COPD in a nutshell for Medical and Nursing students

1. Presented by
Dr. Ajay Kumar Agarwala
Resident (Neurology)
Bangabandhu Sheikh Mujib Medical University,
Dhaka, Bangladesh.
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
OVERVIEW & UPDATE

2. Key facts
 90% of COPD deaths occur in low- and middle-income
countries
 The primary cause of COPD is tobacco smoke
 The disease now affects men and women almost equally
 Not curable, but treatment can slow the progression
2
Chronic obstructive pulmonary disease
(COPD)

3.  3rd leading cause
death in developing world
 Prevalence in Bangladesh
21.25% (above 40 year age)
 Currently total burden about
6 million in BD
(Worldwide 80 million) 3
Picture in Bangladesh
Top 10 Causes of Death
Cancer 13%
Lower Respiratory Infections 7%
Chronic Obstructive Pulmonary
Disease 7%
Ischemic Heart Disease 6%
Stroke 5%
Preterm Birth Complications 4%
Tuberculosis 3%
Neonatal Encephalopathy 3%
Diabetes 3%
Cirrhosis 3%
Source: https://www.cdc.gov/globalhealth/countries/banglade
sh/

4. It is characterized by Progressive air way limitation
that is not fully reversible.
Emphysema
Chronic Bronchitis
Small airway disease
4
What is COPD?

5. 5
By Spirometry

6. 6

7. Risk factors
HOST FACTORS
 Genes
 Male sex
 Ethnicity (Caucasians)
 Airway hyper-
responsiveness
 Poor lung development/
poor growth
EXPOSURE FACTORS
 Tobacco smoke (Unusual if
< 10 pack years)
 Occupational-
dust/fumes/Smokes
 Air pollution
 Persistent Infections
(adenovirus, HIV)
 Low Socioeconomic status
7

8. • Pink puffer
Type A- Emphysema Predominant
• Blue bloater
Type B- Chronic Bronchitis Predominant
Type C- Mixed (MOST COMMON)
8
Types

9. Abnormal permanent dilatation of airspaces distal to
terminal bronchioles (resp. bronchioles, alveolar
ducts and alveoli)
Emphysema
9

10. 10
Pathology of emphysema
Cigarette leads to inflammatory and immune cell
recruitment within the terminal air spaces < 2mm
Release elastolytic and other proteinases that damage
the ECM
Cell death (Endothelial and Epithelial)
Ineffective repair of elastin and other
ECM leads to airspace enlargement

11. Small Airways
• Airway inflammation & edema, fibrosis, cellular
infiltration and destruction of elastic fibers of
respiratory bronchiole and alveolar ducts
• Goblet metaplasia and mucus plugs
• Reduce surfactant leads to airway narrowing and
collapse
• Smooth muscle hypertrophy
• Increased airway resistance
• Narrowing and drop out of small airway
Lung Parenchymal Destruction
• Loss of alveolar attachments
• Perforated alveoli coalesce to form large air spaces
• Decrease of elastic recoil
Airway limitation
Decrease pulmonary
and chest wall
compliance
Airway
hyperinflation
Poor gas exchange
Respiratory failure

12.  Bronchitis is inflammation of the inner lining of the
Bronchi ( Cough & Sputum for most of the days for 3 months
for consecutive 2 years)
Bronchitis
Enlargement of mucus-secreting glands &
goblet cells mainly in large airway
Inflammatory cell infiltrate
(Neutorphil elastase)
Smooth muscle hypertrophy & bronchial
hyper-responsiveness
Increased sputum production and
airway limitation

13. 13
Common Comorbidities

14. COPD Comorbidities
Increased risk of:
Cardiovascular diseases Cardioselective beta-blockers are not
contraindicated in COPD
Osteoporosis
Respiratory infections
Anxietyand Depression
Diabetes
Lung cancer
These comorbid conditions may influence mortality and
hospitalizations and should be looked for routinely, and
treated appropriately.

15. HISTORY
 Dyspnoea
 Fatigue, Morning headache (hypercapnia)
 Cough, Sputum +/-
 Frequent respiratory infection
 Risk exposure (Smoke, pollution etc.)
 Family history
15
How to diagnose?

16. PHYSICAL EXAMINATION
 Pursed lip breathing and use of accessory
respiratory muscles
“ Paradoxical inward movement of the lower rib
cage during inspiration: Hoovers sign”
 Rhonchi, Prolonged expiration, Crackles (if
infection)
 Decreased intensity of breath and heart sound
 Polycythemia, Cyanosis, Digital clubbing
(Malignancy), dependent pitting edema
16
Diagnosis…..(cont.)

17.  Thin with a barrel chest
 Little or no cough or expectoration
 pursed lips and use of accessory
respiratory muscles
 patients may adopt the tripod sitting
position
 The chest may be hyper-resonant &
wheezing may be heard
 Heart sounds are very distant
 Maintain normal PaC02 until late
stage
17
Emphysema PINK
PUFFER

18.  Patients may be obese
 Frequent cough and
expectoration are typical
 Coarse Ronchi and
wheezing may be present
 Earlier hypercapnia so
early secondary
Polycythemia
 Patient may have edema
and cyanosis
18
Chronic
bronchitis BLUE
BLOATER

19. 19
INVESTIGATION
The global initiative for chronic obstructive lung disease
(GOLD) used severity staging based on air flow
limitation.
stage I: MILD, FEV1 > 80% of normal
stage II: MODERATE, FEV1 = 50-79% of normal
stage III: SEVERE, FEV1 = 30-49% of normal
stage IV: VERY SEVERE, FEV1 <30% of normal or
<50% of normal with presence of chronic respiratory
failure present
The FEV1:FVC ratio should be <0.70 for all stages
(Post-bronchodilator)
Spirometry
must to
establish
diagnosis

20. Spirometry: Normal Trace Showing FEV1
and FVC
1 2 3 4 5 6
1
2
3
4
Volume,liters
Time, sec
FVC5
1
FEV1 = 4L
FVC = 5L
FEV1/FVC = 0.8

21. Spirometry: Obstructive Disease
Volume,liters
Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV1 = 1.8L
FVC = 3.2L
FEV1/FVC = 0.56
Normal
Obstructive

22.  Chest X ray
 HRCT
 Lung volumes
1. Helium dilution technique
2. Body plethysmography
 Arterial blood gas (ABG) 22
Investigation…(cont.)
 CBC
 Sputum examination
 ECG
 ECHO
 Alpha 1 Antitrypsin ( if Basal
Emphysema)

23. 23
Emphysema

24. Coarse broncho-
vascular marking
24
Chronic
Bronchitis

25. Centrilobular (centriacinar)
primarily the upper lobes
Occurs with loss of the
respiratory bronchioles in the
proximal portion of the acinus,
with sparing of distal alveoli.
This pattern is most typical for
smokers
25

26. 26
Panlobular emphysema permanent destruction of the entire
acinus distal to the respiratory bronchioles with no "obvious"
associated fibrosis. Usually affect basal part. Common in patient
with Alpha 1 AT deficiency.

27. Paraseptal Emphysema & sub
pleural bullae 27

28. 1. Assessment of COPD
2. Relief of symptoms
3. Prevent frequency and severity of exacerbations
4. Improve quality of life
5. Reduce mortality
28
Goals of management

29.  Modified MRC dyspnoea scale
 Six-minute walk test
 Exercise Oximetry
 COPD assessment test (CAT)
29
Assessment of COPD

30. 30

31. 31
Start pointTurnout point
100 feet/ 30m
100 feet/30m
6 minute walk test

32. 32

33. 33
Pharmacotherapy

34. A B
DC
Gold stage Ⅰ
Gold stage Ⅲ
Gold stage Ⅳ
Combined COPD Assessment (Airway limitation GOLD
assessment + Exacerbation risk + breathlessness)
≥2 episode in
last one 1
year or
≥1 episode
leading to
hosp
admission
≤ 1episode
not leading to
hosp
admission
Gold stage Ⅱ
mMRC 0-1 mMRC ≥ 2
Low risk, Less symptom
High risk, More symptomHigh risk, Less symptom
Low risk, More symptom

35. Patient Characteristic SpirometricClas
sification
Exacerbations
per year
mMRC CAT
A Low Risk
Less Symptoms
GOLD 1-2 ≤ 1 0-1 < 10
B Low Risk
More Symptoms
GOLD 1-2 ≤ 1 >2 ≥ 10
C High Risk
Less Symptoms
GOLD 3-4 >2 0-1 < 10
D High Risk
More Symptoms
GOLD 3-4 >2 >2 ≥ 10
Combined Assessment of COPDWhen assessing risk, choose the highest risk according to GOLD grade
or exacerbation history

36. Patient
category
First recommendation Alternative recomm.
A
Short acting anticholinergic
or Short acting beta2 agonist
as per need (pro re nata)
-Long acting anticholinergic or
-Long acting beta2 agonist or
-Short acting anticholinergic and
Short acting beta2 agonist
B
Long acting anticholinergic
or Long acting beta2 agonist
Long acting anticholinergic and Long
acting beta2 agonist
C
Inhaled corticosterLong
+
Long acting anticholinergic
or Long acting beta2 agonist
-Long acting anticholinergic and
Long acting beta2 agonist or
-LAanticholinergic +PDE4 inhibitor
or
-LAbeta2agonist+ PDE4 inhibitor
D
Inhaled corticosteroid
+
Long acting anticholinergic
and/or Long acting beta2
agonist
LTOT /SURGERY
Inhaled corticosteroid
+
Long acting anticholinergic and Long
acting beta2 agonist or
-LAanticholinergic +PDE4 inhibitor or
-LAbeta2agonist+ PDE4 inhibitor
36
Pharmacotherapy

37.  Oxygen
 Systemic steroid
 Antibiotic (According to C/S)
 Diuretics (If edema)
 Doxapram
 Parenteral Aminophylline
 Low dose benzodiazepines
 Morphine
37
Other drugs

38.  Ultra short acting b2 agonist- Indacaterol
 Long acting muscarinic antagonist- Glycopyronium
bromide
 Phosphodiesterase 4 inhibitor- Roflumilast and
Cilomilast
 Newer generation phosphodiesterase inhibitors-
Doxyphyllin
 Mucolytic and anti-oxidant agent- N acetylcysteine
38
Newer drugs

39.  During exercise
 During exacerbation
 During air travel
 Category D disease (Severe) - LTOT
39
02 Therapy
Temporary Need based

40.  For continuous use at home in patients with chronic
hypoxaemia
 15 to 19 hours per day including sleeping periods
 2-4 L/min For at least 30 days
 Goal: Increase baseline
Pa02 > 60 mmHg
Sa02 > 90%
40
Long term oxygen therapy
(LTOT)

41. Indication
1. Chronic hypoxaemia:
 Pa02 < 55 mmHg + PaC02 rise
 Pa02 > 60 mmHg + {pulmonary
hypertension/peripheral edema/ Nocturnal
hypoxaemia} + PaC02 rise
1. Nocturnal Hypoventilation: (Obesity/ Neuromuscular
disease/Obstructive Sleep apnoea)
2. Palliative use: Pulmonary malignancy or other causes
of disabling dyspnoea.
41
Long term oxygen therapy
(LTOT)

42.  Category C and D disease
 In Category B if steroid shows responsiveness
 Severe exacerbation of COPD
 Frequent exacerbation
Oral Steroid Trial
Differentiation of COPD from Asthma of ACOS
Can it predicts responsiveness to inhaled corticosteroid?
42
When to use inhaled steroid

43.  Smoking cessation & Reduce exposure to noxious
stimuli
 Vaccination (pneumococcal and Influenza vaccine)
 Exercise training & Breathing exercise
 Nutritional and Psychological counseling
 Palliation (Morphine for breathlessness and
Addressing End of life issue)
 Pulmonary rehabilitation (A holistic multidisciplinary
approach for patients with chronic respiratory
impairment) 43
Other mode of management

44. Influenza vaccines can reduce serious illness.
Pneumococcal polysaccharide vaccine is
recommended for COPD patients 65 years and older
and for COPD patients younger than age 65 with an
FEV1< 40% predicted.
vaccines

45. Brief Strategies to Help the
Patient Willing to Quit Smoking
ASSIST For the patient willing to make a quit
ttempt,
offer medication and provide or refer for
counseling or additional treatment to help
the patient quit. For patients unwilling to
quit at the time, provide interventions
designed to increase future quit attempts.
ARRANGE For the patient willing to make a quit
attempt, arrange for followup contacts,

47.  Lung volume reduction surgery
 Bullectomy
 Lung transplantation
47
Surgery

48. 48
Pulmonary
rehabilitation
components
General
exercise
training
Breathing
retraining
Education
Nutritional
advice
Psychological
support

49.  Def: Acute change in baseline dyspnoea, cough and/or
sputum that is beyond normal day to day variation
 Cause: 1. Infection 2. pollution 3. unknown (66% cases)
 Types:
Type1: Mild exace. (Risk factor for poor outcome-
)
(H. Influenzae, S. Pneumoniae, Chlamydia, Viruses)
Type2: Moderate exace. (Risk factor for poor outcome +)
(Type 1 plus Presence of resistant organism)
Type3: Severe exace. (Risk factor for poor outcome +)
(Type 2 plus P. aeruginose, Actinobactor)
Exacerbations

50. 50
Exacerbations
 Investigation:
Chest x ray, ECG, Pulse oximetry, ABG
Sputum for gram stain and C/S
CBC, B. Urea, S. Creatinine S. Electrolytes, B. Sugar
 Management: 1. Home-based 2. Hospital-based
Controlled oxygen: at 24% or 28% should be used with the aim of
PaO2above 60 mmHg or an SaO2 between 88% and 92%
without worsening acidosis
Systemic steroid: If baseline FEV1 is <50 % predicted….30-40 mg
of prednisolone for 7-10 day (Nebulized budesonide if risk of
hyperglycaemia or other steroid side effects)
Antibiotic: Aminopenicillin or a Macrolide. Co-amoxiclav if β-
lactamase-producing organisms are known to be common

51.  Increased intensity or resting dyspnoea
 New sign appearance (cyanosis, edema, arrhythmia)
 Severe underlying disease
 Significant co-morbidities
 Frequent admission
 Diagnostic uncertainty
 Older age
 Inadequate home support
51
Indication for Hospital
admission in exacerbation

52.  Inadequate response to initial emergency therapy
 Change in mental status (lethargy, confusion, coma)
 Persistent of worsening parameters despite oxygen
and Non-invasive ventilation
Hypoxemia (Pa02) ….less than 40 mmHg
Hypercapnia (PaC02)…..more than 60 mmHg
Respiratory acidosis…..pH <7.35
 Need for invasive ventilation
 Haemodynamic instability needing vasopressor
52
Indication for
ICU admission

53.  Able to use long acting bronchodilators
 Need for short acting b2 agonist not more than every 4
hour
 Patient can walk, eat and sleep without awakening by
dyspnoea
 Clinically stable for 12-24 hours
 Fully understand the use of medication
 Good support at home
 Follow up plan home care arrangement completed
53
Discharge criteria

54.  Maintenance pharmacotherapy regimen for home
 Inhaler technique
 Instruction regarding completion of steroid and
antibiotic therapy
 Assess for long term oxygen therapy
 Provide management plan for Comorbidities
 Assurance of a follow up visit within 4-6 weeks
54
Assessment at time of discharge

55.  Measurement of FEV1
 Inhaler technique
 Ability to cope in usual environment
 Understanding recommended treatment regimen
55
Items to assess at F/U visit

56. Respiratory failure
Pulmonary hypertension
Arrhythmias
 Corpulmonale
Secondary infection (Pneumonia)
 Osteoporosis
Complications
56

57. Chronic hypoxia
Pulmonary vasoconstriction
Muscularization
Intimal
hyperplasia
Fibrosis
Obliteration
Pulmonary hypertension
Cor pulmonale
Death
Pulmonary Hypertension in COPD

58. 58

59. 59
Predictors of
BAD prognosis
1) Increased age
2) Declined Post-bronchodilator FEV1
3) Weight loss (Cachexia)
4) Pulmonary hypertension

60. Body mass index
Obstruction of airflow
Dyspnoea
measurement
Exercise capacity
60
BODE index
BODE score of 0-2 has a mortality rate of around 10% at 52 months, When
BODE score 7-10 mortality rate around 80% at 52 months

61. 61
Distinguishing Asthma From COPD
Lung function test:
 Airway hyper responsiveness (Methacholin challenge test)
 Arterial blood gas (Chronically abnormal in COPD)
 DLCO (reduced in COPD)
 PEFR (Diurnal variation less in COPD)
Inflammatory Biomarkers:
 Skin prick tests for atopy,
 Ig E in blood,
 Blood eosinophilia,
 Suptum cell analysis
Imaging :
 Chest X ray
 HRCT

62. Differential Diagnosis:
COPD and Asthma
COPD ASTHMA
Onset in mid-life
Symptoms slowly
progressive
Long smoking history
Dyspnea during exercise
Largely irreversible
airflow limitation
Onset early in life (often childhood)
Symptoms vary from day to day
Symptoms at night/early morning
Allergy, rhinitis, and/or eczema also present
Family history of asthma
Largely reversible airflow limitation

64. Increased but not complete reversibility of the airway obstruction.
2 major and 2 minor required

65. 65
Research Update

66. 66
Beta Blockers in COPD

67. PLoS One. 2014 Nov 26;9(11):e113048. doi: 10.1371/journal.pone.0113048. eCollection 2014.
Beta-blockers reduced the risk of mortality and
exacerbation in patients with COPD: a meta-analysis
of observational studies.
Du Q1, Sun Y1, Ding N1, Lu L1, Chen Y1.
 An extensive search of the EMBASE, MEDLINE and Cochrane was performed to retrieve the
studies of beta-blockers treatment in patients with COPD. The random effects model meta-
analysis was used to evaluate effect on overall mortality and exacerbation of COPD.
 Fifteen original observational cohort studies with a follow-up time from 1 to 7.2 years
were included. The results revealed that beta-blockers treatment significantly decreased
the risk of overall mortality and exacerbation of COPD. The relative risk (RR) for overall
mortality was 0.72 (0.63 to 0.83), and for exacerbation of COPD was 0.63 (0.57 to 0.71). In
subgroup analysis of COPD patients with coronary heart disease or heart failure, the risk
for overall mortality was 0.64 (0.54-0.76) and 0.74 (0.58-0.93), respectively.
 The findings of this meta-analysis confirmed that beta-blocker use in patients
with COPD may not only decrease the risk of overall mortality but also reduce
the risk of exacerbation of COPD. Beta-blocker prescription for cardiovascular
diseases needs to improve in COPD patients.
Beta-blocker use in patients with COPD may not only decrease the risk of overall
mortality but also reduce the risk of exacerbation of COPD.

68. 68
N-AcetylCysteine in COPD

69. Abstract
In order to clarify the possible role of N-acetylcysteine (NAC) in the treatment of patients with
chronic bronchitis and chronic obstructive pulmonary disease (COPD), we have carried out a
meta-analysis testing the available evidence that NAC treatment may be effective in preventing
exacerbations of chronic bronchitis or COPD and evaluating whether there is a substantial
difference between the responses induced by low (≤600 mg per day) and high (>600 mg per
day) doses of NAC.
The results of the present meta-analysis (13 studies, 4155 COPD patients, NAC n=1933; placebo or
controls n=2222) showed that patients treated with NAC had significantly and consistently
fewer exacerbations of chronic bronchitis or COPD (relative risk 0.75, 95% CI 0.66–0.84;
p<0.01), although this protective effect was more apparent in patients without evidence of
airway obstruction. However, high doses of NAC were also effective in patients suffering from
COPD diagnosed using spirometric criteria (relative risk 0.75, 95% CI 0.68–0.82; p=0.04). NAC
was well tolerated and the risk of adverse reactions was not dose-dependent (low doses
relative risk 0.93, 95% CI 0.89–0.97; p=0.40; high doses relative risk 1.11, 95% CI 0.89–1.39;
p=0.58).
The strong signal that comes from this meta-analysis leads us to state that if a patient suffering
from chronic bronchitis presents a documented airway obstruction, NAC should be
administered at a dose of ≥1200 mg per day to prevent exacerbations, while if a patient suffers
from chronic bronchitis, but is without airway obstruction, a regular treatment of 600 mg per
day seems to be sufficient.
69
Influence of N-acetylcysteine on chronic bronchitis or COPD exacerbations: a
meta-analysis Mario Cazzola1 , Luigino Calzetta1 , Clive Page2 , Josè Jardim3 ,
Alexander G. Chuchalin4 , Paola Rogliani1 and Maria Gabriella Matera5
patient suffering from chronic bronchitis with documented airway obstruction,
NAC should be administered at a dose of ≥1200 mg per day to prevent
exacerbations, while if a patient suffers from chronic bronchitis, but is without
airway obstruction, a regular treatment of 600 mg per day seems to be sufficient.

70. Take Home Messages

71. Harrison's Principles of Internal Medicine .19th E
Davidson's principles and practice of medicine. 22nd E
National guideline on Asthma and COPD. 5th E
71
References

72. 72
THANK YOU!

73. 73
“We Rise by Lifting Others”
Robert ingersoll