Chronic Obstructive Pulmonary Disease

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Chronic Obstructive Pulmonary Disease
 
1- Inflammation & fibrosis of the bronchial wall, 
2- Hypertrophy of the submucosal glands and 
 
3- Loss of alveolar tissue � decreases the surface area for gas exchange.
4- Loss of elastic fibers � leads to airway collapse.
Normally the elas�c fibers have 2 func�ons:
1- Recoil of elastic fibers that were stretched during 
of the lung during expiration. 
2- Elastic fibers are attached to the airways,providing radial traction to hold
In persons with COPD : the loss of elastic fibers causes:
1- Predisposes to airway collapse.
2- Increases air trapping. 
3- Impairs the expiratory flow rate.
 
The term COPD encompasses two types of obstructive airway disease: 
• Emphysema, with enlargement of air spaces and destruction of lung tissue.
• Chronic obstructive bronchitis,
Normally, the lung is p
Two recognized causes of emphysema :
 
1- Increased elastase production:
• Cigarette smoke stimulate movement of inflammatory cells into the lungs
proteinases as: elastase ( se
that digests elastin resulting in 
 
2- Inherited deficiency of αααα1-
• Accounts for 1% of all cases of COPD.
• More common in young persons before age of 40 years 
• Smoking & repeated respiratory 
• Human α1-antitrypsin is available for 
 
 
Emphysema is characterized by : 
1- Loss of lung elasticity 
2- Destruction of the alveolar walls and capillary beds.
3- Abnormal enlargement of the air spaces distal to the terminal bronchioles, 
Enlargement of the air spaces leads to 
There are two commonly recognized types of emphysema:
 
1- Centriacinar : 
• Affects the bronchioles in the central part of the 
respiratory lobule ( terminal 
respiratory bronchioles (RB) ), with 
preservation of the alveolar ducts and sacs.
• Most common type of emphysema
Seen predominantly in male smokers
• Centriacinar changes in upper parts of 
 
2- Panacinar 
• Produces initial involvement of 
• More common in persons with 
Also found in smokers in association with centrilobular emphysema.
• Panacinar changes are seen in lower parts of the lung
 
1. Dyspnea : In Emphysema & chronic bronch
- Persons with emphysema have marked dyspnea and struggle
(overventilate) , including prominent use of the accessory muscles. 
- The seated position,which stabilizes chest structures and allows for maximum chest expansion and use of accessory muscles, is preferred.
2. Productive chough : In Chronic Bronchitis
- Cough is productive of thick, purulent sputum owing to
- Sputum viscosity is increased largely as a result of presence of free DNA (of high molecular weight and highly viscous) from lysed cells. 
- Hemoptysis � with increased inflammation and mucosal injury.
- Cough is much less effective owing to �
3. Breath sounds : 
In Emphysema : 
- Decreased in intensity of breathing sound
- Wheezes, when present , are of diminished intensity 
In Chronic Bronchitis : Persistent airway narrowing 
- Produce localized or diffuse wheezing ( responsive to bronchodilators).
- Prolonged expiratory time . 
- Inspiratory & expiratory coarse crackles
4. Cardiac examination : 
- Tachycardia � as in chronic bronchitis, especially with exacerbations 
- Pulmonary hypertension � If hypoxemia is significant and chronic,,, 
• Prominent pulmonary valve closure (increased P
• Elevated jugular venous pressure AND peripheral edema resulting from 
5. Imaging : 
- Hyperinflation with � 1- fla8ened hemidiaphragms 2
- Parenchymal destruction produces : attenuated 
- Pulmonary hypertension produces : proximal pulmonary artery dilation .
- Cardiac size may be increased, suggesting right heart volume overload
- Cystic or bullous changes. 
6. Pulmonary function tests : 
In Emphysema : 
• The loss of elastic recoil in lung tissue supporting the airways results in increased 
dynamic compression of airways, (especially during forced expiration)
are reduced:With premature airway collapse, FEV
• "Expiratory flow-volume curve" shows substantial limitation in flow
In Chronic Bronchitis : 
• Diffuse airway obstruction is demonstrated as a global reduction in expiratory flows 
• expiratory flow-volume curve" shows substantial limitation in flow
 
- Increased RV and FRC, reflecting air trapped in the lung
a- Diffuse airway obstruction 
b- Early airway closure caused by loss of elastic recoil
- TLC is increased � substantial amount of this increase comes from gas trapped in poorly lung units, including bullae. 
7. Arterial blood gases : 
In Emphysema : (Emphysema is a disease of alveolar wall destruction)
- The loss of the alveolar capillaries creates: 
- They may able to maintain nearly normal PO
- Hypercapnia, respiratory acidosis, and a compensatory metabolic alkalosis
In Chronic Bronchitis : 
- In contrast to persons with emphysema, those with chronic obstructive bronchitis are 
increasing their breathing effort ���� " Ventilation
- Hypoxemia (arterial PO2 levels fall below 55 mm Hg) 
vasoconstriction of the pulmonary vessels
eventually, right-sided heart failure with peripheral edema (
- Hypercapnia, Cyanosis, respiratory acidosis, and a compensatory metabolic alkalosis
8. Polycythemia : Chronic hypoxemia (especially in chronic bronchitis) 
The mnemonics “pink puffer” and “blue bloater”
Emphysema & Chronic obstructive bronchitis
 
 
A major difference between the pink puffers 
• Chronic obstructive bronchitis
causes mismatching of ventilation & perfusion
increasing their ventilation; � instead, 
 
• Pulmonary emphysema : there i
- These persons are pink puffers, or
levels until late in the disease. 
 
Chronic Obstructive Pulmonary Disease (COPD) 
Pathogenesis of COPD : (IHLL) 
nflammation & fibrosis of the bronchial wall, 
ypertrophy of the submucosal glands and hypersecretion of mucus 
decreases the surface area for gas exchange. 
leads to airway collapse. 
the elas�c fibers have 2 func�ons: 
Recoil of elastic fibers that were stretched during inspiration provides the force needed to move air out 
 
Elastic fibers are attached to the airways,providing radial traction to hold airways open during expiration
the loss of elastic fibers causes: 
edisposes to airway collapse. 
Impairs the expiratory flow rate. 
types of obstructive airway disease: 
with enlargement of air spaces and destruction of lung tissue.
bronchitis, with obstruction of airways. 
Normally, the lung is protected by antiprotease enzymes as :
 
Two recognized causes of emphysema : 
Increased elastase production: 
movement of inflammatory cells into the lungs, 
serine elastase from neutrophils / metalloelastase from alveolar macrophages
resulting in breakdown of elastin and other alveolar wall components
-proteinase inhibitor (αααα1 – antitrypsin)
1% of all cases of COPD. 
ore common in young persons before age of 40 years . 
repeated respiratory tract infections, � decrease α1-antitrypsin 
ailable for replacement therapy. 
estruction of the alveolar walls and capillary beds. 
bnormal enlargement of the air spaces distal to the terminal bronchioles, 
Enlargement of the air spaces leads to � hyperinflation of the lungs � produces an increase in (TLC).
 
There are two commonly recognized types of emphysema: 
Affects the bronchioles in the central part of the 
terminal bronchioles (TB) & 
respiratory bronchioles (RB) ), with initial 
preservation of the alveolar ducts and sacs. 
ost common type of emphysema. 
een predominantly in male smokers. 
entriacinar changes in upper parts of the lung. 
roduces initial involvement of the peripheral alveoli� Later extends to involve the more central bronchioles. 
ore common in persons with α1-antitrypsin deficiency. 
lso found in smokers in association with centrilobular emphysema. 
changes are seen in lower parts of the lung 
Clinical Manifestations 
a & chronic bronchitis 
marked dyspnea and struggle to maintain normal blood gas levels
, including prominent use of the accessory muscles. 
stabilizes chest structures and allows for maximum chest expansion and use of accessory muscles, is preferred.
In Chronic Bronchitis 
of thick, purulent sputum owing to� ongoing local inflammation & infection. 
largely as a result of presence of free DNA (of high molecular weight and highly viscous) from lysed cells. 
ation and mucosal injury. 
� 1- narrow airway caliber & 2- greater volume and viscosity of secretions.
sound � reflecting decreased airflow. 
Wheezes, when present , are of diminished intensity - Crackles & rhonchi, in superimposed processes as infection 
Persistent airway narrowing & mucus obstruction : 
( responsive to bronchodilators). 
expiratory coarse crackles : � mucus production + defective mucociliary clearance
as in chronic bronchitis, especially with exacerbations of bronchitis or hypoxemia. 
mia is significant and chronic,,, Cardiac examination may 
Prominent pulmonary valve closure (increased P2, pulmonary component of the 2
nd
 heart sound) or 
Elevated jugular venous pressure AND peripheral edema resulting from Rt heart failure. 
fla8ened hemidiaphragms 2- � anteroposterior chest diameter. 
Parenchymal destruction produces : attenuated peripheral vascular markings. 
Pulmonary hypertension produces : proximal pulmonary artery dilation . 
may be increased, suggesting right heart volume overload. 
The loss of elastic recoil in lung tissue supporting the airways results in increased 
(especially during forced expiration)� all flow rates 
With premature airway collapse, FEV1, FVC, FEV1/FVC (FEV1% ratio) ����. 
volume curve" shows substantial limitation in flow. 
Diffuse airway obstruction is demonstrated as a global reduction in expiratory flows & volumes. 
volume curve" shows substantial limitation in flow. 
air trapped in the lung as a result of : 
iffuse airway obstruction (chronic bronchitis) 
caused by loss of elastic recoil (emphysema) 
substantial amount of this increase comes from gas trapped in poorly lung units, including bullae. 
(Emphysema is a disease of alveolar wall destruction) 
The loss of the alveolar capillaries creates: areas of high ventilation relative to perfusion. 
maintain nearly normal PO2 and PCO2 levels despite advanced disease 
Hypercapnia, respiratory acidosis, and a compensatory metabolic alkalosis are common in severe disease.
In contrast to persons with emphysema, those with chronic obstructive bronchitis are unable to 
Ventilation-perfusion mismatching " is common in chronic bronchitis.
arterial PO2 levels fall below 55 mm Hg) at rest tends to be more profound than in emphysema
vasoconstriction of the pulmonary vessels ���� persons with chronic obstructive bronchitis develop 
sided heart failure with peripheral edema (i.e., cor pulmonale). 
respiratory acidosis, and a compensatory metabolic alkalosis. 
Chronic hypoxemia (especially in chronic bronchitis) is associated with erythropoietin
“pink puffer” and “blue bloater” used to differentiate the clinical manifestations of 
Emphysema & Chronic obstructive bronchitis ( In practice, differentiation between t
A major difference between the pink puffers & the blue bloaters is the respiratory responsiveness to the hypoxic stimuli
Chronic obstructive bronchitis is characterized by excessive bronchial secretions and airway obstruction that 
causes mismatching of ventilation & perfusion � Thus, persons with chronic bronchitis are unable to compensate by 
instead, hypoxemia & cyanosis develop. (These are blue bloaters, or nonfighters
there is a proportionate loss of ventilation & perfusi
ffers, or fighters able to overventilate and thus mai
In smokers in whom COPD develops :
- Inadequate antiprotease production and release to neutralize 
- Excess protease production 
Both lead to obstruction of airflow & cause : 
mismatching of ventilation & perfusion.
 
inspiration provides the force needed to move air out 
airways open during expiration 
with enlargement of air spaces and destruction of lung tissue. 
Emphysema
as : αααα1-antitrypsin 
, � resulting in increased release of 
metalloelastase from alveolar macrophages ) � 
breakdown of elastin and other alveolar wall components. 
antitrypsin): 
antitrypsin levels� risk for emphysema . 
bnormal enlargement of the air spaces distal to the terminal bronchioles, 
produces an increase in (TLC). 
Later extends to involve the more central bronchioles. 
1- Reduced elastic recoil: 
 
The lung’s reduced ability to retract (
reduced elastic recoil (increased compliance) of the lung requires an increase in intrathoracic
expiration, resulting in compression of the intrathoracic airways 
 
• Positive pressure in alveoli :
1-
2-
THUS :
Maximal expiratory flow rate (V max) is a function of the ratio between 
 
 
• Respiratory function :
- If 
- V 
 
 
2- Bronchial obstruction : 
 
3- Loss of alveolar wall : 
 
The hypoxia
pulmonary
 
 
4- Loss of pulmonary capillaries : 
• The fluid retention and peripheral oedema is due to failure of excretion of sodium and water by the hypoxic kidney 
rather than Rt. heart failure.
• With severe fluid overload, 
 
to maintain normal blood gas levels with increased ventilatory effort 
stabilizes chest structures and allows for maximum chest expansion and use of accessory muscles, is preferred.
infection. 
largely as a result of presence of free DNA (of high molecular weight and highly viscous) from lysed cells. 
greater volume and viscosity of secretions. 
, in superimposed processes as infection 
defective mucociliary clearance � excessive secretions in the airways. 
or hypoxemia. 
may reveal : 
heart sound) or 
volumes. FEV1, FVC, FEV1/FVC (FEV1%) ����. 
substantial amount of this increase comes from gas trapped in poorly lung units, including bullae. 
common in severe disease. 
unable to maintain normal blood gases by 
is common in chronic bronchitis. 
at rest tends to be more profound than in emphysema � causes reflex 
persons with chronic obstructive bronchitis develop pulmonary hypertension and, 
associated with erythropoietin-mediated increase in hematocrit. 
used to differentiate the clinical manifestations of : 
differentiation between the two types is often difficult ) 
respiratory responsiveness to the hypoxic stimuli. 
 
 
 
Centrilobular emphysema :
• In centrilobular emphysema a 
different bronchioles 
• Patients with 
excessive bronchial secretions and airway obstruction that 
Thus, persons with chronic bronchitis are unable to compensate by 
blue bloaters, or nonfighters ). 
perfusion area in the lung. 
thus maintain relatively normal blood gas 
Panlobu
• In pa
• Patie
In smokers in whom COPD develops : 
production and release to neutralize 
Excess protease production 
(Top) Normal bronchial airway with elastic 
fibers that provide traction and
airway open. 
 
(Bottom) Obstruction of the airway caused by :
(A) hypertrophy of the bronchial wall, 
(B) inflammation and hypersecretion of mucus
(C) loss of elastic fibers that hold the airway open
Both lead to obstruction of airflow & cause : 
mismatching of ventilation & perfusion.Definition : 
Chronic producCve cough of more than 3 months’ duraCon for more than 2 
consecutive years 
� Typically,the
increase in acute exacerbations that produce frankly purulent sputum.
 
Types : 
1- Simple bronchitis
2- Chronic obstructive bronchitis
 
Causes : 
• It's associated with chronic irritation from 
 
In chronic bronchitis, 
1- Inflammation of the major and small airways. 
2- There is edema and hyperplasia of 
excretion into the bronchial tree.
Emphysema 
Reduced elastic recoil: leads to 
The lung’s reduced ability to retract (flaccid lung) can lead to 
reduced elastic recoil (increased compliance) of the lung requires an increase in intrathoracic
expiration, resulting in compression of the intrathoracic airways 
Positive pressure in alveoli : 
- Reduced lung’s elastic recoil generates the positive pressure in the alveoli 
 
- With loss of lung elasticity and hyperinflation of the lungs
for expiration because compliance and resistance are increased 
bronchioles �so, airway pressure increases further
- The airways often collapse during expiration because pressure in surrounding lung tissues exceeds 
airway pressure � Air becomes trapped in lungs, producing an increase in the anteropos
dimensions of the chest, the so-called barrel
- Elastic recoil can be raised by increasing the inspiratory volume
position toward inspiration (barrel chest
 
- Pursed-lip breathing, � increases the resistance to the outflow of air, 
increasing airway pressure. 
 
- External compression produces positive pressure in the alveoli by contraction of expiratory muscles, 
BUT this will also compress the bronchioles 
 
THUS : 
Maximal expiratory flow rate (V max) is a function of the ratio between 
Respiratory function : 
 tidal volume(TV) remains constant : 
1- � functional residual capacity (FRC) 2
 
Vital capacity (VC) is � because of the reduced expiratory volume.
Bronchial obstruction : leads to 
1- � maximum breathing capacity (V˙ max) 
2- � FEV1 . 
3- differing ventilation of various alveoli results in 
Loss of alveolar wall : leads to 
1- diminished diffusion area ���� abnormal diffusion
The hypoxia of underventilated alveoli leads to �vasoconstriction,
pulmonary hypertension, � an increased right ventricular load (cor pulmonale)
Loss of pulmonary capillaries : leads to
1- increase in functional dead space 
2- increased pulmonary artery pressure and vascular resistance
The fluid retention and peripheral oedema is due to failure of excretion of sodium and water by the hypoxic kidney 
rather than Rt. heart failure. 
With severe fluid overload, � tricuspid incompetence
elevated jugular venous pressure (JVP) / ascites / upper abdominal discomfort due to liver swelling.
Centrilobular emphysema : 
In centrilobular emphysema a distribution abnormality
different bronchioles � resulting in hypoxemia. 
Patients with centrilobular emphysema are called 
Panlobular emphysema : 
In panlobular emphysema , an enlargement of the f
Patients with panlobular emphysema are called are
Normal bronchial airway with elastic 
fibers that provide traction and hold the 
) Obstruction of the airway caused by : 
) hypertrophy of the bronchial wall, 
) inflammation and hypersecretion of mucus 
ibers that hold the airway open
 
Chronic Bronchitis 
hronic producCve cough of more than 3 months’ duraCon for more than 2 
consecutive years . 
Typically,the cough has been present for many years, with a gradual 
increase in acute exacerbations that produce frankly purulent sputum.
Simple bronchitis � Chronic bronchitis without airflow obstruction.
hronic obstructive bronchitis� chronic bronchitis with airflow obstruction.
associated with chronic irritation from smoking & recurrent infection
In chronic bronchitis, airway obstruction is caused by : 
nflammation of the major and small airways. 
There is edema and hyperplasia of submucosal glands and excess mucus 
excretion into the bronchial tree. 
) can lead to obstructive lung disease, because : 
reduced elastic recoil (increased compliance) of the lung requires an increase in intrathoracic pressure for 
expiration, resulting in compression of the intrathoracic airways � massive increase in flow resistance.
 
generates the positive pressure in the alveoli : 
With loss of lung elasticity and hyperinflation of the lungs � greater intrathoracic pressure is necessary 
resistance are increased � This causes compression of the 
airway pressure increases further. 
he airways often collapse during expiration because pressure in surrounding lung tissues exceeds 
Air becomes trapped in lungs, producing an increase in the anteropos
barrel chest. 
Elastic recoil can be raised by increasing the inspiratory volume � leading to a shift in the resting 
barrel chest). 
increases the resistance to the outflow of air, � preventing airway collapse by 
positive pressure in the alveoli by contraction of expiratory muscles, 
 � thus bring a massive increase in flow resistance
Maximal expiratory flow rate (V max) is a function of the ratio between elastic recoil (K) and resistance (RL) .
(FRC) 2- � residual volume (RV) 3- � dead space. 
because of the reduced expiratory volume. 
 
differing ventilation of various alveoli results in abnormal distribution � resulting in : Hypoxemia
abnormal diffusion of gases � resulting in : Hypoxemia
vasoconstriction,� increased pulmonary vascular resistance, 
ventricular load (cor pulmonale). 
leads to 
pulmonary artery pressure and vascular resistance ���� with development of " 
The fluid retention and peripheral oedema is due to failure of excretion of sodium and water by the hypoxic kidney 
tricuspid incompetence may develop with : 
elevated jugular venous pressure (JVP) / ascites / upper abdominal discomfort due to liver swelling.
distribution abnormality also develops, because of differing resist
. 
centrilobular emphysema are called “blue bloaters” . 
t of the functional dead space forces them to breathe m
alled are called “pink puffers”. 
 
hronic producCve cough of more than 3 months’ duraCon for more than 2 
cough has been present for many years, with a gradual 
increase in acute exacerbations that produce frankly purulent sputum. 
tis without airflow obstruction. 
with airflow obstruction. 
recurrent infections. 
submucosal glands and excess mucus 
 
pressure for 
increase in flow resistance. 
reater intrathoracic pressure is necessary 
compression of the 
he airways often collapse during expiration because pressure in surrounding lung tissues exceeds 
Air becomes trapped in lungs, producing an increase in the anteroposterior 
shift in the resting 
airway collapse by 
positive pressure in the alveoli by contraction of expiratory muscles, 
increase in flow resistance. 
and resistance (RL) . 
 
Hypoxemia. 
Hypoxemia . 
increased pulmonary vascular resistance, � 
 cor pulmonale"
The fluid retention and peripheral oedema is due to failure of excretion of sodium and water by the hypoxic kidney 
elevated jugular venous pressure (JVP) / ascites / upper abdominal discomfort due to liver swelling. 
, because of differing resistances in 
breathe more deeply. 
1- Lung function tests: 
- Show evidence of airflow limitation
In many patients the airflow limitation is partly reversible 
distinguish between COPD and asthma.
- Lung volumes : be normal or increased; 
- Carbon monoxide gas transfer factor:
 
2- Chest X-ray : see above in clinicalmanifestations
 
3- High-resolution CT scans : when the plain chest X
 
4- Haemoglobin level and PCV 
 
5- Blood gases : 
- At rest� normal - On exercise 
- In more advanced cases � 1- 
 
6- Sputum examination : 
- Strep. pneumoniae and H. influenzae
- Occasionally, Moraxella catarrhalis may cause infective exacerbations.
 
7- Electrocardiogram: is often normal
- P wave is tall (P pulmonale) . 
 
8- Echocardiogram : is useful to assess cardiac function where there is disproportionate dyspnoea.
 
9- α1-Antitrypsin : levels & genotype are worth measuring in
 
Acute exacerbations of COPD
- Exacerbations are episodes of increased dyspnea
- They may or may not be accompanied by other signs of illness, including 
- Presence of cyanosis, peripheral oedema or alteration in consciousness
 
1- Oxygen : ( In patients with an exacerbation of severe COPD, high concentrations of oxygen may cause respiratory depression 
• The aim is maintaining : PaO2 > 60 mmHg 
 
2- Bronchodilator s : 
• Nebulised short-acting β2-agonists
• These may be administered separately or together
 
3- Glucocorticoids : 
• 1- Reduce length of stay 2- hasten recovery
• The GOLD guidelines recommend : 
 
4- Antibiotics : 
• Patients with COPD are frequently colonized 
• Indications: Currently recommended 
• Regimens : Aminopenicillin or a macrolide
 
 
5- Mechanical Ventilatory Support : 
A) Noninvasive positive-pressure ventilation (NIPPV)
• Indications: If, despite above measures, patient remains 
• Its use is associated with reduced requirements for mechanical ventilation and reduced mortality
B) Invasive Mechanical Ventilation : 
• Indications: 
1- Severe respiratory distress despite initial therapy, 
4- markedly impaired mental status 5
 
 
Reducing exposure 
to noxious particles & gases
 
 
Bronchodilators 
 
β-Adrenergic agonists 
 
Antimuscarinic drugs 
Theophyllines 
Phosphodiesterase inhibitors 
 
Corticosteroids 
 
Combination of : 
- Corticosteroid with 
- Long-acting β2 agonist 
 
may protect against lung function decline 
BUT does not improve overall mortality.
 
Oxygen therapy 
 
Long-term oxygen therapy (LTOT)
 
 
 
Other measures 
 
Pulmonary rehabilitation
 
Surgical intervention
 
Lung Transplantation
 
Investigations 
Show evidence of airflow limitation : FEV1: FVC ratio is reduced /and PEFR is low. 
limitation is partly reversible (usually a change in FEV
distinguish between COPD and asthma. 
be normal or increased; 
Carbon monoxide gas transfer factor: is low when significant emphysema is present.
see above in clinical manifestations 
when the plain chest X-ray is normal. 
Haemoglobin level and PCV : can be elevated as a result of persistent hypoxaemia (
On exercise � patients desaturate . 
 resting hypoxaemia and 2- hypercapnia. 
Strep. pneumoniae and H. influenzae are the only common organisms to produce acute exacerbations.
Occasionally, Moraxella catarrhalis may cause infective exacerbations. 
is often normal, BUT In advanced pulmonary hypertensio
P wave is tall (P pulmonale) . - Right bundle branch block (RBBB) - Rt. ventricular hypertrophy.
is useful to assess cardiac function where there is disproportionate dyspnoea.
genotype are worth measuring in: 1- premature disease or 
Acute exacerbations of COPD ���� Presence of hypercarbia (PCO2 >45 mmHg) has important implications for treatment (discussed below).
episodes of increased dyspnea and cough and change in the amount and character of sputum.
They may or may not be accompanied by other signs of illness, including fever, myalgias, and sore throat
cyanosis, peripheral oedema or alteration in consciousness � indicates the need for referral to hospital. 
n patients with an exacerbation of severe COPD, high concentrations of oxygen may cause respiratory depression 
60 mmHg or SaO2 between 88% & 92% without worsening acidosis.
agonists (salbutamol) combined with anticholinergic agent (ipratropium).
These may be administered separately or together. 
hasten recovery 3- reduce chance of subsequent exacerbaCon or relapse for a period of up to 6 m
: oral prednisolone (30 mg ) for a period of 2 weeks.
Patients with COPD are frequently colonized with potential respiratory pathogens 
ded for patients reporting increase in sputum purulence, sputum volume or breathlessness. 
minopenicillin or a macrolide. / Co-amoxiclav if β-lactamase-producing organisms 
pressure ventilation (NIPPV) : 
Indications: If, despite above measures, patient remains tachypnoeic, hypercapnic ,acidotic 
Its use is associated with reduced requirements for mechanical ventilation and reduced mortality
 
evere respiratory distress despite initial therapy, 2- life-threatening hypoxemia, 
markedly impaired mental status 5- respiratory arrest 6- hemodynamic instability
gases 
• Complete cessation of smoking is accompanied by 
• Pharmacologic approaches: 1- Bupropion
- Bronchodilator therapy is central to the 
- Oral bronchodilator therapy may be used in patients who cannot use inhaled 
- Significant improvements in breathlessness may be reported, d
• In mild COPD : Short-acting β2-agonists 
• In moderate & severe COPD : long-acting 
 
• In mild COPD : Short-acting � Ipratropium bromide
• In moderate & severe COPD : long-acting 
• Theophylline preparations: improve breathlessness and quality of life, 
• Roflumilast is an inhibitor with anti-inflammatory properties. 
 
may protect against lung function decline 
not improve overall mortality. 
• Indications : 
- Recommended in patients with severe disease (FEV1 
• Effects : 
- Reduce the frequency and severity of exacerbations
- Regular use is associated with a small improvement 
• Indications : 
- Useful during exacerbations ( BUT
• effects : 
- If there is objective evidence of a substantial 
term oxygen therapy (LTOT) 
 
• long-term domiciliary oxygen therapy
Arterial blood gases measured in clinically stable patients on optimal medical therapy 
 
1- PaO2 < 55 mmHg irrespecCve of PaCO2 
2- PaO2 55–60 mmHg plus
3- Carboxyhaemoglobin of 
 
� Use : at least 15 hrs/day at 2
� Aim : to achieve ���� PaO2
 SaO2 
 
 
1- Vaccination: ���� 1- Influenza vaccine 
2- Mucolytic therapy : ����4-week trial of 
3- Diuretic therapy: � This is necessary for all oedematous patients.
4- α1-Antitrypsin replacement
5- Heart failure : � should be treate
6- Secondary polycythaemia :�
7- Sensation of breathlessness
 
Pulmonary rehabilitation 
• Exercise should be encouraged at all stages 
• Multidisciplinary programmes
 
Surgical intervention 
1- Bullectomy : 
- Patients in whom large bullae compress surrounding
 
2- Lung volume reduction surgery (LVRS) :
- Predominantly upper lobe emphysema 
peripheral emphysematous lung tissue is resected 
 
tation 
 
• Candidates for lung transplantation: 1
• In contrast to LVRS, the anatomic distrib
 
and PEFR is low. 
(usually a change in FEV1 of <15%), and it can be difficult to 
significant emphysema is present. 
can be elevated as a result of persistent hypoxaemia (2ry polycythaemia). 
are the only common organisms to produce acute exacerbations. 
tension : 
Rt. ventricular hypertrophy. 
is useful to assess cardiac function where there is disproportionate dyspnoea. 
premature disease or 2- lifelong non-smokers. 
has important implications for treatment (discussed below). 
and cough and change in the amount and character of sputum. 
fever, myalgias, and sore throat. 
indicates the need for referral to hospital. 
npatients with an exacerbation of severe COPD, high concentrations of oxygen may cause respiratory depression & worsening acidosis) 
without worsening acidosis. 
anticholinergic agent (ipratropium). 
reduce chance of subsequent exacerbaCon or relapse for a period of up to 6 m. 
for a period of 2 weeks. 
s (s. pneumoniae, H. influenzae, M. catarrhalis). 
for patients reporting increase in sputum purulence, sputum volume or breathlessness. 
producing organisms susceptible. 
tachypnoeic, hypercapnic ,acidotic (PaCO2 > 45 mmHg / pH < 7.35)
Its use is associated with reduced requirements for mechanical ventilation and reduced mortality 
threatening hypoxemia, 3- severe hypercarbia and/or acidosis, 
hemodynamic instability 
Pharmacotherapy
is accompanied by � 1- improvement in lung function 
Bupropion 2- Nicotine replacement therapy as: gum, transdermal patch, inhaler
Bronchodilator therapy is central to the management of breathlessness. - Compound bronchodilators, a selective 
Oral bronchodilator therapy may be used in patients who cannot use inhaled devices efficiently.
Significant improvements in breathlessness may be reported, despite minimal changes in FEV1 
agonists � Salbutamol or Terbutaline . 
acting β2 agonists � Formoterol or salmeterol
pratropium bromide (improves symptoms and produces acute improvement in 
acting � Tiotropium bromide (improve symptoms and reduce exacerbations
improve breathlessness and quality of life, BUT their use is limited by
inflammatory properties. � It is used as an adjunct to bronchodilators for the maintenanc
Inhaled Corticosteroids (ICS)
severe disease (FEV1 < 50%) who report two or more exacerbaLons requiring anLbioLcs or oral steroids per year .
educe the frequency and severity of exacerbations. 
th a small improvement in FEV1 (but ICS do not alter the natural history of the FEV1 declin
Oral Corticosteroids Prednisolone 
BUT maintenance therapy contributes to osteoporosis 
If there is objective evidence of a substantial degree of improvement in airflow limitaLon (FEV1 increase 
inhaled corticosteroids (beclometasone
term domiciliary oxygen therapy (LTOT) will benefit patients who have:
Arterial blood gases measured in clinically stable patients on optimal medical therapy on at least two occasions 3 weeks apart
irrespecCve of PaCO2 and FEV1 < 1.5 L 
plus secondary polycythaemia, pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia
Carboxyhaemoglobin of <3% (i.e. paLents who have stopped smoking).
at least 15 hrs/day at 2–4 L/min 
O2 > 60 mmHg or 
SaO2 > 90 % 
vaccine (annually) 2- Polyvalent pneumococcal vaccin
week trial of Carbocysteine (Reduce sputum viscosity 
This is necessary for all oedematous patients. 
Antitrypsin replacement:�Weekly or monthly infusions of α1-antitrypsin
should be treated. 
� requires venesection if the PCV is >55% 
ensation of breathlessness: � an be reduced by either promethazine or 
 Although opiates are the most effective treatment for intractable breathlessness they depress ventilation and carry the
Nonpharmacologic Therapies
should be encouraged at all stages 
Multidisciplinary programmes that incorporate: 1- Physical training 2- Disease education and nutrition
Patients in whom large bullae compress surrounding normal lung tissue, who otherwise have minimal airflow limitation and a lack of generalised
Lung volume reduction surgery (LVRS) : Patients with : 
ominantly upper lobe emphysema - with preserved gas transfer - No evidence of pulmonary hypertension,
peripheral emphysematous lung tissue is resected �
1- <65 years 2- have severe disability despite m
ic distribution of emphysema AND presence of pulmona
• A fall in pulmonary artery pressure
• Substantial improvement in 
 
 
 
7.35)
 
Pharmacotherapy 
improvement in lung function 2- deceleraCon in the rate of FEV1 decline 
gum, transdermal patch, inhaler 3- varenicline, 
Compound bronchodilators, a selective β2 agonist and an anCmuscarinic agent, are used.
devices efficiently. 
espite minimal changes in FEV1 � reflecting improvements in lung emptying that reduce dynamic hyperinflation 
salmeterol . 
(improves symptoms and produces acute improvement in FEV1 ). 
improve symptoms and reduce exacerbations BUT does not affect the decline in FEV1 )
their use is limited by : 1- side-effects 2- unpredictable metabolism 
It is used as an adjunct to bronchodilators for the maintenance treatment of COPD patients.
Inhaled Corticosteroids (ICS) 
50%) who report two or more exacerbaLons requiring anLbioLcs or oral steroids per year .
ICS do not alter the natural history of the FEV1 decline). 
Prednisolone 30 mg daily should be given for 2 weeks
maintenance therapy contributes to osteoporosis "other side effects" should be avoided ) . 
degree of improvement in airflow limitaLon (FEV1 increase >15%), � prednisolone should be discontinued and replaced by 
inhaled corticosteroids (beclometasone 40 μg twice daily adjusted according to response)
will benefit patients who have: 
on at least two occasions 3 weeks apart : 
pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia
3% (i.e. paLents who have stopped smoking). 
pneumococcal vaccine (single dose) 
educe sputum viscosity + can reduce the number of acute exacerbations) 
antitrypsin have been recommended for : 1-paLents with serum levels below 310 mg/L & 2
or dihydrocodeine 
Although opiates are the most effective treatment for intractable breathlessness they depress ventilation and carry the
 
Nonpharmacologic Therapies 
isease education and nutritional counselling reduce symptoms 
normal lung tissue, who otherwise have minimal airflow limitation and a lack of generalised
o evidence of pulmonary hypertension, � benefit from 
� with the aim of reducing hyperinflation and decreasing the
espite maximal medical therapy 3- free of comorbid c
 pulmonary hypertension are not contraindications to lu
A fall in pulmonary artery pressure : was achieved if oxygen was given for 15 hours daily, 
Substantial improvement in mortality: was only achieve if 
deceleraCon in the rate of FEV1 decline . 
, nicotinic acid receptor agonist/antagonist. 
2 agonist and an anCmuscarinic agent, are used. 
reflecting improvements in lung emptying that reduce dynamic hyperinflation 
does not affect the decline in FEV1 ). 
unpredictable metabolism 3- drug interactions. 
e treatment of COPD patients. 
50%) who report two or more exacerbaLons requiring anLbioLcs or oral steroids per year . 
30 mg daily should be given for 2 weeks 
 
prednisolone should be discontinued and replaced by : 
g twice daily adjusted according to response) 
pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia 
of acute exacerbations) . 
paLents with serum levels below 310 mg/L & 2-abnormal lung function.
Although opiates are the most effective treatment for intractable breathlessness they depress ventilation and carry the risk of respiratory failure.
reduce symptoms 3- Improve health status and enhance confidence.
normal lung tissue, who otherwise have minimal airflow limitation and a lack of generalised emphysema, � considered for bullectomy.
benefit from lung volume reduction surgery (LVRS),
with the aim of reducing hyperinflation and decreasing the work of breathing. 
orbid conditions ( liver, renal diseases). 
ations to lung transplantation. 
was achieved if oxygen was given for 15 hours daily, 
 oxygen was given for 19 hours daily. 
 
 
reflecting improvements in lung emptying that reduce dynamic hyperinflation . 
abnormal lung function.
risk of respiratory failure. 
status and enhance confidence.considered for bullectomy. 
(LVRS), in which: