Chronic Obstructive

Pulmonary Disease (COPD)

GAO Bao-an MD
Respiratory Department,
The First College of Clinical Medical Science,
Three Gorges University
E-mail: 222xiaozhao@163.com
The learner will…
● Master clinical manifestation, diagnosis, and
principal protocols of prophylaxis and treatment
of COPD.
● Be familiar with the pathophysiology of COPD.
● Understand COPD is common and frequently-
occurring disease. Incidence is high, and
complication is serious.
World’s Top Ten Killers (WHO)
World’s Top Ten Killers (WHO)
Why COPD is Important ?
• COPD is the only chronic disease that is
showing progressive upward trend in both
mortality and morbidity.
• It is expected to be the third leading
cause of death by 2020
ⅠDefinition
Chronic obstructive pulmonary
disease is defined as
--‘a disease state characterized by the
presence of airflow obstruction due to
chronic bronchitis or emphysema; the
airflow obstruction is generally progressive,
may be accompanied by airway hyper-
reactivity, and may be partially reversible’
American Thoracic Society 1995/ATS
New Definition
• Chronic obstructive pulmonary disease (COPD) is
a preventable and treatable disease state
characterized by airflow limitation that is not fully
reversible.
• The airflow limitation is usually progressive and
is associated with an abnormal inflammatory
response of the lungs to noxious particles or
gases, primarily caused by cigarette smoking.
• Although COPD affects the lungs, it also
produces significant systemic consequences.

American Thoracic Society 2004/ATS

Ⅱ Epidemiology
◎COPD is the 4th leading cause of death in the United States
(behind heart disease, cancer, and cerebrovascular
disease).
◎ In 2000, the WHO estimated 2.74 million deaths worldwide
from COPD.
◎ In 1990, COPD was ranked 12th as a burden of disease;
by 2020 it is projected to rank 5th
◎ Approximately 14 million Indians are currently suffering
from COPD.
◎ Approximately 32.8 million Chinese are currently suffering
from COPD.
The Indian J Chest Dis & Allied Sciences 2001; 43:139-47
ZHONG Nanshan GARD. China
 Percent Change in Age-Adjusted
Death Rates, U.S., 1965-1998
Proportion of 1965 Rate
3.0
Coronary Stroke Other CVD COPD All Other
2.5 Heart Causes
Disease
2.0

1.5

1.0

0.5

–59% –64% –35% +163% –7%

0
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
 Overall prevalence of COPD in China
Urban Rural Total
prevalence of COPD(%)

14 12.7 12.4
12.1
12
10 8.8 8.2
7.8
8
4.9 5.4 5.1 #
6
4
2
0
Male Female * Total

* Male VS Female: P<0.01; # Urban VS Rural: P<0.01

 Ⅲ Risk factors for COPD
★Tobacco smoking (most common cause)
★Smoke from home cooking and heating fuel
★Occupational dust and chemicals
★Gender: More common in men. M:F ratio is
5%:2.7% (in India) and12.4%:5.4% (in
China)
★ Increasing age
★ Others:
Infection, nutrition, socioeconomic status
and deficiency of alpha1 antitrypsin
Ⅳ Pathology of COPD
Inflammation of small airway and destruction of alveolar wall

cilia

Nonsmoker COPD
A B

A Hypertrophy of airway
smooth muscles
B Squamous metaplasia
replace columnar epithelium
focally
C Enlarged submucosal
C glands
Ⅴ Pathogenesis of COPD

1 Abnormal airway inflammation

2 Reactive oxygen species

3 Imbalance of protease-antiprotease
 AIRWAY INFLAMMATION OF COPD

Cigarette smoke Noxious particles or gases

? Alveolar macrophage
CD8
+

lymphocyte
Neutrophil chemotactic factors
Cytokines (IL-8, interleukin)
Mediators

Neutrophil

PROTEASE Neutrophil elastase

PROTEASES MatrixCathepsins
INHIBITORS
- metalloproteinases

Alveolar wall destruction Mucus hypersecretion

(Emphysema) (Chronic bronchitis)
 REACTIVE OXYGEN SPECIES IN COPD
ANTIOXIDANTS
Vitamins C and E
N-acetyl cysteine
Anti-proteases
α 1-AT NF-κB

Proteolysis
IL-8 TNF-
a
O2-, H202 α
Neutrophil
OH., ONOO-
recruitment

Mucus secretion
Isoprostanes Plasma leak Bronchoconstriction
PROTEASE-ANTIPROTEASE IMBALANCE IN COPD

α 1-Antitrypsin
SLPI
Neutrophil elastase
Elafin
Cathepsins
TIMPs
MMP-1, MMP-9,
MMP12
Granzymes, perforins
Others……..
Ⅵ Pathophysiology of COPD
▲ Increased mucus production and reduced mucociliary
clearance
– cough and sputum production
▲ Loss of elastic recoil, Increase smooth muscle tone,
Pulmonary hyperinflation
– airway collapse (emphysema)
▲ Gas exchange abnormalities
– hypoxemia and/or hypercapnia (dyspnea, cyanosis)
▲ Pulmonary hypertension: hypoxemia, decreasing capillary
bed
– chronic cor pulmonale (systemic edema)
Ⅶ Diagnosis of COPD
1 Symptoms
• Cough and mucoid sputum
• Dyspnea-slowly
progressive
• Wheeze
• Edema (If cor pulmonale)
• Winter exacerbations
 Key indicators for COPD diagnosis
Chronic cough Present intermittently or every day
often present throughout the day;
seldom only nocturnal

Chronic sputum Present for many years, worst in

winters. Initially mucous sputum
production becomes purulent with
exacerbation
Dyspnea that is Progressive (worsens over time)
Persistent (present every day)
Worse on exercise
Worse during respiratory infections

Acute bronchitis Repeated episodes

History of exposure to risk Tobacco smoke

occupational dusts and chemical
factors smoke from home cooking and
heating fuel
2 Signs
• barrel chest
(hyperinflation)
• Low, flat diaphragm
• Decreased expansion
chest
• Diminished breath
sound, prolonged
expiration, or wheeze
• cyanosis
3 Assistant examination

Chest imaging: Chest x-ray plate, Computer

Tomograph scan
Pulmonary function testing
Other exam: blood routine test, electrocardio-
graph, arterial gas analysis, sputum culture,
etc.
Normal COPD
(emphysema)
 C
O
P
D

Normal
Pulmonary function testing
Spirometry
• Diagnosis
• Assessing severity
• Assessing prognosis
• Monitoring progression
• FEV1 – Forced expired volume in the
first second
• FVC – Total volume of air that can be
exhaled from maximal inhalation to
maximal exhalation
• FEV1/FVC% – The ratio of FEV1 to
FVC, expressed as a percentage.
Arterial blood gas analysis
In the early stages, mild or moderate hypoxemia (PaO2
﹤60mmHg) without hypercapnia.
As the disease progresses, hypoxemia becomes more
severe and hypercapnia (PaCO2﹥50mmHg) happens.
Hypercapnia occurs with increasing frequency as the
FEV1 falls below 1 L.
Blood gas abnormalities worsen during acute
exacerbations and may worsen during exercise and
sleep.
4 COPD classification based on Spirometry
Severity Post bronchodilator Post bronchodilator
FEV1/FVC % FEV1% predicted

At risk (0 stage) >70 >80

Mild (1 stage) <70 >80
Moderate < 70 50-80
(2 stage)
Severe (3 stage) < 70 30-50

Very severe < 70 <30

(4 stage)

SPIROMETRY is not to substitute for clinical judgment in the

evaluation of the severity of disease in individual patients.
5 Relationship between COPD and chronic
bronchitis, emphysema, asthma.
Chronic bronchitis is characterized by
‘chronic productive cough for at least 3 months
in each of 2 successive years for which other
causes, such as infection with tuberculosis,
carcinoma of the lung, or chronic heart failure,
have been excluded.
Two types: simple type and wheezing type
Three stages: acute attack phase, chronic
procrastinate phase, and clinical remission
stage.
Emphysema is characterized by
abnormal permanent enlargement of the
airspaces distal to the terminal bronchioles with
destruction of their walls and without obvious
fibrosis. Destruction is defined as irregular
enlargement of respiratory airspaces; the orderly
appearance of the acinus and its components is
disturbed and may be lost.
Asthma is characterized by
airway inflammation that is manifested by
airway hyper-responsiveness to a variety of
stimuli and by airway obstruction that is
reversible spontaneously or in response to
treatment; reversibility may be incomplete in
some patients.
Relationship between COPD and chronic
bronchitis, emphysema, asthma.

Bronchitis
Asthma

COPD

Emphysema
Ⅷ Differential diagnosis
COPD Smoking (occupational ) history. Onset after middle age.
chronic cough, sputum, dyspnea. Symptoms develop
slowly. Airflow obstruction is not reversible fully.

Asthma Family history. Onset from children. Expiratory dyspnea

(cough) in night or morning especially. Allergic symptoms
(rhinitis, eczema). Airflow obstruction is fully reversible.

Heart failure Heart diseases history (hypertension, angina, rheumatic

valvular disease). Dyspnea and edema. Small crackles of
low lung. No airflow obstruction. Enlarged heart (X ray).
Chronic cough, large pyoid sputum in the morning on
arising especially. Persistent middle-large crackles.
Bronchiectasis Finger clubbing, CT shows dilated airway (tram lines,
signet ring appearance, and grapelike cluster)
Low fever, night sweat, loss weight, cough, hemoptysis.
Tuberculin skin test (PPD, purified protein derivative)
Tuberculosis ( ＋ ).
bacterium test ( ＋ )(sputum smear or culture). X ray plate
shows special manifestations. Spirometry is normal.
 Finger
clubbing
grapelike cluster

signet ring appearance

Ⅸ Prognosis and Course
Disease Course of a Patients with COPD
Symptoms

Exacerbations

Exacerbations
Deterioration
Exacerbation
s
End of Life

FEV1 < 0.75L

mortality rate is 30% at 1 year
mortality rate is 95% at 10 year
Ⅹ Treatment of COPD
1 general therapy
⊙ Smoking cessation; ⊙ physical activity;
⊙ nutrition; ⊙ oxygen therapy.

2 pharmacotherapy for stable COPD

⊙ bronchodilators; ⊙ expectorant;⊙ antioxidants; ⊙
corticosteroid (some patients need); ⊙surgery

3 therapy for exacerbation (acute attack)

⊙ antibiotics; ⊙ bronchodilators;⊙ controlled oxygen;
⊙corticosteroid; ⊙mechanical ventilation;
⊙treat complications (pneumothorax, heart failure, etc)
 Smoking cessation
5

4
FEV1 (liters)

3
smoking
2

1
Stop

0
10 15 20 25 30 35 40 45 50 55 60 65 70 75 80
Age (Years)
Smoking cessation
• Stops accelerated decline in FEV1
• Improves possibility of oxygen therapy benefits
• 3-6 months after quitting: end of cough/phlegm
production
• 1 year: lung function increased 30mls
• 1 year: risk of Small Cell Lung Cancer halved
• 5 years: risk of any lung cancer halved
– No progression of COPD
– Sporting performance enhanced
• Methods of smoking cessation
– Counseling; Nicotine replacement; Behavior
modification
Physical activity

● Walk, jogging
(30 minutes for at least twice a week )
● pursed-lip breathing
● Abdominal breathing
● Qi gong, or Indian yoga
Nutrition
Low BMI, high mortality
BMI (body mass index) ＝ weight (kg)/high2(m2)
BMI﹤21 kg/m2, mortality rise

Respiratory quotient (RQ)

Protein: 0.8
Fat: 0.71
Carbohydrate: 1.0
Oxygen therapy
Long-term O2 therapy prolongs life in hypoxemic
COPD patients. It needs more than 15 hours a day.
criteria: PaO2 ≤55 mmHg (SaO2,arterial saturation
<= 88%).
O2 is administered by nasal cannula at a flow
rate sufficient to achieve a PaO2 ＝ 60
mmHg (SaO2 ＝ 90%), usually ≤ 3 L/min
with the patient at rest.
Expectorants Antioxidants
★ammonium chloride ☆Vitamine C
0.3-0.6, tid, po. 0.1-0.3, tid, po.
★bromhexine ☆Vitamine E
16mg, tid, po. 0.1-0.2, tid, po.
★ambroxol
☆N-acetyl cysteine
30mg, tid, po.
0.2, tid or 0.6, qd
★gelomyrtol
300mg, tid, po. ☆T.C.M
★T.C.M.
 Bronchodilators
• Short-acting β2-agonist –
Salbutamol
• Long-acting β2-agonist -
Salmeterol and Formoterol
• Anticholinergics –
Ipratropium, Tiiotropium
• Methylxanthines –
Theophylline, Aminophylline
Steroids
• Oral – Prednisone
• Inhaled - Fluticasone,
Budesonide
Management based on GOLD
Surgery

Lung volume reduction surgery:

thoracoscope
Lung transplantation:
Single-lung
Double-lung
 Therapy for exacerbation
(acute attack)
(1)Antibiotics (common G-)
bacteria: hemophilus influenza, pseudomonas
cef Ⅲ, Imipenem, Amikacine, etc
(2)Bronchodilators
Salmeterol, 200ug, q6h-q12h, inhaling
Aminophylline, 0.25, iv drop, Bid
(3)Corticosteroid
Methiprednisone 40mg-80mg, iv drop Qd
Dexamethsone 10mg, iv drop Qd
(4) Controlled oxygen:
O2 is administered by nasal cannula at a flow
rate sufficient to achieve a PaO2 ≈ 60mmHg
(SaO2≈90%), usually ≤ 3 L/min.
(5)Mechanical ventilation (respiratory failure)
Noninvasive positive pressure ventilation
Bi-PAP (Bilevel positive airway pressure)
Invasive positive pressure ventilation
（ usually nasotracheal intubation ）
Nasal/face mask
NIPPV: BiPAP
nasotracheal intubation