Download COPD 2012

Dr Dhaher Jameel Salih Al-habbo
FRCP London UK
Assistant Professor Department of
Medicine.College of Mdicine
University of Mosul


COPD preventable and treatable lung disease
with some extrapulmonary effects
(muscle weakness,↑circulating inflammatory
markers, impair water salt and excretion,
altered fat metabolism and ↑prevalence of
osteoporosis)

Collapse of intrathoracic airways during expiration

Increase V/Q mismach↑dead space volume

Flattening of the diaphragm and ↑horizontal
alignment of intercostal muscles please the
respiratory muscles at a mechanical disadvantage
with ↑ work of breathing..
Emphysema can be divided according to the
pattern of enlarged air space
Emphysema is usually centriacinar involving
respiratory bronchioles, alveolar ducts and
centrally located alveoli.
Panacinar and paraseptal emphysema with
blebs or giant bullae.








Occurs in Cigarette smokers 10-12 years
after starting .
Affects 10-15% of smokers
"Sputum, spasm, and swelling“.
Chronic excessive mucus secretion .
Hypertrophy of mucus-secreting glands .
Smooth muscle hyperplasia.
Bronchial Hyperresponsivenes
Occurs in 50% of COPD patients
Any patient who coughed up sputum on most
days of at least 3 consecutive months for
more than 2 successive years.
This inflammation eventually leads to scarring
of the lining of the bronchial tubes.
 Chronic bronchitis affects people of all ages,
but is higher in those over 45 years old.
 Incidence of chronic bronchitis in Females
are increased by more than twice in
comparison to males
pathological process of permanent destructive
enlargement of the airspaces distal to the
terminal bronchioles.
Begins with the destruction of air sacs (alveoli)
in the lungs where oxygen from the air is
exchanged for carbon dioxide in the blood.
Damage to the air sacs is irreversible and
results in permanent "holes" in the tissues of
the lower lungs.




Enquiry should be made as about the
presence of oedema and morning headaches
which may suggest hypercapnia.
Breath sounds are typically quiet; crackles
may accompany infection or bronchiactasis.
Leg oedema usually due to failure of salt and
water excretion due to hypoxic and
hypercapnic kidney.
Right heart seldom “fails” in COPD
Clinical examination of the chest in mild to
moderate disease might be normal.
Variable numbers of inspiratory and
expiratory low to medial pitched ronchi are
audible in most patients.
Crackles(cripitations)which may disappear
after coughing may be audible over the
lower zones.
Ronchi, especially on forced expiration.
A reduction in the length of the trachea
palpable above the sternal notch.
Trachea descent during inspiration (Tracheal
Tug).
Contraction of sternomastoid and scalene
muscles on inspiration
Excavation of the suprasternal and
supraclavicular fossae during inspiration,
together with indrawing of the costal
margins and intercostal spaces.
Increased antero-posterior diameter of the
chest relative to the lateral diameter; loss of
cardiac dullness.
Loss of weight common (often stimulates
unnecessary investigation).
Pursed lip breathing-physiological response
to decrease air trapping.
Flapping tremor and bounding pulse (due to
hypercapnia).
Peripheral oedema which may indicate
corpulmonale.
Raised JVP, right ventricular heave, loud
pulmonary second sound, tricuspid
regurgitation


Pink puffers; Thin and breathless and
maintain a normal PaCO2 until the late
stage of disease
Blue bloaters; They tolerate hypercapnia
earlier and may develop oedema and
secondarypolycythaemia




Chest x-ray;To Look for lung cancer,bullae.
Complete blood count to document
polysthaemia and to exclude anaemia.
For young with basal emphysema α1antiproteinaseassay.
Lung function test to document obstructive
ventilatory defect with partial response to
bronchdilatores
Age 30…a robust
young man
Age 51…riding
into the sunset
Arterial Blood Gas (ABG):
1-Markedly reduced arterial pO2
2-Elevated arterial pCO2 (40-50) mmHg
B-Pulmonary Function Tests:
Residual Volume increased .
FEV1 decreased ,FEV1/FVC decreased .
FEF 25-75 (mid-flows) decreased
Diffusion capacity (DLCO) near normal








A-Smoking cessation.
B-Bronchodilators.
C-Corticosteroids.
D-Pulmonary rehabilitation.
E-Oxygen therapy.
F-Surgical intervention.
G-Other measures.
H-Palliative care.
E-Oxygen therapy





Arterial blood gases in clinically stable patients on
optimal medical therapy on at least two occasion 3
weeks apart:
PaO2<7.3kPa(55mmHg) irrespective of PaCO2 and
FEV1<1.5l.
PaO2 7.3-8 kPa(55-60mmHg)plus pulmonary
hypertension, peripheral oedema or nocturnal
hypoxaemia.
Patient stopped smoking
Use at least 15hours/day at 2-4L/min to achieve a
PaO2>8kPa(60mmHg) with out unacceptable rise in PaCO2


Treatments for AAT deficiency emphysema
including AAT replacement therapy (a lifelong process) and gene therapy are currently
being evaluated.
It is hoped that a clinical trial on gene
therapy will take place within the decade.


Although there is little evidence of a
direct benefit of vaccination in patients
with COPD, It is recommend that;
Pneumococcal vaccination and annual
influenza vaccination should be offered to
all patients with COPD in an attempt to
reduce both disease-specific mortality
and mortality from all causes.