are effective
and one of these should be prescribed in the
absence of CI.
� Treatment is cost-effective
GOLD 2020
165

166. E - Cigarette
‘Vaping’
166

167. Some facts:
� E-Cigarettes contain Nicotine. Youths are esp. vulnerable to nicotine
addiction.
� E-Cigarettes come in flavours that are appealing to children.
� In some cases, E-Cigarettes have exploded.
� Long-term health effects on users and bystanders (2nd hand smokers) not
known.
� E-Cigarettes can be used to smoke or vape marijuana, herbs, waxes, or
oils.
� ‘Popcorn lung’ (Bronchiolitis obliterans) – it is sometimes caused by
breathing in a chemical – Diacetyl, a butter flavoured substance - used
to flavour microwave popcorn.
� Severe acute lung injury, eosinophilic pneumonia & other form of lung
injury.
� Banned in INDIA in 2019.
E - Cigarette167

168. 3rd hand smoking
� Smoke left behind – the harmful toxins that
stay in place where people have smoked
previously.
�
� 3rd hand smoke can be found in walls, on
the seats of cars, and even in someone’s
hair.
� Harmful too.
168

169. Davidson’s
Annual Decline in FEV1169

170. Smoking Cessation
Davidson’s
170

171. Brief strategies to help patient willing to quit
ASK Systematically identify tobacco user at every
visit, query tobacco use status & record
ADVICE Strongly urge all tobacco users to quit.
In a clear, strong & personalised manner, urge
to quit
ASSESS Determine willingness to quit in a fixed time
frame
ASSIST Aid in quitting. Help with a quit plan; provide
practical counseling, social support,
Pharmacotherapy, supplemental material
ARRANGE Schedule follow up contact – either in person or
via telephone
Smoking Cessation
GOLD 2020
171

172. Vaccinations172

173. GOLD 2020
Vaccinations173

174. 174

175. Interventional therapy in stable COPD
� Lung Volume Reduction Surgery: Improves survival in
severe emphysema with upper lobe emphysema and
low post-rehabilitation exercise capacity (Evidence
A)
� Bullectomy: In selected patients, dyspnea, improved
lung function & exercise tolerance (Evidence C)
� Transplantations: In appropriately selected cases with
very severe COPD, lung transplantation has been
shown to improve the quality of life & functional
capacity (Evidence C)
� Bronchoscopic interventions: In selected advanced
emphysema patients – Endobronchial valves, Lung
coils, Vapor ablation
GOLD 2020
175

176. GOLD 2020
176

177. 177

178. Pulmonary Rehabilitation
� Exercise should be encouraged at all stages and
patients reassured that breathlessness, whilst
distressing, is not dangerous.
� Multidisciplinary programmes that incorporate
physical training, disease education and
nutritional counseling reduce symptoms, improve
health status and enhance confidence.
� Most programmes include 2–3 sessions per week
for 6 and 12 weeks, and are accompanied by
demonstrable and sustained improvements in
exercise tolerance and health status.
Davidson’s
178

179. Basic Breathing Exercises in COPD
179

180. Incentive Spirometer
180

181. Incentive Spirometer - Inspiration/Expiration
181

182. Pulmonary Rehabilitation -1
182

183. Pulmonary Rehabilitation -2
183

184. Pulmonary Rehabilitation - 3
184

185. Davidson’s
Prognosis185

186. Palliative Care, End of life support
& Hospice care in COPD
� All clinicians managing patients with COPD
should be aware of the effectiveness of
palliative approaches to symptom control
and use these in their practice
� Should include: Discussions with patients and
their families about their views on
resuscitation, advance directives and place
of death preferences
GOLD 2020
186

187. Palliative Care, End of life support
& Hospice care in COPD
� Opiates, Neuromuscular electrical stimulation
(NMES), O2 and fans blowing air on the face
can relieve breathlessness (Evidence C)
� In malnourished patients, nutritional
supplementation may improve respiratory
muscle strength & overall health status
(Evidence B)
� Fatigue can be improved by self-management
education, pulmonary rehabilitation, nutritional
support & mind-body interventions (Evidence B)
GOLD 2020
187

188. Davidson’s
OLD AGE188

189. Davidson’s
OLD AGE189

190. OLD AGE
Davidson’s
190

191. OLD AGE
Davidson’s
191

192. 192
Approach to conditions contributing to functional decline in COPD
Risk Factor COPD-specific
mechanism
Screening Treatment
Falls ● Gait & balance
impairment
● Muscle
weakness
● Nutritional
deficiencies
● H/o prior falls
● Observe the
patient getting
out of chair for
balance/gait
difficulties
Targeted treatment of
fall risk factors
Physical impairment ● Decreased
exercise
capacity
● Upper & lower
limb weakness
● 6 minute walk
test
● Short physical
performance
Battery
Pulmonary
rehabilitation
Cognitive
impairment
● Systemic
inflammation
● Vascular
disease
● Hypoxia
● Mini-COG ● For hypoxemia:
Continuous O2
therapy
● Pulmonary
rehabilitation
COPD in Elderly

193. Summary
� COPD is treatable & preventable – main phenotypes are
Chronic bronchitis & Emphysema, though
pathophysiologically they are considered together.
� Patient may often have many co-morbidities.
� Tobacco smoking is the major risk factor, & smoking
cessation is the key in halting the progression. ‘Childhood
disadvantage factors’ are imp. risk considerations.
� Incessant progression will end in Chronic cor pulmonale &
Chronic type 2 RF – which during exacerbations (often
due to LRTI), will go for a/c on c/c type 2 RF, needing
ventilatory support.
� Pharmacologic therapy should be individualised, - can
reduce symptoms, reduce exacerbations & improve
health status.
193

194. Summary (Contd..)
� Inhaler technique should be assessed regularly.
� Influenza & Pneumococcal vaccinations
decreases LRTIs.
� Pulmonary rehabilitation improves symptoms,
quality of life.
� In patients with chronic resting hypoxemia, long-
term O2 therapy improves survival.
� In patients with severe hypercapnia & a h/o
hospitalisation for a/c RF, long-term NIV may
decrease mortality & prevent re-hospitalisation.
194

195. Case scenario
� 45 Yr old male, chronic smoker.
� Admitted with: h/o cough & expectoration many
months in a year x 5 years, progressive shortness of
breath x 1 year, worsened 1 week.
� H/o fever, cough with yellowish sputum,
headache.
� P/E: BMI 28%, Temp 38C, RR 28, PR 112/mnt, high
vol, BP 110/66, Drowsy, Central cyanosis +, Pedal
edema b/l, Flapping tremor +, JVP �, RS – B/l
wheezes & creps,
� What is the likely diagnosis?
� What investigations you will order to arrive at
diagnosis?
� What findings you expect in ABG ?
� What is the emergency management?
195

196. Case scenario
� 60 yr old male, seen in OPD.
� H/o progressive breathlessness x 6 years.
� Smoking: 20 cigarette packs/yr x 35 years.
� H/o Systemic HTN – on Metoprolol 50mg OD.
� P/E: Dyspneic, not cyanosed, no pedal edema,
BMI 20%, BP 160/80, RR 24, PR 100, Temp - N
� RS: Barrel shaped chest, Trachea central,
Accessory muscles used, Campbell sign +ve.
� What is your suspicion ?
� What other findings on RS exam you expect ?
� How will you confirm your suspicion ?
� What advice you will offer ?
196

197. What will be your advice if a COPD patient
wants to fly in an aeroplane ?
197

198. Thank You
198