Copd 2012

Department of Pulmonary Medicine
Chronic Obstructive
Pulmonary Disease
(COPD)
Dr. Rahul Magazine
M.D. (Medicine); D.T.C.D.
Dept. of Pulmonary Medicine

DEFINITION
COPD, a common preventable and treatable
disease, is characterized by persistent airflow
limitation that is usually progressive and
associated with an enhanced chronic
inflammatory response in the airways and the
lung to noxious particles or gases.

Chronic bronchitis has been defined as the
presence of chronic productive cough for 3
months during each of two successive years in
a patient in whom other causes of chronic
cough have been excluded.
Emphysema is defined as a condition of the
lung characterized by abnormal permanent
enlargement of the air spaces distal to the
terminal bronchioles accompanied by
destruction of their walls and without obvious
fibrosis.

EPIDEMIOLOGY
• COPD ranked sixth as the cause of death
in 1990, but will become the third leading
cause of death worldwide by 2020.
• The prevalence of COPD is appreciably
higher in smokers and ex-smokers than in
nonsmokers, in those over 40 years than
those under 40, and in men than in
women.

RISK FACTORS
 Exposure to particles
Tobacco smoke
Indoor air pollution from heating and cooking
with biomass in poorly vented dwellings
(among women in developing countries)
Occupational dusts (organic and inorganic)
Outdoor air pollution
 Genes (α1 anti-trypsin deficiency)
 Airway hyperresponsiveness
 Lung Growth and Development
 Oxidative stress
 Gender
 Age
 Respiratory infections
 Socioeconomic status

PATHOLOGY
• Large Airway
Mucous gland enlargement and goblet cell
hyperplasia.
• Small Airways
Airway wall thickening
Peribronchial fibrosis
Luminal inflammatory exudate
Airway narrowing (obstructive
bronchiolitis)

• Lung parenchyma
Alveolar wall destruction
Apoptosis of epithelial and endothelial cells
• Pulmonary vasculature
Thickening of intima
Endothelial cell dysfunction,
INFLAMMATORY CELLS: Macrophages, T
lymphocytes, few neutrophils or eosinophils

PATHOPHYSIOLOGY
Peripheral airway obstruction
Air trapping during expiration
Hyperinflation
Functional Residual Capacity increased

PATHOPHYSIOLOGY
• Gas Exchange Abnormalities
• Mucus Hypersecretion
• Pulmonary Hypertension

PATHOGENESIS
The inflammation in the respiratory tract of
COPD patients appears to be an
amplification of the normal inflammatory
response of the respiratory tract to chronic
irritants such as cigarette smoke

Smoking
Lung Inflammation
Oxidative Stress
COPD Pathology
Proteinases

CLINICAL FEATURES
Symptoms
 Breathlessness
Progressive (worsens over time)
Usually worse with exercise
Persistent (present every day)
 Chronic cough, which is often, but not
invariably, productive.
 Wheeze

 History of exposures to risk factors:
A smoking history of at least 20 pack
years is usual before symptoms develop
Smoke from home cooking and heating
fuels
Occupational dusts and chemicals
 Family history of COPD
 Weight loss and anorexia are features of severe
COPD
 Sleep quality is impaired in advanced COPD
 Hemoptysis

Clinical signs
General examination
• Tachypnoea,
• Prolonged forced expiratory time (more
than 5 s)
• Adopting pursed lipped breathing on
expiration which reduces expiratory airway
collapse.

• Use of the accessory muscles of respiration
• Adopt the position of leaning forward, supporting
themselves with their arms to fix the shoulder
girdle
• Tar-stained fingers
• Cyanosis in advanced disease
• Flapping tremor
• Weight loss
• Finger clubbing is not a feature of COPD

Examination of Chest
Inspection and Palpation
• Signs of overinflation: barrel-shaped with a
kyphosis and an apparent increased
anterior/posterior diameter, horizontal ribs,
prominence of the sternal angle, and a wide
subcostal angle. Distance between the
suprasternal notch and the cricoid cartilage
(normally three finger-breadths) may be
reduced.
• Pursed lip breathing, use of accessory muscles
• An inspiratory tracheal tug
• Hoover's sign

• Indrawing of the suprasternal and supraclavicular
fossas and of the intercostal muscles
Percussion
• Hyper resonant note
• Decreased hepatic and cardiac dullness
Ausculatation
• Breath sounds may have a prolonged expiratory
phase, or may be uniformly diminished
• Wheeze
• Crackles may be heard particularly at the lung bases

Cardiovascular Examination
• Difficulty in localizing the apex beat
• Signs of pulmonary artery hypertension
• Signs of right heart failure
SYSTEMIC FEATURES:
Skeletal muscle wasting
Osteoporosis
Anxiety and Depression
Increased risk of cardiovascular disease, respiratory
infections diabetes, lung cancer

Type A: Pink Puffer
(Emphysema Predominant)
• Major complaint is dyspnea,
• Cough is rare, with scant clear, mucoid sputum.
• Patients are thin, with recent weight loss
common.
• They appear uncomfortable, with evident use of
accessory muscles of respiration.
• Chest is very quiet without adventitious sounds.
• No peripheral edema.

Type B: Blue Bloater
(Bronchitis Predominant)
• Major complaint is chronic cough, productive of
mucopurulent sputum
• Dyspnea usually mild, though patients may
note limitations to exercise.
• Patients frequently overweight and cyanotic but
seem comfortable at rest.
• Peripheral edema is common.
• Chest is noisy, with rhonchi invariably present

MANAGEMENT

Assessment
• COPD Assessment Test (CAT): An 8-item
measure of health status impairment in
COPD
• Breathlessness Measurement using the
Modified British Medical Research Council
(mMRC) Questionnairewell to other
measures of health statusand predicts
future mortality risk.

INVESTIGATIONS
Hematocrit
Polycythemia can develop in the presence
of arterial hypoxemia, especially in
continuing smokers, and can be identified
by hematocrit > 55%.

• Spirometry:
The presence of a postbronchodilator
FEV1/FVC < 0.70 confirms the presence of
persistent airflow limitation and thus COPD

Spirometry: Normal Trace Showing
FEV1 and FVC
1 2 3 4 5 6
1
2
3
4
Volume,liters
Time, sec
FVC5
1
FEV1 = 4L
FVC = 5L
FEV1/FVC = 0.8

Spirometry: Obstructive Disease
Volume,liters
Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV1 = 1.8L
FVC = 3.2L
FEV1/FVC = 0.56
Normal
Obstructive

Classification of Severity of Airflow
Limitation in COPD
(Based on Post-Bronchodilator FEV1)
In patients withFEV1/FVC < 0.70
GOLD I: Mild; FEV1 ≥ 80% predicted
GOLD II: Moderate; 50% ≤ FEV1 < 80%
predicted
GOLD III: Severe; 30% ≤ FEV1 < 50%
predicted
GOLD IV: Very Severe; FEV1 < 30% predicted

• Imaging
Chest X-ray Signs of hyperinflation
(flattened diaphragm and an increase
in the volume of the retrosternal air
space), hyperlucency of the lungs,
and rapid tapering of the vascular
markings.
Computed tomography (CT)

• Arterial blood gas measurement
• Exercise testing
• Alpha-1 antitrypsin deficiency
screening (when COPD develops under 45
years or with a strong family history of COPD.)
• Other investigations, including
electrocardiography, echocardiography,
radionucleotide scintigraphy, and magnetic
resonance imaging.

TREATMENT
1. Smoking Cessation
• Counseling
• Pharmacotherapy
Nicotine replacement products (nicotine
gum, inhaler, nasal spray, transdermal
patch, sublingual tablet, or lozenge)
Other pharmacotherapy:The antidepressants
bupropion and nortriptyline. Varenicline,
a nicotinic acetylcholine receptor partial
agonist that aids smoking cessation by
relieving nicotine withdrawal symptoms and
reducing the rewarding properties of nicotine

Drugs Used in COPD
β2-agonists
Short-acting
(Salbutamol, Terbutaline)
Long-acting
(Formoterol, Salmeterol)

Drugs Used in COPD
Anticholinergics
Short-acting
Ipratropium bromide
Oxitropium bromide
Long-acting
Tiotropium

Drugs Used in COPD
Combination short-acting β 2-agonists
plus anticholinergic in one inhaler
Salbutamol/Ipratropium
Methylxanthines
Aminophylline
Theophylline (SR)

Drugs Used in COPD
Inhaled glucocorticosteroids
Beclomethasone, Budesonide,
Fluticasone, Triamcinolone
Combination long-acting β 2-agonists plus
glucocorticosteroids in one inhaler
Formoterol/Budesonide
Salmeterol/Fluticasone

Drugs Used in COPD
Phospodiesterase-4 inhibitor: Roflumilast
Systemic glucocorticosteroids
Prednisone, Methyl-prednisolone

OTHER PHARMACOLOGIC
TREATMENTS
• Alpha-1 antitrypsin augmentation therapy.
• Vaccines:
Influenza vaccine (reduces serious illness and
death)
Pneumococcal vaccine (reduces incidence of
CAP)

OTHER PHARMACOLOGIC
TREATMENTS
• Mucolytic agents (ambroxol, carbocysteine,
iodinated glycerol)
Patients with viscous sputum may benefit
from mucolytics; overall benefits are very
small.
• Antibioticsefits are very small
• Antioxidant agents
• Immunoregulators
• Antitussives

OTHER PHARMACOLOGIC
TREATMENTS
Oxygen Therapy
Can be administered in three ways: longterm
continuous therapy, during exercise, and to relieve
acute dyspnea.
The primary goal of oxygen therapy is to increase
the baseline PaO2 to at least 8.0 kPa (60 mm Hg)
at sea level and rest, and/or produce an SaO2 at
least 90%, which will preserve vital organ function
by ensuring adequate delivery of oxygen.

The long-term administration of oxygen(> 15
h/d) to patients with chronic respiratory
failure has been shown to increase survival.
Long-term oxygen therapy is generally
introduced in patients with COPD, who have
PaO2 at or below 55 mm Hg or SaO2 at or
below 88%, with or without hypercapnia

OTHER TREATMENTS
• Non invasive ventilation with LTOT in
a some selected patients may improve
survival
• Rehabilitation

Surgical Treatments
Bullectomy
Lung volume reduction surgery
Lung transplantation

Only three interventions influence the natural
history of patients with COPD.
1.Smoking cessation
2.Oxygen therapy in chronically hypoxemic
patients
3.Lung volume reduction surgery in selected
patients with emphysema.
There is currently suggestive, but not definitive,
evidence that the use of inhaled glucocorticoids may
alter mortality rate.

Patien
t
Characteristic Spirometric
Classification
Exacerbation
s per year
mMRC CAT
A
Low Risk
Less Symptoms
GOLD 1-2 ≤ 1 0-1 < 10
B
Low Risk
More Symptoms
GOLD 1-2 ≤ 1 > 2 ≥ 10
C
High Risk
Less Symptoms
GOLD 3-4 > 2 0-1 < 10
D
High Risk
More Symptoms
GOLD 3-4 > 2 > 2
≥ 10
Combined Assessment

Management of Stable
COPD

Managing Stable COPD

MANAGE
EXACERBATIONS
An exacerbation of COPD is defined as an
event in the natural course of the disease
characterized by a change in the patient’s
baseline dyspnea, cough, and/or sputum
that is beyond normal day-to-day
variations, is acute in onset, and may
warrant a change in regular medication in
a patient with underlying COPD.

 The most common causes of COPD
exacerbations are viral upper respiratory
tract infections and infection of the
tracheobronchial tree. .
 Streptococcus pneumoniae, Hemophilus
influenzae, and Moraxella catarrhalis are
the most common bacterial pathogens
involved in COPD exacerbations.

Inhaled bronchodilators (particularly
inhaled Β 2-agonists with or without
anticholinergics) and oral
glucocorticosteroids are effective
treatments for exacerbations of COPD.
Antibiotics if clinical signs of airway
infection (e.g., increased sputum,
purulence)

 Noninvasive mechanical ventilation in
exacerbations improves respiratory acidosis,
increases pH, decreases the need for
endotracheal intubation, and reduces PaCO2,
respiratory rate, severity of breathlessness,
the length of hospital stay, and mortality.
 Medications and education to help prevent
future exacerbations should be considered as
part of follow-up

OXYGEN THERAPY

INTRODUCTION
Oxygen is the substrate that cells use in the
greatest quantity and upon which aerobic
metabolism and cell integrity depend. Since the
tissues have no storage system for oxygen, a
continuous supply at a rate that matches
changing metabolic requirements is necessary
to maintain aerobic metabolism and normal
cellular function.

PRINCIPLES
In general, maintain SaO2 >90%, though
preferably >95%.

Devices For Providing
Oxygen
• Oxygen supply (cylinder or wall unit)
• Nasal cannula
• Face mask
• Venturi mask

NASAL CANNULA
• The nasal cannula is a low-flow oxygen administration
system designed to add oxygen to room air when the
patient inspires.
• A nasal cannula provides up to 44% oxygen.
• The ultimate inspired oxygen concentration is
determined by the oxygen flow rate through the
cannula and how deeply the patient breathes (tidal
volume).

• Increasing the oxygen flow by 1 L/min
(starting with 1 L/min) will increase the
inspired oxygen concentration by
approximately 4%:
— 1 L/min: 21% to 24%
— 2 L/min: 25% to 28%
— 3 L/min: 29% to 32%
— 4 L/min: 33% to 36%
— 5 L/min: 37% to 40%
— 6 L/min: 41% to 44%

FACE MASK
• A simple face mask delivers low oxygen
flow to the patient’s nose and mouth. A
partial rebreathing mask consists of a face
mask with an attached reservoir bag

• A face mask can supply up to 60% oxygen
with flow rates of 6 to 10 L/min. A face
mask with oxygen reservoir
nonrebreathing mask) provides up to 90%
to 100% oxygen with flow rates of 9 to 15
L/min. In this system a constant flow of
oxygen enters an attached reservoir.

Use a face mask with a reservoir for patients who
Are seriously ill, responsive, and have adequate
ventilation but require high oxygen concentrations

VENTURI MASK
• A Venturi mask enables a more reliable and
controlled delivery of oxygen concentrations
from 24% to 50%. Use the Venturi mask for
patients who retain carbon dioxide (CO2).
Patients who have chronic high levels of CO2 in
their blood and moderate-to-severe hypoxemia
may develop respiratory depression if the drive
stimulating them to breathe (oxygen) is
reduced.

• Delivered oxygen concentrations can be
adjusted to 24%, 28%, 35%, and 40%
using a flow rate of 4-8 L/min and 40% to
50% using a flow rate of 10-12 L/min.

MONITORING
Adequacy and changes in arterial oxygen
saturation can be continuously monitored
by pulse oximetry and intermittent or
continuous invasive blood gas analysis.

REFERENCES
• Harrison's Principles of Internal Medicine, 18th
Edition
• GOLD. 2011 (revised)
• Murray & Nadel's Textbook of Respiratory
Medicine, 4th ed.
• CMDT 2010

THANK YOU

Copd 2012

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