1. Department of Medicine Manipal College of Medical Sciences
C O P D
ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal

2. Chronic obstruction of lung airflow.
DEFINATION
Chronic obstruction of lung airflow
which is permanent & progressive
over time

3. COPD is comprised primarily of.
COPD is comprised primarily of
Chronic bronchitis
Emphysema

4. .
Asthma also is a pulmonary disease in which there is obstruction to the flow of air out of the lungs
obstruction in asthma usually is reversible
Between "attacks" of asthma the flow of air through the airways usually is good
(With execptions)

5. Emphysema and Ch.Bronchitis
are two ends of spectrum of COPD with various shades in between
Emphysema and Ch.Bronchitis .

6. Defining feature of COPD is irreversible airflow limitation during forced expiration FEV1(<80%) & FEV1/FVC (<70%) are reduced
EMPHYSEMA
a result of a loss of
elastic recoil due to
lung tissue destruction
Pathology
starts beyond terminal
bronchioles
CHR. BRONCHITIS
increase in resistance of the
conducting airways due to
accumulation of inflammatory
mucous exudates in the lumens
of small airways
Thickening of their walls
Pathology confined
up to terminal bronchioles

7. Ch. Bronchitis
Emphysema

8. Chronic Bronchitis Inflammation & swelling of the airways lining
narrowing and obstruction of airways due to
Hyperplasia of mucus-producing glands
Over production of mucous - further obstruction of the airways - increases
likelihood of bacterial lung infections

10. Reid index - chronic bronchitis
Ratio of the thickness of mucous gland layer to thickness of wall between epithelium & cartilage.
Normal Reid index is less than 0.4
is increased in chronic bronchitis.

11. Pulmonary capillary bed relatively undamaged .
Pulmonary capillary bed relatively undamaged
Centrilobular Emphysema present to a variable degree

12. Centrilobular emphysema
Normal
Pulmonary vessels in between alveoli are undamaged

13. Body responds by decreasing ventilation and increasing cardiac output.
Compared to Emphysema
Air way narrowing is more
Pulmonary circulation is less affected
Body responds by decreasing ventilation and increasing cardiac output.
due to rapid circulation in a poorly ventilated lung – increase in physiological shunt leading to
Hypoxemia
Polycythemia
V/Q mismatch

14. Eventually, hypercapnia and respiratory acidosis develop
Leading to pulmonary artery vasoconstriction and pulmonary hypertension with cor pulmonale
Patients have signs of right heart failure and are known as
“Blue bloaters"

15. Emphysema Permanent enlargement of the air spaces distal to
the terminal bronchioles, with destruction of their
walls
reduces the elasticity of the lung
collapse of the bronchioles
obstructing airflow out of the alveoli
Inspiration
Expiration

16. Air trapping in the alveoli
Inability of the lung to shrink during exhalation
Amount of air inhaled is reduced
Less air for the exchange of gasses in lungs
Trapped air compress adjacent less damaged
lung tissue compromising their function .

17. Panacinar emphysema
Destruction of the alveoli – blood vessels obstrcted/destroyed
reduced diffusing capacity of the lung for carbon monoxide (DLCO)

18. Now identify them

19. Normal lung

20. Emphysematous lung

21. Destruction of the alveolar walls decreases the
number of capillaries gas exchange decreases
(decreased DLCO)
due to relatively limited blood flow through a fairly well oxygenated lung – increase in physiological dead space with normal blood gases and pressures in the lung, (in contrast to the blue bloaters.)
The body compensates with
lowered cardiac output
hyperventilation .
V/Q mismatch

22. Normally expiration is passive process- effortless
extra effort required to exhale due to collapse of airways
Lungs are already inflated due to air trapping so more effort required to inhale further
Work of breathing is increased
Reduced gaseous exchange increase the
Breathing rate

23. Because of low cardiac output, rest of body suffers from tissue hypoxia and pulmonary cachexia. Eventually, develop muscle wasting and weight loss and are identified as
“Pink puffers"

24. Causes for cachexia in emphysema
Increased work of breathing
Low cardiac out put
Increase in TNF alpha and other mediators of inflammation

25. Pulmonary capillary bed relatively damaged
EMPHYSEMA
Pulmonary capillary bed
relatively damaged
V/Q mismatch - relatively limited
blood flow through a fairly well
oxygenated lung with normal
blood gases & pressures in the
Lung - Dead Space
Body compensates with
lowered cardiac output and
Hyperventilation
CHR. BRONCHITIS
Pulmonary capillary bed
relatively undamaged
V/Q mismatch – rapid
circulation in a poorly ventilated
lung, leading to hypoxemia and
Polycythemia
Shunt
Body responds by
increasing cardiac output
& decreasing ventilation .

26. Chronic Asthma Obstruction to the flow of air is due to
inflammation of the airways -thickening of the
airway walls lead to scarring and fixed airway
obstruction
spasm of smooth muscles - bronchospasm reversible
subsides spontaneously or
with the use of bronchodilators

27. Etiology

28. Smoking responsible for 90% of COPD
not all cigarette smokers develop COPD-15% will (don’t tell this to smokers)
Smokers with COPD have higher death rates
than non smokers with COPD
Have more frequent respiratory symptoms
coughing,
shortness of breath
passive smoking – equally harmful

29. MECHANISM
Irritation of cigarette smoke attracts cells to the lungs that promote inflammation.
They release elastase -breaks down the elastic fibers in lung tissue
Increases mucus production
Decreases ciliary motility

30. 2. Air pollution Role of outdoor air pollution – unclear
most common cause of COPD in non
industrialized world is indoor air pollution due to
indoor stoves used for cooking – biomass fuel
3. Occupational pollutants:
Cadmium & Silica - increase the risk of COPD

31. Alpha-1 antitrypsin deficiency
Genetic disorder
Accounts for less than 1% of the COPD
Enzyme elastase is found normally in lungs.It can
break down the elastin and damage the airways
and alveoli
Alpha-1 antitrypsin produced by liver block the
damaging effects of elastase on elastin. .

32. Alpha-1 antitrypsin deficiency causes
1. Early on set of emphysema- homozygos
2. Accelerated emphysema in smokers- hetrozygos
3. Chronic liver disease leading to cirrhosis due to
their defective release leading to intra hepatic
accumulation .

33. Clinical features of COPD

34. Progressive exercise intolerance Alteration in mental status
Patients with COPD present with a combination of signs and symptoms of
chronic bronchitis
emphysema
Symptoms
Worsening dyspnea
Progressive exercise intolerance
Alteration in mental status
In addition, some important clinical and historical differences exist between the types of COPD .
Common
symptoms

35. Chronic bronchitis Emphysema
Productive cough, with progression over time to intermittent dyspnoea
Cough and sputum on most days -at least 3 consecutive months for at least 2 successive years
Morning headache – CO2 retention
Hemoptysis – usually small
Frequent & recurrent pulmonary infections
Progressive cardiac/respiratory failure over time, with oedema and weight gain
Emphysema
A long history of progressive dyspnea with late onset of nonproductive cough
Occasional mucopurulent relapses
Eventual cachexia and respiratory failure .

36. 0 No breathlessness except with strenuous exercise
19.29 MODIFIED MRC DYSPNOEA SCALE
Grade Degree of breathlessness
0 No breathlessness except with strenuous exercise
1 Breathlessness when hurrying on the level or walking up a slight hill .

37. 2 Walks slower than contemporaries on level ground because of breathlessness or has to stop for breath when walking at own pace
3 Stops for breath after walking about 100 m or after a few minutes on level ground
4 Too breathless to leave the house, or breathless when dressing or undressing

38. Exclude Infection malignancy & other causes
Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation
Exclude
Infection
malignancy &
other causes

39. Physical
Examination

40. Barrel shaped chest sternum more arched spine unduly concave
AP diam > Trans diamt (5 : 7)
horizontal ribs

41. Emphysema

42. Normal
Compare it with
Previous one

43. Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration)
COPD
Normal
TLC
IRV
TLC IC VT
ERV
FRC RV

44. Laboured breathing – pursed lip breathing
Increased hollow in supraclavicular & suprasternal space
Indrawing of intercostal spaces
Accessory muscles of inspiration / expiration active

45. Apical impulse/Apex beat – not visible/palpable
Tracheal span reduced - < 2 c.m.
Tracheal tug – may be present
Indicates the severity of disease
Apical impulse/Apex beat – not visible/palpable

46. Hyper resonant note, liver & cardiac dullness diminished or obliterated
Breath sounds –diminished, vesicular with prolonged expiration
Ronchi or wheeze during expiration
Crepitations may be present more during inspiration

47. pump handle action of the upper 8 ribs
Inspiration:
result of active contraction
Diaphragm
External intercoastals
pump handle action of the upper 8 ribs
increases the AP diameter of the chest
bucket handle action of the lower 4 ribs
increases the transverse diameter of the chest
resulting in costal elevation & lateral expansion

48. dimension by upper ribs; Pump- Handle Motion
Increase in A-P
dimension by upper ribs; Pump- Handle Motion
                            
mywebpages.comcast.net/wnor/respap.gif

49. Increase in transverse dimension by lower ribs; Bucket-handle motion
                            
mywebpages.comcast.net/wnor/respap.gif

50. Hutchison's Clinical Methods (22E) page 55
Movement of the chest Body: Look at the chest movements. Are they symmetrical? If they seem to be diminished on one side, that is likely to be the side on which there is an abnormality. Intercostal recession - a drawing-in of the intercostal spaces with inspiration - may indicate severe upper airways obstruction, as in laryngeal disease, or tumours of the trachea. In COPD the lower ribs often move inwards on inspiration instead of the normal outwards movement

51. Hoover's sign
refers to the inspiratory retraction of the lower intercostal spaces
results from alteration in dynamics of diaphragmatic contraction due to hyperinflation resulting in traction on the rib margins by the flattened diaphragm
Seen in up to 70% of patients with severe obstruction can be an excellent marker for severe airway obstruction

54. Features of CO2 narcosis
headache
Flapping tremors
full & bounding pulse
Warm & moist extrimites
Detoriation of consciousness
Papilloedema

55. Chronic bronchitis Emphysema Patients may be obese.
Frequent cough and expectoration are typical.
Use of accessory muscles of respiration not so prominent
Coarse rhonchi and wheezing may be heard on auscultation.
Patients may have signs of right heart failure - edema & cyanosis.
Emphysema   
Patients may be very thin with a barrel chest.
Typically have little or no cough or expectoration.
Breathing may be assisted by pursed lips & use of accessory respiratory musls.
chest hyper resonant
wheezing may be heard; heart sounds very distant
Overall appearance is more like classic COPD exacerbation. Rt H.F. usually not seen till late .

56. Finger clubbing
is not consistent with COPD and should alert the physician to potentially more serious pathology.
persistent crepts
raise the possibility of bronchiectasis

57. .
INVESTIGATIONS

58. PFT Obstructive pattern
Reduced FEV1 to <80% predicted (FEV1 is the measurement of choice to assess progression of COPD)
FEV1/FVC < 0.7
Minimal bronchodilator reversibility (<15%, usually <10%)
Raised total lung volume, FRC, and residual volume because of emphysema, air trapping, and loss of elastic recoil

59. PEFR diary – less than 20% variation
Decreased TLCO and kCO because presence of emphysema decreases surface area available for gas diffusion
PEFR diary – less than 20% variation
No change in FEV1: FVC with exercise (absence of exercise induced bronchospasm)
TLCO=CO transfer factor for whole lung KCO=gas transfer coefficient

60. Flow Volume Curves
25%
50%
75%
In early C.O.P.D. FEV1 may be normal but FEF25%-75% is reduced

61. Pulmonary function tests
(Summary)
Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio
Poor/absent reversibility with bronchodilators
FVC normal or reduced
Normal or increased total lung capacity (TLC)
Increased residual volume (RV)
Normal or reduced diffusing capacity .

62. Arterial blood gas  
Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity
pH usually is near normal due to renal compensation in chronic disease
Generally, consider any pH below 7.3 a sign of acute respiratory compromise ? .

63. These patients tend to retain sodium.
Serum chemistry  
These patients tend to retain sodium.
Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels serum potassium should be monitored carefully.
Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia .

64. CBC - Polycythemia Hematocrit > 50

65. Chronic bronchitis is associated with
Chest radiography 
Chronic bronchitis is associated with
increased bronchovascular markings
Cardiomegaly
Features of pulmonary hypertension .

68. Emphysema is associated with a
small heart
hyperinflation
flat hemidiaphragms
possible bullous changes

69. SUBPLEURAL BULLAE
Bleb
BULLAE

70. . .

72. BLEBS

73. Chest radiography Chronic bronchitis associated with increased broncho
vascular markings
cardiomegaly.
Emphysema
associated with
small heart
hyperinflation
flat hemidiaphram
possible bullous changes.

74. CT scan Is useful -detection, characterisation and quantification
-more sensitive than the chest X-ray at detecting bullae.

76. Pulse oximetry does not offer as much information as ABG analysis.
When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status. .

77. ASSESSMENT OF SEVERITY OF COPD GOLD CRITERIA
Global Initiative for Chronic Obstructive Lung Disease

78. cough, sputum production Normal spirometry
Stage
Symptoms
Characteristics
0: at risk
cough, sputum production
Normal spirometry
I : mild COPD ,,
(With or without)
FEV1/FVC < 70%
FEV1 ≥ 80% predicted
IIA: moderate COPD
FEV1 = 50 – 80%
IIB: Potential for severe exacerb.
FEV1 = 30 – 50%
severe COPD
FEV1 < 30% predicted
Or < 50% with signs of resp.failure or CCF

79. Management

80. EMERGENCY TREATMENT .

81. Acute exacerbation

82. Treat bronchospasm and inflammation
Treat hypoxia
Treat bronchospasm and inflammation
Treat any underlying cause if present
Infection
Pneumothorax
Assess the need for intensive care

83. Initial treatment 1. Sit the patient up in bed
2. Oxygen: Adequate oxygen should be given to relieve hypoxia
With administration of oxygen, PO2 and PCO2 rise but not in proportion to the very minor changes in respiratory drive

84. Supply the patient with enough oxygen to maintain a near normal saturation (above 90%)
do not be concerned about oxygen supplementation leading to clinical deterioration
If the patient's condition is that tenuous, intubation most likely is needed anyway .

85. 3. Bronchodilators

86. short-acting beta-agonist short-acting anticholinergics
Bronchodilator  
short-acting beta-agonist
short-acting anticholinergics
given initially by nebulizer therapy .

87. stimulation of receptors relaxes airway smooth muscles
It help in COPD by-
stimulation of receptors relaxes airway smooth muscles
increases mucociliary clearance
decreases mucous production
Delivered by-
Nebulizer
M D I with space halers – if nebulizer not available
Parentral in refractory cases .

88. Nebulization with short acting bronchodilators
Salbutamol 5mg or
Terbutaline 10mg
administered with O2
repeat up to every minutes if required
continuous nebulization of salbutamol 10mg/h if inadequate response to initial treatment
Monitor Serum K+ regularly to prevent hypokalemia as a side effect

89. Anticholinergics
act via inhibition of cyclic guanosine monophosphate (GMP)–mediated bronchoconstriction.
decrease mucus production
improve mucociliary clearance
Ipratropium bromide -agent of choice
Add ipratropium bromide 0.5mg 6 hourly if initial response to –Beta-2 agonists is poor

90. In severe airflow obstruction combination of.
In severe airflow obstruction
combination of
Ipratropium
Salbutamol/albuterol
provide better broncho dilatation than used alone

91. Obtain iv access
4. Start Steroids:
Hydrocortisone - 200mg intravenously
Repeat 6 – 8 hourly
Or Methylprednisolone: 1-2 mg/kg IV q6h; not to exceed 125 mg
Follow up with oral corticosteroid - Prednisolone (40 to 60 mg / day) in tapering doses
(steroids should still be used in pregnant women as the risk of foetal anoxia from the asthma is high)

92. 5. Antibiotics Antibiotics in chest infection Prefferably a
purulent sputum/ or fever
abnormal CXR
raised WBC
should provide coverage against
Pneumococcus
H influenzae
Legionella species
Gram-negative enterics
Prefferably a
fluroquinolone or
Co Amoxyclav 650 m.g.X 3 or
Doxycyclline 100 m.g. X 2

93. Monitoring progress Pre- and post-nebulizer peak flows
Repeated arterial blood gases 1-2 hourly or according to response especially if SaO2 <93%

94. If response not brisk or patient's condition is deteriorating
Continue oxygen and nebulized beta2-agonist every 15 minutes
7. magnesium sulphate iv single dose
1.2-2g infused over 20 minutes
8. iv Aminophylline infusion
Loading dose: 250mg (4-5mg/kg) iv in 20 min
Maintenance infusion: mg/kg/h (250mg in 1 litre N saline at 2- 4 ml/kg/h)

95. Consider iv salbutamol infusion
Loading dose: µg over 10 minutes
Maintenance infusion: 5 -20µg/min (5mg in 500ml saline at 1- 3ml/min)
Side Effects:
tremor
tachycardia
hypokalaemia
hyperglycaemia
Summon anaesthetic help

96. Indications for admission to intensive care unit
Hypoxia (PaO2 <8kPa (60mmHg) despite FiO2 of 60%
Rising PaCO2 or PaCO2 >6kPa (45mmHg)
Exhaustion, drowsiness, or coma
Respiratory arrest
Failure to improve despite adequate therapy

97. Heliox (ie, mixture of helium and oxygen) inhalation may be tried
NON INVASIVE POSITIVE PRESSURE VENTILATION
continuous positive airway pressure
(CPAP)
biphasic positive airway pressure (BiPAP)
prevents airways collapse & air trapping
reduces the need for endotracheal intubation
Heliox (ie, mixture of helium and oxygen) inhalation may be tried .

98. definitive airway management via Intubation & mechanical ventilation.
When every thing fails
definitive airway management via
Intubation & mechanical ventilation

99. high risk of complications overall mortality of ~13%.
life saving
high risk of complications overall mortality of ~13%.
hypotension in ~38%
Barotrauma seen in ~14%
pneumothorax
pneumo-mediastinum
subcutaneous emphysema

100. On-going therapy
continue nebulized beta2-agonist, reducing to 4-hourly and withdraw after hours
Peak flow rate should be measured before and after each nebulizer
Maintain O2 sats >92%

101. Continue nebulized ipratropium bromide 6-hourly until the condition is improving
Continue steroids, hydrocortisone 100mg q6h iv switching to mg o d oral prednisolone when able to swallow, and continue for days
Monitor serum K+ daily and supplement as necessary

102. Discharge
PEF should be 75% of best without significant morning dipping
should be established on inhalers with no requirement for nebulizers for hours prior to discharge.

103. Ambulatory patients

104. Smoking cessation

106. Aids for stopping smoking
Nicotine patch
Medicines
Nicotine gum

107. Inhaled Corticosteroids (ICS) Pulmonary rehabilitation Physiotherapy
Oxygen therapy
Bronchodilators
Inhaled Corticosteroids (ICS)
Pulmonary rehabilitation
Physiotherapy
Annual influenza & pneumococcal vaccine
Surgical intervention

108. Oxygen therapy
LTOT via an oxygen concentrator for patients in respiratory failure, with
PaO2 < 55 mm / Hg (7.3 kPa) with any PCO2
PaO2 of 7.3 – 8 kPa (55 – 60 mm) with any of:
secondary polycythaemia
peripheral oedema
pulmonary hypertension present
FEV1 < 1.5 liters
use for a minimum of 15 hours per day (including
Sleep)

109. LONG-TERM DOMICILIARY OXYGEN THERAPY (LTOT)
improves survival,
reduces secondary polycythaemia
prevents progression of primary pulmonary hypertension.
Use at least 15 hours/day at 2-4 litres/min to achieve a PaO2 > 8 kPa (60 mmHg) without unacceptable rise in PaCO2
MUST STOP SMOKING

110. a. N O T
PaO2 < 55 mm SaO2 < 88%- while awake
Decrease in PaO2 > 10 mm & SaO2 > 5%
while asleep
c. Supplementation during exercise
when after exercise the gas saturation comes down

111. Bronchodilators Ipratropium bromide
by M.D.I. – 2 puffs (36-72 mcg) X 6h Nebul.
Long acting beta2 agonist
Salmeterol
Bambuterol
less expensive than above
rapid onset
more side effects
Theophylline -have other effects on diaphragm, resp centre etc

112. Inhaled corticosteroids (ICS)
reduce the frequency & severity of exacerbations
recommended in patients with severe disease 1.FEV1 < 50%
2.two or more exacerbations requiring antibiotics or oral steroids per year.
previuos response to steroids
during acute exacerbation
concomitent asthma
Has no role in modifying the disease as opposed to bronchial asthma (no need to give early in disease)
The combination of ICS with long-acting β2-agonists produces further improvement in breathlessness and reduces the frequency and severity of exacerbations.
(Role of oral CS)

113. Incentive Spirometry

114. QUIZ
How much capitation fee will be charged at MCOMS if she takes admission ?
COMPLICATIONS

115. COPD Cor pulmonale Due to Treatment (P.T.) pneumothorax Cachexia Acute
exacerbations
Respiratory
failure
Secondary
polycythemia

116. Cor pulmonale caused by pulmonary hypertension
This leads to enlargement and subsequent failure of the right side of the heart

117. pneumothorax
consider in all patients with COPD with acute exacerbation
Due to rupture of
subpleural bullae
Blebs

118. Acute exacerbations due to
Acute infections – preventive role of pneumococcal and influenza vaccine
Recent increase in size of bullae

119. Secondary polycythemia due to hypoxia
Increases blood viscosity
Pulmonary hypertension
thrombosis
Hematocrit > 60 then phlebotomy is done

120. Acute or chronic respiratory failure Acute
Due to infections
Associated with resp. acidosis
Chronic
Type I
Type II in severe COPD when FEV1< 1 liter
Associated with features of CO2 narcosis

121. Cachexia Increased work of respiration Reduced appetite and absorbtion
Release of inflammatory mediators (TNF alfa)

122. Bronchial Asthma Vs COPD

123. airflow obstruction due to inflammation & increased airway hyper-responsive ness & bronchospasm which is
variable over short periods of time
reversible with treatment
Mostly by allergens in atopic persons
Mostly affects the young people
Chronic obstruction of lung airflow which is permanent & progressive over time
Due to the chemical
irritation of the airways
caused by smoke(ing)
Disease of middle aged & elderly
cause
Age group

124. Chest normal in between the attacks
Airway obstruction due to
Smooth muscle spasm
oedema
Chest normal in between the attacks
Emphysematous changes do not occur
Does not progress to cor pulmonale or type II respiratory failure
Pathogenesis
Due to
Loss of elastic recoil: Emphysema
Remodeling of the air way: Ch Bronchitis
Features of air way obstruction always seen
Seen after some years
Many cases develop these complication
Clinical features
Complications

125. Pulmonary Function Test
Obstructive picture +
FEV1 ≥ 15% (and 200 ml) increase following administration of a bronchodilator/trial of corticosteroids
> 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary
FEV1 ≥ 15% decrease after 6 mins of exercise
Normal in between attacks. Hyper inflated lungs at the time of acute attack
Obstructive pattern +
Minimal bronchodilator reversibility (<15%, usually <10%)
< 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary
No change in FEV1: FVC with exercise (absence of exercise induced bronchospasm)
Shows
Emphysematous changes with bullae
Features of pulmonary hypertension
X ray chest