You are on page 1of 23

Internal medicine

Topic: COPD
Lec #: 4

Dr: mousa malkawy


Date: 26-10-2009
COPD-Definition

A disease state characterized by airflow limitation that is not fully reversible and usually
it is progressive and associated with abnormal inflammatory response of the lungs to
noxious particles or gases. It is a preventable but not treatable disease.
 Although asthma is a chronic and obstructive disease but its not classified as a chronic
obstructive pulmonary disease (COPD).
 COPD is not fully reversible, but asthma is reversible one.
 the inflammatory response in COPD differ from that of asthma; in asthma the main cells
are CD4+ with eosinophiles, basophiles and mast cells while COPD the main inflammatory
cells are CD8+ with neutrophiles .
 COPD is smoke related and only in 10% its not related to smoke.
 Unlike asthma, COPD cant be curable or once the pt has COPD he will never go back to
mild or reverse his condition, but some associated symptoms can be relieved by
medication.

COPD-Classification
 COPD could be a component of one of two inflammatory diseases leading to airflow
limitation at the level of small airways :
1. The first component is obstructive bronchiolitis (chronic bronchitis) where
theres inflammation mainly in the small airway with fibrosis lead to narrowing and
airflow obstruction.
2. The second component is emphysema where theres destruction of the elastic
tissue in the lung and walls of alveoli, so the alveoli that are normally patent by the
elastic tissue will be collapsed leading to airflow obstruction.
 To diagnose a pt with COPD he\she must have permanent airflow limitation by pulmonary function
test, what ever the cause of airflow limitation (it may be a from of ch.bronchitis, emphysema or both).

Chronic bronchitis
CLINICALLY: The presence of cough and sputum production most of the day for at
least 3 months in 2 consecutive years without the presence of underlying
parenchymal disease or other causes for the cough or the sputum.

Chronic bronchitis define clinically, any one who is smoker with cough and sputum production
for 3m for 2 consecutive years is diagnosed as chronic bronchitis.
In some lung disease like bronchiectsis or interstitial lung diseases theres a cough most of the
day, but we dont consider them as a chronic bronchitis because theres underlying parenchymal
pathology in those diseases or the cough and sputum here is explained by other diseases.
Most of the pt in chronic bronchitis denies the presence of cough and sputum as they consider it
as a part of smoke, but if you ask them do you cough early morning to clear your airways they
say yes, which is characteristic for chronic bronchitis.

Emphysema
Permanent airspace enlargement beyond the terminal bronchioles where gas
exchange take place due to alveolar destruction.
 Emphysema is diagnosed pathologically, not
clinically.
 In the pic, look where the pathology of
emphysema take place, its distal to terminal
bronchiole where gas exchange take place
(respiratory bronchiole, alveolar ducts and
alveolar sacs )

To understand COPD better 


Ch. Bronchitis affects the airways (mainly small airways) while emphysema affects the air sacs and
parenchyma of the lung.
In COPD, less air flows in and out of the airways because of one or more of the following:
1. The airways and air sacs lose their elastic quality 2.The walls between many of the air sacs are destroyed
 This is mainly the effect of emphysema (1+2)
3. The walls of the airways become thick and inflamed (swollen) 4.The airways make more mucus than usual,
which tends to clog the airways.
This is mainly the effect of ch.bronchitis (3+4)
In emphysema, the walls between many of the air sacs are damaged, causing them to lose their shape,
elasticity and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and
larger air sacs instead of many tiny ones.
In chronic obstructive bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the
lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.

If you look at this diagram, you will see that theres overlap between asthma, emphysema,
chronic bronchitis and COPD.
For example you might have pt have chronic bronchitis but without COPD, bcz he doesnt
has airflow obstruction like area 1 and 11.
You might have pt with emphysema (diagnosed by C.T scan) and you do pulmonary function
test then you find that there's no airway obstruction so this is emphysema without COPD
Some pts have both asthma and COPD, like those who are already asthmatic and they are
smoker so they will get asthma and emphysema at the same time.
In COPD you must have airflow limitation by pulmonary function test.
2

Prevalence - risk factors


Burden of COPD is like this
12.1 million adults has COPD in 2001
Estimated number now is 16 millions
14 million undiagnosed  this is bcz most of the pts justify and relate their cough to smoke itself and
consider it normal so they will be undiagnosed until the symptoms become severe enough to make
them go for diagnosis.
4th leading cause of death in USA  it's predicted if the same rate of smoking is continuing, at year
2020 COPD will become the 3rd leading cause of death. So it's a lethal disease different from asthma.

This figure is just to show you that most of the killing diseases are going down, heart diseases and stroke are
decreasing, and stroke doesn't increase but in COPD the rate of death are increasing.

Here to show you that the prevalence of COPD related death is increasing in females, and this bcz smoke
among females is increasing.

Clinical Risk Factors


 Smoking  the most important single risk factor, 90% of COPD is related to smoke. But 20% of
smokers develop COPD and that's due to other factors affect each smoker separately including genetic
factor.
 Airway hyperresponsiveness
 Environmental exposures  those who exposed to dust and air pollution are more likely to develop
COPD.
 Atopy  like asthma, atopic diseases increase the risk.
 Antioxidant deficiency (vit. C & E)
 Bronchopulmonary dysplasia (neonatal chronic lung disease)  like those who are born
prematurely are more likely to develop this disease.
 Except for smoking, the rest are considered minor factors.

Molecular and genetic risk factors


 Alpha one anti-protease deficiency  this is very rare disease, less than 1% of COPD is related to
this factor, pts develop emphysema due to this in the 40yrs of their age but if they are smoker, smoke
will accelerate the development of emphysema earlier in the late twenties and early thirties.
 Gene polymorphisms : mostly the genes that are affected are :
Tumor necrosis factor alpha
Microsomal epoxide hydrolase
Transforming growth factor beta 1
 In the case of gene polymorphism, this will make COPD run in families (familial) and of
course increase the risk in first degree relatives especially those who are smokers.

Risk Reduction
 Smoking cessation  the most important, if you want to prevent COPD just stop smoking bcz if
COPD happened you will not be fine again bcz of the permanent damage in the lung.
 Exposure avoidance
 Physical activity  those who are smokers and they are on regular exercises are less likely to develop
COPD
 Anti-inflammatory therapy (ICS, Statins)  so far studies shows that inhaled corticosteroids
doesnt affect the airway obstruction which happen in COPD, but it can prevent the exacerbation of
COPD, also few studies have shown that Statins will decrease the progression of COPD but it's not
proved so far.
 N-acetylcysteine  like vit C, E. N-acetylcysteine which act as anti oxidant may help in decreasing
the risk.

Prevalence of Smoking in Jordan


 Adults above age 25 year :
Males 48%

Females

10.5%

 School children 13-15 year " those who are experimenting smoking for the first time " :
Males 26%

Females
4

11.5%

Pathology of COPD
C h a n g e s in

L a r g e A ir w a y s o f C O P D
P a tie n ts

M u c u s h y p e r s e c r e tio n
N e u t r o p h ils in

s p u tu m

S q u a m o u s m e t a p la s ia o f e p it h e liu m
N o b a s e m e n t m e m b r a n e t h ic k e n in g
G o b le t c e ll
h y p e r p la s ia

? M a c ro p h a g e s
? C D 8

M u c u s g la n d

ly m p h o c y te s

h y p e r p la s ia

L ittle in c r e a s e in
a ir w a y s m o o th m u s c le
S o u rc e :

P e te r

J . B a r n e s , M2 0D

Here if you notice the pathology will affect large and small airways:
Large airways  increase Neutrophiles in sputum and macrophages which both driven by CD8+ cells, S.M
and B.M not largely affected (unlike asthma), mucous and goblet cells hyperplasia leading to mucous
hypersecretion.
Small airways Why COPD is progressive and irreversible, bcz as you see we have structural changes in
addition to fibrosis affecting small airways (peribronchial fibrosis) leading to airways narrowing and
limitation which is not reversible, B.M is not thickened as in asthma which is reversible, so fibrosis is
permanent change which is not reversible make COPD irreversible

C h a n g e s

in

S m a ll A ir w a y s
P a t ie n t s

in

In fla m m a to r y

D is r u p te d

C O P D

e x u d a te

in

lu m e n

a lv e o la r a tt a c h m e n t s

T h ic k e n e d w a ll w it h in f la m m a to r y c e lls
- m a c r o p h a g e s , C D 8 + c e lls , fib r o b la s t s
P e r ib r o n c h i a l f i b r o s is
L y m p h o id

f o llic le

S o u r c e :

P e t e r

J . B a r n e s , M2 1D

Changes in the Lung Parenchyma in COPD


Patients

Here the changes that happens in


COPD at the Level of parenchyma
(Emphysema), you see alveolar
Wall and Septa destruction that
Normally give support to the
Airways, the damage Result in
Reduce elasticity and collapsed
Airways.

Alveolar wall destruction

Loss of elasticity
Destruction of pulmonary
capillary bed
? Inflammatory cells
macrophages, CD8+ lymphocytes
Source: Peter J. Barnes, 22
MD

C O P D

A S T H M A

C ig a r e t t e s m o k e

A lle r g e n s
Y

E p c e lls

C D 4 + c e ll
(T h 2 )

M a s t c e ll

A lv m a c r o p h a g e E p c e ll s

C D 8 + c e ll
(T h 1 )

E o s in o p h i l

S m a ll a ir w a y n a r r o w in g
A lv e o la r d e s tr u c tio n

B r o n c h o c o n s tric tio n
A H R

R e v e r s ib le

N e u t r o p h il

A i r f lo w L im it a t io n

Ir re v e rs ib le
23

Sou rce:

P e te r J . B a rn e s, M D

This is to show you the difference between asthma and COPD, in asthma the inflammatory response
mediated by CD4+ " eosinophiles, mast cells" although there is airflow limitation but it's at the level of
bronchi "large airways" and it's reversible so we don't consider it as apart of COPD. In COPD the
inflammatory response mediated by CD8+ (macrophages, neutrophiles) in addition to airflow limitation in
the small airways with alveolar destruction that is not reversible

First pic: in a + b: this is pathology of a smoker who didn't develop COPD, as we said 20% of smokers
develop COPD but not all of them. In c + d: here is a late stage where there are excessive exudates in the
airways with peribronchial fibrosis leading to permanent airflow limitation.
Second pic: this is emphysema related to smoke; the emphysema which is developed due to smoke is
centriacinar (centrilobular) which affect the respiratory bronchiole, while emphysema due to alpha one antiprotease deficiency is panacinar (pan lobular) affect the respiratory bronchiole, alveolar ducts and sacs.

COPD-diagnosis
Diagnosis of COPD done mainly by 
1. Clinical feature
2. Pulmonary function test
3. Radiology

1. Clinical features
the most important one that we depend on when we diagnose COPD, any one who has cough, sputum
production with SOB and he is smoker ( more than 20 pack/year ) or has risk factors he is candidate to
have COPD.

D ia g n o s is o f C O P D
E X P O S U R E T O
F A C T O R S

S Y M P T O M S
c o u g h
s p u tu m
s h o rtn e s s o f b re a th

R IS K

to b a c c o
o c c u p a tio n
in d o o r /o u td o o r p o llu tio n


S P IR O M E T R Y
2 7

One phenotype of COPD where there is


predominantly ch.bronchitis is what is
called Blue Bloater, these pts are usually
obese, smoker, have cor pulmonale and
chronic respiratory failure, they are
cyanosed and edematous as a result of
right sided heart failure and cor pulmonale
 all of theses are character of blue
bloater

The other phenotype is what is called pink


buffer, pt here have predominantly
emphysema, those pts have severe shortness
of breath but the don't have cyanosis and
they are thin.

 Most of the cases in COPD have both component ch.bronchitis and emphysema bcz
both of them are related to smoke.

D iffe r e n tia l D ia g n o sis:


C O P D a n d A sth m a
A s th m a

COPD
O n s e t in m id -life

S y m p to m s s lo w ly
p ro g re s s iv e
L o n g s m o k in g h is to ry
D y s p n e a d u rin g e x e rc is e
L a rg e ly irre v e rs ib le
a irflo w lim ita t io n

O n s e t e a rly in life (o fte n


c h ild h o o d )

S y m p to m s v a r y fro m d a y to
d a y a n d u s u a lly w o rs e a t n ig h t

O th e r a to p ic d is e a s e s o r fa m ily
h is to ry o f a to p y .

L a rg e ly re v e rs ib le a irflo w
lim ita tio n
30

This to differentiate between asthma and COPD just by history and clinical features alone.
1. We haven't seen pts who have COPD less than 40yrs of age but majorities of asthma
are young and children.
2. Asthma is intermittent disease while COPD is chronic and progressive.
3. smoking history is much more important in COPD

2. Pulmonary function tests


Once we suspect COPD we do pulmonary function test to confirm, bcz pts might have chronic bronchitis
without COPD, COPD as we said mean that we have airway obstruction and this is confirmed by pulmonary
function test which is done by spirometer.

Remember these terms:


FEV1 (forced expiratory volume at one second): maximum volume of air that can be
forced out or expired within one second after taking deep breath.
FVC (forced vital capacity): This measures the amount of air you can exhale with force after
you inhale as deeply as possible.

TLC (total lung capacity): the volume of the lung achieved at the end of maximal
inspiration. TLC = RV (residual volume) + IRV (inspiratory reserved volume) + TV (tidal
volume) + ERV (expiratory reserved volume)
TV: the amount of air inspired or expired with each breath (normal passive breath
not forced one).
IRV: maximum amount of additional air that can be inspired from the end of
normal inspiration.
ERV: maximum amount of additional air that can be expired from the end of
normal expiration
RV: the volume of air remains in the lung after maximal expiration.
VC (vital capacity): TLC-RV, volume achieved by maximal forceful expiration after
maximal inspiration

Pulmonary function test

COPD

FEV1/FVC

< 70

FEV1

variable

Airway resistance

increased

Total lung capacity

increased

Residual volume

increased

Diffusion capacity
chronic bronchitis
emphysema

normal
decreased

The hallmark of COPD is a reduction in FEV1/FVC ratio, the normal ratio is >= 70 80 % which
mean that70%-80% of inspired air must be expired at 1st second , in COPD it's a must to find this ratio
(< 70%) and that's bcz there's obstruction which prevent more than 70% of the inspired air to be
expired. This is called vital capacity maneuver where we ask the pt to take deep breath and expire it
and measure the expired air during the first second.
10

FEV1 alone is variable among COPD pts according to the severity.


Airway resistance is increased
TLC is increased, RV is increased especially in emphysema  bcz there's more air stay in the lung
that not fully expired as the normal person does.
Diffusion capacity, if the pt is predominantly has ch.Bronchitis then diffusion capacity is normal while
in emphysema the diffusion capacity is decreased  this is bcz in emphysema the pathology is at the
site where gas exchange take place ( distal to terminal bronchiole) which mean decrease gas exchange
, but in ch.bronchitis those sites will not be affected .

 According to this we can determine the severity of COPD as following


Stage I: Mild
Stage II: Moderate
Stage III: Severe
Stage IV: Very Severe

FEV1/FVC < 0.70


FEV1 > 80%
FEV1/FVC < 0.70
50% < FEV1 < 80%
FEV1/FVC < 0.70
30% < FEV1 < 50%
FEV1/FVC < 0.70
FEV1 < 30% or
FEV1 < 50% plus
chronic respiratory failure

11

3. Radiology

This is C.T scan shows centrilobular


emphysema, you can notice dark
spots which indicate smoke pigments,
and it usually affects the upper lobes
of the lungs

This is x-ray shows extreme emphysema,


you can see low flat diaphragm with
hyper-inflated lungs.

This is more severe one with


subpleural emphysematous spaces;
this type could lead to pneumothorax
if these could rupture.

This is panlobular emphysema which


mostly affects the lower lobes of the
lung, its characteristic of alpha one
antiprotese deficiency.

12

This is bullous emphysema, where small


bulla coalesce together to form large
bullae.

Treatment and management of COPD


Goals of COPD Management
1. Relieve symptoms

the most important goals, if these two are


Achieved all others will be improved.

2. Prevent disease progression


3. Improve exercise tolerance
4. Improve health status
5. Prevent and treat complications
6. Prevent and treat exacerbations
7. Reduce mortality

13

Treatment
Prevent disease progression
A. Smoking cessation: the only thing that can prevent disease progression is probably
smoking cessation, if you stop smoking the disease will stay as it is and it will not
deteriorate more, you will not go back to normal but you will keep the pulmonary
function as it is or it might improve a little in the first one or two years.
B. Vaccines: all smokers who have COPD should receive the influenza vaccine and
probably the pneumococcal vaccine, the evidence for influenza vaccine is stronger but
usually we give pneumococcal once and we give influenza annually.
Improve pulmonary function
Medical treatment
Rehabilitation
Surgical treatment
Treat complications

Smoking cessation
It's advisable that any physician who sees pts to ask pts about smoking even if the disease
that the pts come for is not smoke related, and they found by adopting this policy (ask the pts
to quit smoking) that high percent of smokers will quit smoking, we have to adopt what is
called the five As: Ask the pt if he is smoker, advice him to quit smoking even if this
disease is not smoke related, assess his willingness to quit smoking, assist pts in quitting
smoking bcz some pts tell you that they tried to quit but they failed so if they failed you can
offer them 1.nicotine replacement therapy 2.nicotene patches or gum 3. Give them
antidepressant which is useful in smoking cessation 4. Recently varenicline was introduced
which is nicotine receptor agonist  30-40% of smoker might quit only by assisting them in
quitting, and you have to arrange for follow up for these pts.

14

Age

4040-50

5050-55

6060-70

5555-60

Indeterminate

FEV1 (%) Relative to Age 25

100
Susceptible
Smokers

80
60 Symptoms

Not Susceptible

Stopped smoking
at 45 (mild COPD)
Stopped smoking
at 65 (severe COPD)

40 Disability
20 Death

0
20

30

40

50
60
Age (years)

70

80

90

Courtesy of D.ODonnell.
D.ODonnell. Adapted from Fletcher CM, Peto R. Br Med J.
J. 1977;1:1645.

As I said only 20% of smokers develop COPD, and this is probably genetically
determined.
around the age of twenty we reach the maximum pulmonary function, after the age of
20 we start aging process then we will get a decline in our FEV1, in normal people after the
age of twenty they will loss around 20-30 ml of their FEV1 every year.
In COPD pts there is what is called rapid accelerator, they loss 70-80 ml of their FEV1
every year.
Number 1 in the box above, this person is not susceptible (not smoker = no COPD) so
he is probably can live around age 90 with reasonable pulmonary function.
Number 2 in the box, those who are susceptible (smoker) by age of 60 they will die, but
if they stopped smoking at age of 45 (# 3) they will go back and only loss 20-30 ml of their
FEV1 every year after quitting instead of the 70-80ml lost when they were smokers and
they will live around the age of 80 instead of 6o. So it's not late to quit smoking bcz if you
quit you will have more years to live.

Smoking Cessation and FEV1 Decline


2.8
2.7
Sustained Quitters
Continuing Smokers

2.6
2.5

5y
r

4y

3y
r

2y
r

2
n
re
e

1y
r

2.4
Sc

Post bronchodilator FEV1

2.9

Anthonisen et al. JAMA 1994;272:14971505

15

This is to show you that after you


quit smoking (the upper line) the
FEV1 will improve in the first year
and after that it will start to decline
again as usual (20-30 ml/ year) .

Medical treatment

In medical treatment of COPD we do stage treatment according to the symptoms:


As we said before we start treatment with smoking cessation and then we offer vaccination  this is
applied for all stages of COPD pts.

If pts have mild symptom  we give them short acting beta two agonist
If pts have moderate symptoms  we give them long acting beta two agonist + anticholinergic
medication.

If pts have severe symptoms  we give them inhaled corticosteroids in addition to the previous
protocol (long acting beta two agonist + anticholinergic medication)

If pts have very severe symptoms  we add long term oxygen therapy if they have respiratory failure
in addition to the previous protocols (inhaled corticosteroids + long acting beta two agonist +
anticholinergic medication)

Protocols here differ from that in asthma, in asthma we used inhaled corticosteroids
in initial stages but here inhaled corticosteroid is used in severe and very severe cases.

16

Surgical Treatment
 Lung volume reduction surgery
 Bullectomy
 Lung transplantation  we do it only if the pt have alpha one antitrypsin deficiency.

Lung volume reduction surgery: we use this


type of surgery only in very severe cases of smoke
related emphysema but not in ch.bronchitis, we do
pulmonary function test and we find that FEV1 is
less than 30% which indicate a very severs case
then we do high resolution C.T scan and if we
find that emphysema predominantly affecting the
upper lobes of the lung which is characteristics
finding
in
smoke related emphysema (
centrilobular emphysema) then we can remove the
severely affected upper lobes of the lung which
give more space for the relatively normal lung
tissue down which then improve oxygenation,
exercise tolerance and survival.
So this type of surgery is only done in severe cases
of smoke related emphysema and it must affect
predominantly the upper lobes of the lung.
If the pt has large bullous that compress the
normal lung tissue we do what is called
Bullectomy, but these are very rare.

17

Acute Exacerbations of COPD


Definition:
COPD exacerbation is a period in the natural course of the disease that is characterized by a worsening of a
patient's baseline symptoms -- such as dyspnea, cough and/or sputum production.

Signs and Symptoms of a COPD Exacerbation


The main symptom of an acute exacerbation of COPD is abrupt increase in breathlessness (SOB) for 24-48 h
which is often accompanied by the following:
Increased cough and sputum production
Change in the color and/or thickness of the sputum

the major ones.

Wheezing
Chest tightness
Fever

Causes of COPD Exacerbation: Infection, Air Pollution


The top two causes of an exacerbation are infection (50% of exacerbation is due to infection and mainly it's
bacterial) of the airways or lungs and air pollution (environmental factors). In one-third of all COPD
exacerbation cases, however, the cause cannot be identified.

Therapy for Acute Exacerbations


Oxygen therapy : we use this if the pt have chronic respiratory failure to correct
hypoxemia

Bronchodilators : Bronchodilator dosages are increased during acute exacerbations to


decrease acute bronchospasm, usually we give nebulizers of short acting beta two agonist and
anticholinergic therapy

Antibiotics: Approximately 50% of acute exacerbations are due primarily to the bacterial
infection, most important of these are Streptococcus pneumoniae (causing pneumonia),
Haemophilus influenzae (causing flu), and Moraxella catarrhalis (causing pneumonia).

 We always give antibiotic in COPD exacerbation even if the cause is not related to infection.
18

We decide the type of antibiotic according to the severity of infection.


 In asthma we don't give antibiotic for exacerbation, bcz exacerbation of asthma is only due to
viral infection.

Corticosteroids

Assisted ventilation-mechanical ventilation :


Patients with acute exacerbations of COPD have a risk for developing respiratory failure.
Respiratory failure occurs when respiratory demand exceeds the ability of the respiratory system
to respond. Without aggressive intervention at the point of respiratory failure, the patient can die.

Mechanical ventilation:
Mechanical ventilation is a means by which air is pushed into a patient's lungs by the ventilator instead
of the patient using his respiratory muscles to draw in air. Mechanical ventilation therefore reduces or
eliminates the patient's work of breathing, and the patient continues to receive air into his lungs and
passively exhale without any work. There are two commonly used methods for mechanical ventilation in
COPD: noninvasive and invasive.
Invasive Ventilation
the more traditional means is invasive ventilation: an endotracheal tube, a small-diameter plastic tube,
is placed into the trachea and then connected to a ventilator, which pushes air into the lungs. Invasive
ventilation can be administered to patients who are unconscious or heavily sedated, and it is more
effective than noninvasive ventilation.
Noninvasive Ventilation
Noninvasive ventilation is used in a conscious, cooperative patient. In this method, oxygen is delivered
through a mask that forms a seal around the nose or mouth and nose. The advantages are that the
mask can be periodically removed and the patient's natural protection against secretions getting into the
lower airway is preserved.

Respiratory Failure and COPD

If pts have respiratory failure with stable COPD we have to supply them with oxygen

Respiratory failure has two type

1. Type one respiratory failure (hypoxemic): here there is decrease in PaO2 only,
PaO2 < 55mmhg (7.3 kPa).

2. Type two respiratory failure (hypercapnic): here there's decrease in PaO2 and
increase in PaCO2, PaCO2 > 55mmhg (7kPa).

19


Now if a pt has (PaO2 < 55 mmhg) or (PaO2 between 55-60 mmhg + evidence of chronic hypoxemia
such as polycythemia or cor pulmonale)  they are candidate for long term oxygen therapy, those
therapy include one of two :
o We give them oxygen cylinder that can be replaced every 24-48h or
o We give them what is called oxygen concentrators, a machine that provide oxygen that have
higher concentration than that found in the ambient air by taking the atmospheric air and
keep the nitrogen out of it, characterized by easy accessibility than the oxygen cylinder
These studies have shown that pts who have
COPD with chronic respiratory failure, giving
them oxygen will improve the survival in these
pts.

This slide shows those who have type two


respiratory failure if it's transient, bcz some pts
during exacerbation they retain Co2 and after
exacerbation they recur to type one  those who
have chronic or transient type two failure the
mortality rate will be higher than those who have
type one failure.

20

Prognostic Factors
 BMI & FFMI  if a COPD pt has low body mass index (<=21) the mortality rate is higher than that
who has high body mass index

 Airway hyperresponsiveness
 Acute exacerbations
All these increase mortality rate in COPD pts
 Respiratory failure
 Hypercapnea
 BODE index
 The most important prognostic factor we depend on is the percentage predicted of FEV1,
the more the reduction the more severe the disease is and the higher mortality rate is.

BODE index
B: BMI

O: airway obstruction

4 year survival
0-2 points
3-4 points
5-6 points
7-10 points

D: Dyspnea

80%
67%
57%
18%

21

E: Exercise capacity

COPD and Co-Morbidities


COPD is considered as asystemic disease, accordingly COPD patients are at increased
risk for:





Myocardial infarction, angina


Osteoporosis
Respiratory infection
Depression
Diabetes
Lung cancer

 

Thx for all

22

You might also like