Asthma and COPD

Isabelita M. Samaniego MD, MOH, FPAFP

Ma. Eufemia M. Collao, MD, DPAFP
FCM 3 – College of Medicine
Pamantasan ng Lungsod ng Maynila

01/09/09 1
01/09/09 2
Session Objectives

 To describe the symptomatology in asthma &

COPD
 To describe the disease severity according to
lung function based on GINA and GOLD.
 To describe the definition of disease control &
treatment objectives for asthma & COPD
 To describe the national objectives for health
for asthma & COPD.

01/09/09 3
 Symptomatomatology
 Asthma  COPD
 Intermittent & feeling  Frequent cough usually
well in between wet mostly in the
 Frequent to persistent morning.
& rarely feeling  Can become so well
completely well that asthma is
 Intermittent cough seemingly cured
frequently dry  Never full recovery
usually getting
progressively worse

01/09/09 4
Disease Severity According to lung
function GINA & GOLD
Asthma COPD
Stage 0 =FEV1> 80%
None
( At risk) =FEV1/FVC>70%
Stage 1 = FEV1 > 80%
Step 1= PEFR or FEV1 > 80%
( Mild) = FEV1/FVC < 70%
( Intermittent)
Stage 2= 50% < FEV1 < 80%
Step 2 = PEFR or FEV1 > 80% Moderate =FEV1/FVC < 70%
( Mild persistent)

Stage 3 = 30% < FEV1 < 50%

Step 3 = PEFR < 60% orFEV1 < 80% Severe =FEV1/FVC < 70%
(Moderate Persistent)

Stage 4=FEV1 < 30%

Step 4 PEFR or FEV1 < 60%
( Very severe) = FEV1/FVC < 70%
( Severe persistent)
01/09/09 Chronic Resp. & heart failure 5
Definition of Disease Control &
Treatment Objectives for Asthma &
COPD
 Asthma= GINA  COPD= GOLD
 Minimal episodes
 No emergency visits
 Minimal need for prn B2 agonist
 No limitations on activities,
including exercise
 PEF variability <20%
 ( Near normal PEF)
 Minimal or no adverse effects from
medicine.
Summary:
To achieve total absence of symptoms of
wheeze, breathlessness & cough, normal or
near normal lung function.
 Prevent disease progression
 Relieve symptoms
 Improve exercise tolerance
 Improve health status
 Prevent & treat exacerbations
 Prevent & treat complications
 Reduce mortality
 Minimize side effects
Summary :
To prevent the progression of the disease ( lung
function deterioration) & to improve the
health status or quality of life of patients as
much as possible.

01/09/09 6
01/09/09 7
Goal
 To reduce asthma-related mortality and
morbidity

01/09/09 8
 Health Status Objectives
 Limit the prevalence of asthma to no more
than 12%
 Risk Reduction Objectives
 Increase the awareness of patient and
family on factors that trigger or precipitate
asthma to 30%
 Increase knowledge of the signs and
symptoms of asthma by patients, families
and the general public to 50%

01/09/09 9
 Services and Protection Objectives

 Establish baseline data on the prevalence

of asthma in the Philippines in 2000
 Expand the coverage of asthma clubs in
coordination with the National Asthma
Movement to 75%
 Operationalize Asthma Education
Prevention and Control Programs in 2000

01/09/09 10
 Philippine Report on
Asthma 2004

01/09/09 11
Epidemiolgy
 Asthma is a common disease
 Highest prevalence in UK, Australia, NZ

 Increasing trend for all ages, sex, and racial

groups
 Prevalence increasing by 4%/yr
 Higher among children than adults (esp males),
blacks than whites, impoverished children

 International Study of Asthma and Allergies in Children

( ISAAC) , 1995

01/09/09 12
Philippine Picture
 No available nationwide data on asthma
prevalence.
 Limited reports: prevalence of 12% in
children 13-14y/o and 17-22% in older
age grps
 Lung Center (1996) reported a
prevalence of 22% in adults

01/09/09 13
Current Concepts
 During the last four decades, asthma has
been considered primarily as a dse of airway
smooth muscle.
 But, based on the National Institute of Health
guidelines (1997) concept shifted to airway
inflammation
 Release of inflammatory mediators from eosinophils
and masts cells –
 persistent bronchial inflammation –
 structural abn:
 fibrosis, inc sm muscle mass & mucus glands,
 inc epithelial shedding and thickening of the reticular
basement membrane,
 fiibronectin deposition in the subepithelial layer
01/09/09 14
Asthma
 Definition: A chronic reactive airway disorder
that produces episodic reversible airway
obstruction via bronchospasm, increased
mucous secretions and mucosal edema
 Classifications:
 Extrinsic Asthma (atopic asthma)
 Results from sensitivity to specific external allergens
 Intrinsic Asthma (non-atopic asthma)
 No extrinsic substance can be identified; usually
preceded by severe respiratory infection

01/09/09 15
 It causes recurring episodes of wheezing,
breathlessness, chest tightness, and
coughing particularly at night or in the early
morning
 Common risk factors:
 Domestic dust mites, Animals with fur, Coakroach
 Pollens and molds, Occupational irritants
 Tobacco smoke, Respiratory (viral) infections
 Exercise, Strong emotional expressions
 Chemical irritants and drugs

01/09/09 16
 Severity can be intermittent, or it can be
persistently mild, moderate or severe;
treatment decisions are based on severity
 Should take into account stepwise approach
to pharmacologic treatment to achieve and
maintain control of asthma
 Attacks are episodic, but airways
inflammation is chronically present
 Medications should be taken daily to maintain
to control symptoms, improve lung function
and prevent attacks
 Asthma requires a partnership between the
patient and health care professional
01/09/09 17
Current Concepts on Asthma as
a Disease
 Airway thickening by 50-300% of
normal
 Leading to airway remodelling
 Resulting to:
 Inc airway hyperresponsiveness
 Non-reversibility of airway obstruction and
residual obstruction after bronchodilator
and anti-inflammatory therapy
 Accelerated dec in FEV in some asthmatic
patients

01/09/09 18
Diagnosis of Asthma
 History, PE, and objective measurements of
variable airflow obstruction and/or bronchial
hyperresponsiveness
 But, Hx and PE may not be reliable at times.
 Thus, an objective measure is needed to dx
accurately
 Screening strats: Hx, PE
 Strats for confirmation: FEV1, PEFR, Airway
hyperresponsiveness

01/09/09 19
History
 Asthma should be suspected in any
patient who has any of the following:
 Cough: worsens at night
 Wheeze
 Difficulty in breathing
 Chest tightness
 Dxc accuracy increases as more symptoms are
present
 Dx is strengthened if:
 (+) hx of waxing and waning of symptoms provoked
usu by allergens, irritants, exercise, viral infection;
 (+)FHx;
 improvement after use of anti-asthma meds
01/09/09 20
Physical Examination
 Note that PE may be normal in px with
asthma
 Wheezes are characteristic but not specific
for asthma
 Thus, px may have normal auscultation but
has significant airway obstruction
 A better parameter for significant airway
obstruction: prolonged forced expiratory time
(6 secs or more) = correlates with moderate
to severe a.o.

01/09/09 21
 Forced Expiratory Volume in 1
second (FEV 1)
 Spirometry to document airflow obstruction in
asthma

 Variable airflow obstruction documented via:

 Spontaneous variability in FEV
 Improvement noted 15 mins after inhaled B2-
agonist administration

 Significant: 12% (200ml at least) improvement in

FEV1
 Or: at least 20% improvement in FEV1 after a week
with or without oral steroids, or after 2 wks of
inhaled steroids

01/09/09 22
Peak Expiratory Flow Rate

In the absence of spirometry, home

measurement of PEF may be used +
Response to B2-agonist
 PEF variability is computed as
 mean percentage difference b/w post-
bronchodilator pm value & pre-
bronchodilator am value x several wks or
 Minimum am pre-bronchodilator PEF x 1wk
(Min%/ Max)
asthma if variability of 20% or more

01/09/09 23
Peak Expiratory Flow Rate
 May also be used in clinics, ER and hospital
 If with an improvement of 20% or more in the
PEFR 15 mins after administration of 200-
400ug of inhaled salbutamol or other
equivalent, may be used as indicator of
asthma
 PEFR is more suited for monitoring rather
than for diagnosis
 Thus, it is more of an adjunct to spirometry;
not as substitute

01/09/09 24
Airway Hyperresponsiveness

 If asthma is still suspected in patients

with normal FEV1
 Documentation via:
 Methacholine or histamine inhalation
challenge
 Best to use if the pretest probability of
having asthma based on sx is 30-70%
 A negative test is more reliable in excluding
a dx of asthma

01/09/09 25
Asthma Classification
 According to
 Etiology
 And severity (clinical condition on
presentation whether the patient is in acute
state or chronic state)
 Etiology: limited because no
environmental cause can be identified
 A rigorous search for a SPECIFIC
environmental cause should be part of the
initial assessment

01/09/09 26
 Severity:
 Acute state (in exacerbation)
 Chronic state

01/09/09 27
New Classification of Chronic Asthma
Severity
Parameter S E V E R I T Y
Persistent
Intermittent Mild- Severe
Moderate
Daytime Sx less than wkly wkly daily
Nocturnal Less than Monthly- nightly
awakening monthly wkly
Rescue B2 Less than wkly Wkly-daily Several times
use daily

PEF or FEV More than 80% 60-80 Less than 60

Control Prn B2 agonist LABA + ICS ICS+LABA+
01/09/09
OCS 28
 Six-Part Program to Manage
and Control Asthma
1) Educate patients to develop a partnership in
asthma care
2) Assess and monitor asthma severity
3) Avoid exposure to risk factors
4) Establish individual medication plans for long-
term management in children and adults
5) Establish individual plans to manage asthma
attacks
6) Provide regular follow-up care

01/09/09 29
Goals for successful
management of asthma
 Minimal or no symptoms, including nighttime
symptoms
 Minimal asthma episodes or attacks
 No emergency visits to physicians or hospitals
 Minimal need for reliever medications
 No limitations on physical activities and exercise
 Nearly normal lung function
 Minimal or no side effects from medications

01/09/09 30
Part 1: Educate Patients to
develop a partnership in asthma
care
 Patient can learn to:
 avoid risks factors and take medications correctly
 Understand the difference between “controllers”
and “reliever” medications
 Monitor their status using symptoms and if
available PEF
 Recognize signs that asthma is worsening and
take action
 Seek medical help as appropriate

01/09/09 31
Part 1: Educate Patients to
develop a partnership in asthma
care
 Asthma management plans should cover:
 Prevention steps for long-term control: asthma
risk factors to avoid & daily medication to take
 Action steps to stop attacks

 Ongoing education presented at every patient

visit, is the key to success in all aspects of
asthma management

01/09/09 32
Part 2: Assess and monitor
Asthma Severity
 Monitoring includes review of symptoms and
if possible measurement of lung function
 Regular visits (1-6 months interval) even after
control of asthma is established
 Addressing patient’s concern, fears and
expectations related to asthma to ensure
compliance and adherence to asthma
management

01/09/09 33
Part 3: Avoid Exposure to Risk
Factors
 Specific Immunotherapy, directed at

treating an underlying allergy to grass and

other pollen, domestic mites, animal dander,
or alternaria, may be considered when
avoiding allergens is not possible or
appropriate medications fail to control asthma
symptoms.
 Primary prevention of asthma is not yet
possible, but promising leads are being
actively investigated

01/09/09 34
Part 4: Establish Individual Medication
Plans for Long-term Management in
Children and Adults
 Stepwise Approach
 Used to classify asthma and severity and guide
treatment
 The number and frequency of medications
increase (step up) as the need for asthma therapy
increases, and decreases (step down) when
asthma is under control

01/09/09 35
 Gain Control
 First approach: Establish control promptly with a
high level of therapy and then step down.

 Ex: Add a short course oral glucocorticosteroid and /or

a higher dose if inhaled glucocorticosteroid + long-acting
B2 agonist to the therapy that corresponds with the
patient’s level of asthma severity

 Second approach: Start treatment at the step

most appropriate to the level of asthma severity
and step up if necessary

01/09/09 36
 Step up: if control is not achieved and
sustained. Improvement should be achieved
within 1 month. Review patient’s medication
technique, compliance and avoidance of risk
factors

 Step down: if control is sustained for at least

3 months; follow a gradual stepwise reduction
in treatment. Goal is to decrease treatment to
the least medication necessary to maintain
control

01/09/09 37
 Review treatment every 3 to 6months once
asthma is under control

 Consult with an asthma specialist when other

conditions complicate asthma (sinusitis), the
patient does not respond to therapy, or
treatment at 3 or 4 required

01/09/09 38
 Acute Asthma Management
Initial Assessment
History, PE, PEF or FEV1

Initial Therapy
Bronchodilators; O2 if needed

Good Response Respiratory Failure

Incomplete/Poor Response

Observe for at Add Systemic Admit to

least 1 hour Glucocorticosteroid ICU

If Stable
Discharge Good Response Poor Response

Admit to Hospital

01/09/09 39
 Stepwise approach to long-term
management of asthma
 Criteria in the choice of treatment:
 Severity of asthma
 Current treatment
 Pharmacological properties
 Availability of the various forms of asthma
treatment
 Economic considerations Cultural preference
 Differing health care system

01/09/09 40
Part 5: Establish Individual Plans
to Manage Asthma attacks
 Mild attacks can be treated at home if patient
is prepared and has a personal asthma
management plan that includes action steps
 Moderate attacks may require, and severe
attacks usually require, care in a clinic or
hospital
 Monitor response to treatment
 Evaluate symptoms, if possible, peak flow
 In hospital: assess O2 saturation, consider arterial
blood gas measurement, exhaustion, etc

01/09/09 41
Part 6: Provide Regular Follow-
up Care
 Once asthma control is established, regular
follow-up visits, at 1-6 months intervals as
appropriate
 During visits, monitor and review treatment
plans, medications and level of asthma
control

01/09/09 42
01/09/09 43
01/09/09 44
Goal
 Morbidity and Mortality from lifestyle-related
diseases are reduced and the quality of life of
those who are suffering from such diseases
is improved.

01/09/09 45
 National Objective
 Mortality from degenerative or lifestyle-
related diseases is reduced.
 Indicator
 Mortality rate from COPD per 100,000
population
 Target
 Less than 20.8 deaths per 100,000
population (PHS, 2000)

01/09/09 46
 Strategic Thrusts for 2005 to 2010

 Implement sound, long-term and sustained Healthy

Lifestyle promotion programs
 Promote information, education and advocacy
campaigns
 Translate and implement provisions of the tobacco
laws as local ordinances and develop community
infrastructure supportive of healthy lifestyle
 Pursue training of clinicians and other frontline
healthcare providers
 Manage risk behaviors and risk factors
 Strengthen networking and collaboration
 Support and implement financial risk protection
measures

01/09/09 47
Definition
 COPD is a disease state characterized by
airflow limitation that is not fully reversible.
 The airflow limitation is usually both
progressive and associated with an abnormal
inflammatory response of the lungs to
noxious particles or gases
 Diagnosis should be considered in any
patient who has symptoms of cough, sputum
production, or dyspnea, and/or history of
exposure to risk factors for the disease.
01/09/09 48
Components of COPD that may
coexist
with
 Chronic Bronchitis
Emphysema
 Small airway disease ( Obstructive
Bronchiolitis)
 Chronic Asthma with only partial reversibility

01/09/09 49
Risk Factors

 Smoking – 85%
 Coal
 Isocyanates
 Silica
 Cadmium
 Other dust

01/09/09 50
Classification of Severity of
COPD
 Stage 0: At Risk
 Normal spirometry
 Chronic symptoms (cough, sputum production)

 Stage I: Mild COPD

 FEV1/FVC < 70%
 FEV1 80% predicted
 With or without chronic symptoms (cough, sputum
production)

01/09/09 51
 Stage II Moderate
 FEV1/FVC ,70%; 50% FEV1<80% predicted
 w/ or w/o chromic symptoms

 Stage III Severe COPD

 FEV1/FVC ,70%; 30% FEV1<50% predicted
 w/ or w/o chromic symptoms

 Severe IV Severe COPD

 FEV1/FVC ,70%; 30% FEV1<50% predicted
 Plus chronic respiratory failure

01/09/09 52
Stages of COPD
( Australian New Zealand
Guidelines)COPDX
Stage Postbronchodilator FEV1

Mild 60-80% predicted

Moderate 40-59% predicted

Severe < 40% predicted

01/09/09 53
EPIDEMIOLOGY
 Prevalence and morbidity data greatly
underestimate the total burden of COPD
because the disease is usually not diagnosed
until it is clinically apparent and moderately
advanced

 Mortality data also underestimate COPD as a

cause of death because the disease is more
likely to be cited as a contributory than as an
underlying cause of death, or may not be
cited at all
01/09/09 54
G lobal Initiative for Chronic
bstructive
O ung
L isease
D
01/09/09 55
 GOLD Structure
GOLD Executive Committee
Sonia Buist, MD – Chair
Roberto Rodriguez-Roisin, MD – Co-Chair

Science Committee Dissemination/Implementation

Task Group
Klaus Rabe, MD, PhD - Chair Christine Jenkins, MD - Chair

01/09/09 56
 GOLD Executive
Committee

S. Buist, Chair, US N. Khaltaev, Switzerland WHO

A. Anzueto, US ATS M. Lopez, Uruguay ALAT
P. Calverley, UK E. Nizankowska, Poland
T. DeGuia, Philippines
Y. Fukuchi, Japan APSR
K. Rabe , Netherlands
C. Jenkins, Australia R. Rodriguez-Roisin, Spain
J. Kiley, US NHLBI T. van der Molen,
A. Kocabas, Turkey Netherlands
C. Van Weel, Netherlands
WONCA
01/09/09 57
 GOLD Science
Committee

K. Rabe, Chair M. Decramer

A. Agusti, Y. Fukuchi
A. Anzueto P. Jones
P. Barnes R. Rodriguez-
S. Buist
Roisin
P. Calverley
J. Vestbo
J. Zielinski
01/09/09 58
 Description of Levels of
Evidence
Evidence Sources of Evidence
Category
A Randomized controlled trials
(RCTs). Rich body of data

B Randomized controlled trials

(RCTs). Limited body of data

C Nonrandomized trials
Observational studies.

D Panel consensus judgment

01/09/09 59
 GOLD
Structure
GOLD Executive Committee
Sonia Buist, MD – Chair
Roberto Rodriguez-Roisin, MD – Co-Chair

Science Committee Dissemination/Implementation

Task Group
Klaus Rabe, MD, PhD - Chair Christine Jenkins, MD - Chair

01/09/09
GOLD National Leaders - 60
 Saudi Arabia Bangladesh
Slovenia Germany Ireland
Australia Yugoslavia Croatia
Philippines Brazil Canada
Austria Taiwan
United States Portugal
Thailand ROC
Norway Greece Malta
Moldova China
Syria South Africa
United Kingdom Hong Kong ROC
Italy New Nepal Chile Israel
ArgentinaZealand Mexico
Pakista Russia
United Arab Emirates
n Peru Japan
Poland Korea
GOLD National
Netherland
Leaders Egypt s
Switzerland India Venezuela Georgia
Macedonia France
Czech Iceland Denmark
Turkey Slovakia Belgium
Republic
Romania Columbia Ukraine Singapore Spain
Uruguay
01/09/09
Sweden Albania Kyrgyzstan Vietnam61
 GOLD Website
Address

http://www.goldcopd.o
rg

01/09/09 62
 GOLD Objectives

■Increase awareness of COPD

among health professionals,
health authorities, and the
general public.
■Improve diagnosis, management
and prevention of COPD.
Stimulate research in COPD.
■01/09/09 63
Global Strategy for Diagnosis,
Management and Prevention of
COPD

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 ■ Practical 64
 Definition of COPD
■ COPD is a preventable and treatable disease
with some significant extrapulmonary effects
that may contribute to the severity in
individual patients.

■ Its pulmonary component is characterized by

airflow limitation that is not fully reversible.

■ The airflow limitation is usually progressive

and associated with an abnormal
inflammatory response of the lung to noxious
particles or gases.
01/09/09 65
 Classification of COPD
Severity
by Spirometry
Stage I: Mild FEV /FVC < 0.70
1

FEV1 > 80% predicted

Stage II: Moderate FEV1/FVC < 0.70

50% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.70

30% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70

FEV1 < 30% predicted or
01/09/09 FEV1 < 50% predicted plus 66
 “At Risk” for COPD
■ COPD includes four stages of severity classified by
spirometry.

■ A fifth category--Stage 0: At Risk--that appeared in

the 2001 report is no longer included as a stage of
COPD, as there is incomplete evidence that the
individuals who meet the definition of “At Risk”
(chronic cough and sputum production, normal
spirometry) necessarily progress on to Stage I: Mild
COPD.

■ The public health message is that chronic cough and

sputum are not normal remains important - their 67
01/09/09
presence should trigger a search for underlying
Global Strategy for Diagnosis,
Management and Prevention of
COPD

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 ■ Practical 68
 Burden of COPD: Key Points

 COPD is a leading cause of morbidity and

mortality worldwide and results in an economic
and social burden that is both substantial and
increasing.
 COPD prevalence, morbidity, and mortality vary
across countries and across different groups
within countries.
 The burden of COPD is projected to increase in
the coming decades due to continued exposure
to COPD risk factors and the changing age
structure of the world’s population.
01/09/09 69
 Burden of COPD:
Prevalence
 Many sources of variation can affect estimates of
COPD prevalence, including e.g., sampling
methods, response rates and quality of
spirometry.
 Data are emerging to provide evidence that
prevalence of Stage I: Mild COPD and higher is
appreciably higher in:

- smokers and ex-smokers

- people over 40 years of age
- males
01/09/09 70
 COPD Prevalence Study in Latin
America
The
prevalence of
post-
bronchodilator
FEV1/FVC <
0.70 increases
steeply with
age in 5 Latin
American
Cities

Source: Menezes AM et al. Lancet 2005

01/09/09 71
 Burden of COPD: Mortality

 COPD is a leading cause of mortality worldwide

and projected to increase in the next several
decades.
 COPD mortality trends generally track several
decades behind smoking trends.
 In the US and Canada, COPD mortality for both
men and women have been increasing.
 In the US in 2000, the number of COPD deaths
was greater among women than men.

01/09/09 72
 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
01/09/09 73
Source: NHLBI/NIH/DHHS
 Of the six
leading
causes of
death in the
United
States, only
COPD has
been
increasing
steadily since
01/09/09
Source: Jemal A. et al. JAMA 74
 COPD Mortality by Gender,
U.S., 1980-2000

70
Number Deaths x

60

50 Men

40
Women
30

20
1000

10

0
1980 1985 1990 1995 2000

01/09/09 Source: US Centers for Disease Control and 75

Global Strategy for Diagnosis,
Management and Prevention of
COPD

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 ■ Practical 76
Risk Factors for COPD

Genes Lung growth and

Exposure to particles development
● Tobacco smoke Oxidative stress
● Occupational dusts, Gender
organic and inorganic Age
● Indoor air pollution from Respiratory infections
heating and cooking with Socioeconomic status
biomass in poorly
ventilated dwellings Nutrition
● Outdoor air pollution Comorbidities

01/09/09 77
 Risk Factors for
COPD
Nutrition

Infections

Socio-economic
status

01/09/09
Aging Populations 78
Global Strategy for Diagnosis,
Management and Prevention of
COPD

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 ■ Practical 79
01/09/09 80
 Changes in Large Airways of COPD
Patients

Mucus hypersecretion Neutrophils in sputum

Squamous metaplasia of epithelium

No basement membrane thickening
Goblet cell
hyperplasia ↑ Macrophages

↑ CD8+ lymphocytes
Mucus gland hyperplasia
Little increase in
airway smooth muscle

Source: Peter J. Barnes,

01/09/09 81
MD
 Changes in the Lung Parenchyma in COPD
Patients

Alveolar wall destruction

Loss of elasticity

Destruction of pulmonary
capillary bed

↑ Inflammatory cells
macrophages, CD8+ lymphocytes

Source: Peter J. Barnes,

01/09/09 82
MD
 Changes in Pulmonary Arteries in COPD
Patients

Endothelial dysfunction

Intimal hyperplasia

Smooth muscle hyperplasia

↑ Inflammatory cells
(macrophages, CD8+ lymphocytes)

Source: Peter J. Barnes,

01/09/09 83
MD
 Pathogenesis of
COPD
Cigarette smoke
Biomass particles Host factors
Particulates Amplifying mechanisms

LUNG INFLAMMATION
Anti-oxidants
Anti-proteinases

Oxidative
stress Proteinases

Repair
mechanisms

COPD PATHOLOGY
01/09/09 84
Source: Peter J. Barnes,
Inflammatory Cells Involved in
COPD Cigarette smoke
(and other irritants)

Epithelial Alveolar
cells macrophage

Chemotactic factors

CD8+
Fibroblastlymphocyte

Neutrophil Monocyte
Neutrophil elastase
PROTEASESCathepsins
MMPs

Mucus hypersecretion
Fibrosis Alveolar wall destruction
(Obstructive (Emphysema)
bronchiolitis)
01/09/09 Source: Peter J. Barnes,
85
MD
 Oxidative Stress in COPD Macrophage Neutrophil

Anti-proteases
SLPI α 1-AT NF-κ B

Proteolysis IL-8 TNF-α

↓ HDAC2 O2-, H202
Neutrophil
OH., ONOO- recruitment
↑Inflammation
Steroid
resistance

Isoprostanes Plasma leak Bronchoconstriction

↑ Mucus secretion
01/09/09 Source: Peter J. Barnes,
86
MD
Differences in Inflammation and its Consequences: Asthma and COPD
ASTHMA COPD
Allergens
Cigarette smoke

Y Y
Y

Ep cells Mast cell

Alv macrophage Ep cells

CD4+ cell Eosinophil

CD8+ cell Neutrophil
(Th2)
(Tc1)
Bronchoconstricti
on Small airway narrowing
AHR Alveolar destruction

Airflow Limitation
Reversible Irreversible
01/09/09 87
Source: Peter J. Barnes,
 Air Trapping in
COPD Mild/moderate Severe
Inspiration Normal
COPD COPD
small
airway

alveolar attachments loss of elasticity loss of alveolar attachments

Expiration

closure

↓ Health Dyspnea Air trapping

status ↓ Exercise capacity Hyperinflation
01/09/09 88
Source: Peter J. Barnes,
 Pulmonary Hypertension in
COPD
Chronic hypoxia

Pulmonary vasoconstriction
Muscularization
Pulmonary hypertension Intimal
hyperplasia
Fibrosis
Cor pulmonale Obliteration

Edema
Death

01/09/09 89
Source: Peter J. Barnes, MD
 Inflammation in COPD Exacerbations

Bacteria Viruses Non-infective

Pollutants

Macrophages
Epithelial
cells

TNF-α IL-8 IL-6

Neutrophils

Oxidative stress

01/09/09 90
Source: Peter J. Barnes,
Global Strategy for Diagnosis,
Management and Prevention of
COPD

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 ■ Practical 91
Four Components of COPD
Management

1. Assess and monitor

disease

2. Reduce risk factors

3. Manage stable COPD

● Education
● Pharmacologic
● Non-pharmacologic

• Manage exacerbations
01/09/09 92
GOALS of COPD
MANAGEMENT
VARYING EMPHASIS WITH DIFFERING
• Relieve symptoms
SEVERITY

• Prevent disease progression

• Improve exercise tolerance
• Improve health status
• Prevent and treat
complications
• Prevent and treat
01/09/09 93
Four Components of COPD
Management

• Assess and monitor

disease

• Reduce risk factors

• Manage stable COPD

● Education
● Pharmacologic
● Non-pharmacologic

• Manage exacerbations
01/09/09 94
Management of Stable COPD
Assess and Monitor COPD: Key
Points
A clinical diagnosis of COPD should be
considered in any patient who has
dyspnea, chronic cough or sputum
production, and/or a history of exposure to risk
factors for the disease.
The diagnosis should be confirmed by
spirometry. A post-bronchodilator FEV1/FVC
< 0.70 confirms the presence of airflow
limitation that is not fully reversible.
Comorbidities are common in COPD and
01/09/09 95
Diagnosis of
COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
shortness of breath
indoor/outdoor pollution
➨

SPIROMETRY
01/09/09 96
Management of Stable COPD
Assess and Monitor COPD:
Spirometry
Spirometry should be performed after the
administration of an adequate dose of a short-
acting inhaled bronchodilator to minimize
variability.
A post-bronchodilator FEV1/FVC < 0.70
confirms the presence of airflow limitation
that is not fully reversible.
Where possible, values should be compared
to age-related normal values to avoid
overdiagnosis
01/09/09 of COPD in the elderly. 97
 Spirometry: Normal and
Patients with COPD

01/09/09 98
 Differential Diagnosis:
COPD and Asthma
COPD ASTHMA
• Onset in mid-life • Onset early in life (often
childhood)
• Symptoms slowly
progressive • Symptoms vary from day to day
• Long smoking history • Symptoms at night/early morning
• Dyspnea during exercise • Allergy, rhinitis, and/or eczema
also present
• Largely irreversible airflow
limitation • Family history of asthma
• Largely reversible airflow
limitation
01/09/09 99
COPD and Co-
Morbidities
COPD patients are at increased risk for:
• Myocardial infarction, angina
• Osteoporosis
• Respiratory infection
• Depression
• Diabetes
• Lung cancer

01/09/09 100
COPD and Co-
Morbidities
COPD has significant extrapulmonary

(systemic) effects including:

• Weight loss
• Nutritional abnormalities
• Skeletal muscle dysfunction

01/09/09 101
Four Components of COPD
Management

• Assess and monitor

disease

• Reduce risk factors

• Manage stable COPD

● Education
● Pharmacologic
● Non-pharmacologic

01/09/09
• Manage exacerbations 102
Management of Stable COPD
Reduce Risk Factors: Key
Points
 Reduction of total personal exposure to
tobacco smoke, occupational dusts and
chemicals, and indoor and outdoor air
pollutants are important goals to prevent
the onset and progression of COPD.

 Smoking cessation is the single most

effective — and cost effective —
intervention in most people to reduce the
risk of developing COPD and stop its
01/09/09 103
Brief Strategies to Help the
Patient Willing to Quit Smoking
• ASK Systematically identify all
tobacco users at every visit.
• ADVISE Strongly urge all tobacco
users to quit.
• ASSESS Determine willingness to
make a quit attempt.
• ASSIST Aid the patient in quitting.

• ARRANGE Schedule follow-up contact.

01/09/09 104
Management of Stable COPD
Reduce Risk Factors: Smoking
Cessation
 Counseling delivered by physicians and
other health professionals significantly
increases quit rates over self-initiated
strategies. Even a brief
(3-minute) period of counseling to urge a
smoker to quit results in smoking cessation
rates of 5-10%.

 Numerous effective pharmacotherapies for

smoking cessation are available and
pharmacotherapy is recommended when
01/09/09 105
Management of Stable COPD
Reduce Risk Factors: Indoor/Outdoor Air
Pollution

 Reducing the risk from indoor and outdoor

air pollution is feasible and requires a
combination of public policy and protective
steps taken by individual patients.

 Reduction of exposure to smoke from

biomass fuel, particularly among women and
children, is a crucial goal to reduce the
prevalence of COPD worldwide.

01/09/09 106
Four Components of
COPD
Management

• Assess and monitor

disease

• Reduce risk factors

• Manage stable COPD

● Education
● Pharmacologic
● Non-pharmacologic

01/09/09
• Manage exacerbations 107
 Management of Stable COPD
Manage Stable COPD: Key
Points
 The overall approach to managing stable COPD
should be individualized to address symptoms and
improve quality of life.
 For patients with COPD, health education plays an
important role in smoking cessation (Evidence A) and
can also play a role in improving skills, ability to cope
with illness and health status.
 None of the existing medications for COPD have been
shown to modify the long-term decline in lung
function that is the hallmark of this disease (Evidence
A). Therefore, pharmacotherapy for COPD is used to
decrease symptoms and/or complications.
01/09/09 108
 Management of Stable COPD
Pharmacotherapy:
Bronchodilators
 Bronchodilator medications are central to the
symptomatic management of COPD (Evidence A).
They are given on an as-needed basis or on a
regular basis to prevent or reduce symptoms
and exacerbations.
 The principal bronchodilator treatments are ß2-
agonists, anticholinergics, and methylxanthines
used singly or in combination (Evidence A).
 Regular treatment with long-acting
bronchodilators is more effective and convenient
than treatment with short-acting bronchodilators
01/09/09 109
Management of Stable COPD
Pharmacotherapy:
Glucocorticosteroids
 The addition of regular treatment with
inhaled
glucocorticosteroids to bronchodilator
treatment is appropriate for symptomatic
COPD patients with an FEV1 < 50%
predicted (Stage III: Severe COPD and Stage
IV: Very Severe COPD) and repeated
exacerbations (Evidence A).

 An inhaled glucocorticosteroid combined

with a long-acting ß2-agonist is more
01/09/09 110
Management of Stable COPD
Pharmacotherapy:
Glucocorticosteroids
 The dose-response relationships and
long-term safety of inhaled
glucocorticosteroids in COPD are not
known.

 Chronic treatment with systemic

glucocorticosteroids should be avoided
because of an unfavorable benefit-to-
risk ratio (Evidence A).
01/09/09 111
Management of Stable COPD
Pharmacotherapy:
Vaccines
 In COPD patients influenza vaccines
can reduce serious illness (Evidence
A).

 Pneumococcal polysaccharide vaccine

is recommended for COPD patients 65
years and older and for COPD patients
younger than age 65 with an FEV1 <
40% predicted (Evidence B).
01/09/09 112
Management of Stable COPD
All Stages of Disease
Severity
 Avoidance of risk factors
- smoking cessation
- reduction of indoor pollution
- reduction of occupational exposure
 Influenza vaccination

01/09/09 113
 Therapy at Each Stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe

 FEV1/FVC < 70%

 FEV1 < 30%

 FEV1/FVC < 70%
predicted
 FEV1/FVC < 70%
or FEV1 < 50%
 FEV1/FVC < 70%  30% < FEV1 < 50%
predicted plus
 50% < FEV1 < 80% predicted
chronic respiratory
 FEV1 > 80% predicted failure
predicted
Active reduction of risk factor(s); influenza vaccination
Add short-acting bronchodilator (when needed)
Add regular treatment with one or more long-acting
bronchodilators (when needed); Add rehabilitation
Add inhaled glucocorticosteroids if
repeated exacerbations
Add long term
oxygen if chronic
respiratory failure.
Consider surgical
01/09/09 114
treatments
Management of Stable COPD
Other Pharmacologic
Treatments
 Antibiotics: Only used to treat
infectious exacerbations of COPD
 Antioxidant agents: No effect of n-
acetylcysteine on frequency of
exacerbations, except in patients not
treated with inhaled
glucocorticosteroids
 Mucolytic agents, Antitussives,
Vasodilators: Not recommended in
01/09/09 115
 Management of Stable COPD
Non-Pharmacologic
Treatments
 Rehabilitation: All COPD patients benefit
from exercise training programs,
improving with respect to both exercise
tolerance and symptoms of dyspnea and
fatigue (Evidence A).

 Oxygen Therapy: The long-term

administration of oxygen (> 15 hours per
day) to patients with chronic respiratory
failure has been shown to increase
01/09/09 116
Four Components of COPD
Management

1. Assess and monitor

disease

2. Reduce risk factors

3. Manage stable COPD

● Education
● Pharmacologic
Revised 2006
● Non-pharmacologic

01/09/09
• Manage exacerbations 117
Management COPD Exacerbations

Key Points
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.”
01/09/09 118
Management COPD Exacerbations

Key Points
The most common causes of an
exacerbation are infection of the
tracheobronchial tree and air pollution, but
the cause of about one-third of severe
exacerbations cannot be identified
(Evidence B).

Patients experiencing COPD exacerbations

with clinical signs of airway infection
(e.g., increased sputum purulence) may
benefit from antibiotic treatment (Evidence
01/09/09 119
B).
Manage COPD Exacerbations

Key Points

 Inhaled bronchodilators
(particularly inhaled ß2-agonists
with or without
anticholinergics) and oral
glucocortico- steroids are
effective treatments for
exacerbations of COPD (Evidence
01/09/09 120
 Management COPD Exacerbations

Key Points
 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
(Evidence A).
 Medications and education to help prevent
future exacerbations should be considered
as
01/09/09
part of follow-up, as exacerbations affect
121
Global Strategy for Diagnosis,
Management and Prevention of
COPD

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 ■ Practical 122
Translating COPD Guidelines into Primary
Care

KEY POINTS
 Better dissemination of COPD guidelines and
their effective implementation in a variety of
health care settings is urgently required.
 In many countries, primary care practitioners
treat the vast majority of patients with COPD
and may be actively involved in public health
campaigns and in bringing messages about
reducing exposure to risk factors to both
patients and the public.

01/09/09 123
Translating COPD Guidelines into Primary
Care

KEY POINTS
 Spirometric confirmation is a key
component of the diagnosis of COPD and
primary care practitioners should have
access to high quality spirometry.
 Older patients frequently have multiple
chronic health conditions. Comorbidities
can magnify the impact of COPD on a
patient’s health status, and can complicate
the management of COPD.

01/09/09 124
Global Strategy for Diagnosis,
Management and Prevention of
COPD
SUMMARY

■ Definition,
Classification
■ Burden of COPD
■ Risk Factors
■ Pathogenesis,
Pathology,
Pathophysiology
■ Management
01/09/09 125
■
Global Strategy for Diagnosis,
Management and Prevention of COPD:
Summary
 COPD is increasing in
prevalence in many countries
of the world.
 COPD is treatable and
preventable.
 The GOLD program offers a
strategy to identify patients
and to treat them according to
01/09/09 126
 Global Strategy for Diagnosis,
Management and Prevention of COPD:
Summary
 COPD can be prevented by avoidance
of risk factors, the most notable being
tobacco smoke.
 Patients with COPD have multiple
other conditions (comorbidities) that
must be taken into consideration.
 GOLD has developed a global network
to raise awareness of COPD and
disseminate information on diagnosis
01/09/09 127
 WORLD COPD DAY
November 14, 2007

Raising COPD Awareness

Worldwide
01/09/09 128
Global Initiative for Chronic
Obstructive Lung Disease
(GOLD)
 Conducted in collaboration with the US National
Heart Lung and Blood Institute (NHLBI) and WHO.
 Goal:
 To increase awareness of COPD and decrease morbidity
and mortality from the disease
 Aims :
 to improve prevention and management of COPD through
a concerted worldwide effort of people involved in all facets
of health care and health care policy, and
 to encourage a renewed research interest in this extremely
prevalent disease

01/09/09 129
GOLD Workshop Report: 4
Components of COPD
Management Plan
1) Assess and monitor disease
2) Reduce risk factors
3) Manage stable COPD
4) Manage exacerbations

01/09/09 130
Component 1: Assess and
Monitor Disease
 KEY POINTS:
 Diagnosis of COPD is based on history of
exposure to risk factors and the presence of
airflow limitation that is not fully reversible, w/
or without the presence of symptoms
 Patients who have chronic cough and sputum
production with a history of exposure to risk
factors should be tested for airflow limitation,
even if they do not have dyspnea
01/09/09 131
 For the diagnosis and assessment of COPD,
Spirometry is the gold standard, as it is the
most reproducible, standardized, and
objective way of measuring airflow limitation.
 Health care workers involved in the diagnosis
and management of COPD patients should
have access to spirometry
 Measurement of arterial blood gas tensions
should be considered in all patients with
FEV<40% predicted or clinical signs
suggestive of respiratory failure or right heart
failure

01/09/09 132
Component 2: Reduce Risk
Factors
 KEY POINTS:

 Reduction of total personal exposure to

tobacco smoke, occupational dusts and
chemicals and indoor and outdoor air
pollutants are important goals to prevent the
onset and progression of COPD
 Smoking cessation is the single most
effective- and cost effective – way in most
people to reduce the risk of developing
COPD and stop its regression
01/09/09 133
 Brief tobacco dependence counseling is
effective and every tobacco user should be
offered at least this treatment at every visit to a
health care provider
 Several effective pharmacotherapies for tobacco

dependence are available and at least one of

these medications should be added to
counseling if necessary and in the absence of
contraindications
 Progression of many occupationally induced

respiratory disorders can be reduced or

controlled through a variety of strategies aimed
at reducing the burden of inhaled particles and
gases
01/09/09 134
Component 3: Manage Stable
COPD
 KEY POINTS:
 The overall approach to managing stable
COPD should be characterized by a stepwise
increase in treatment, depending on the
severity of the disease
 Health education can play a role in improving
skills, ability to cope with illness, and health
status

01/09/09 135
 Pharmacotherapy for COPD is used to decrease
symptoms and/or complications
 Bronchodilator medications are central to the
symptomatic management of COPD, which are
given on as-needed basis or on a regular basis to
prevent or reduce symptoms
 Regular treatment with long-acting bronchodilators
is more effective and convenient than treatment with
short-acting bronchodilators, but more expensive
 Addition of regular treatment with inhaled
glucocortisteroids to bronchodilator treatment is
appropriate for symptomatic COPD patients - stage
III and IV- and repeated exacerbations

01/09/09 136
Component 4: Manage
Exacerbations
 KEY POINTS:
 Most common causes of an exacerbation are
infection of the tracheobronchial tree and air
pollution, but 1/3 of the cause of severe
exacerbations cannot be identified
 Inhaled bronchodilators are effective
treatment for exacerbation of COPD

01/09/09 137
 Those with clinical symptoms of infections
benefit from antibiotic treatment
 Non-invasive intermittent positive pressure
ventilation (NIPPV) in exacerbations
improves the blood gases and pH, reduces
hospital mortality decreases the need for
invasive mechanical ventilation and
intubation and decreased the length of
hospital stay

01/09/09 138
 Symptomatic therapy-
 A) Short acting bronchodilators
 B) Long acting inhaled anticholinergic agents
( tiotropium)
 C) Salmeterol – long acting B 2 agonist, formoterol
 Moderate- Severe COPD- FEV1 < 50% predicted
with two exacerbation per year.
 Inhaled corticosteroids
 Combined B 2 agonist and inhaled corticosteroids
 Theophyllines, mucolytics may still have a role

01/09/09 139
 Pulmonary Rehabilitation – 7-8 weeks
improve exercise capacity and quality of life.
 Oxygen therapy –appropriate for patients
who are hypoxemic at rest ( PaO2 less than
or equal to 5.5 mm Hg or 56 to 59 mm Hg
with evidence of end organ effects of the
hypoxemia )
 Treatment of exacerbation

01/09/09 140
01/09/09 141