JMFV D2017

Chronic Obstructive Pulmonary Disease

Dr. I Lanzona, 2016 Pulmo Workbook • Clinical Definition (old)
2016 Global Strategy for the Diagnosis, Management, & Prevention of COPD o Chronic Bronchitis
o Presence of chronic productive cough in
Generalities
most days of the week for 3 months of a year
2 common obstructive diseases: COPD & Asthma
for more than 2 consecutive years in the
absence of other specific causes (asthma,
Statistics
bronchiectasis, cystic fibrosis)
• Worldwide mortality
• Anatomic Definition (old)
o 1990: 6th leading cause of mortality
o Emphysema – dysfunctional elastic fibers
o 2001: 5th leading cause of mortality
o An abnormal permanent enlargement &
o 2020: Will become the 3rd leading cause of
destruction of the (alveoli) gas-exchanging
mortality worldwide
surfaces of the lung distal to the terminal
§ Due to increased incidence in
bronchioles without obvious fibrosis
smoking especially in young females
o Pathogenesis
(relative to previous years)
§ Mucous secretion and accumulation
• Dyspnea – most common problem & is associated
§ Thickening of alveolar walls
with the Burden of COPD:
§ Inflammation damages surrounding
o More frequent hospital visits/admissions
alveoli
o Loss of productivity – more absences from
§ Alveoli are prone to collapse because
work
they have no cartilage
o Disability
§ Added stress from inflammation
o Decline in Quality of Life
causes collapse of alveoli
• Disability Adjusted Life Years (DALYs)
§ End results:
o Indicates loss of productive years in terms of
days absent from work due to COPD • Air trapping
o 7th cause in high income countries • Increase in residual
o 10th in low income countries volume
o 2% worldwide • Lung hyperinflation
Chronic Emphysema
BOLD Study Bronchitis
• Burden of Obstructive Lung Disease Initiative Clinical Definition Anatomic Definition
• A population-based study which aimed to determine “Blue bloaters” “Pink puffers”
the
o Prevalence of COPD
o International variation in the prevalence of
COPD
• Methods
o 12 sites; n=9,425 patients
o Spirometry was used to measure lung
function pre & post bronchodilator
administration *Standard diagnosis of COPD Sputum Copious Scant
is via Spirometry Patients are Patients are
o Questionnaires were used to assess usually holding a malnourished from
§ Health status cup/tissue for increased work of
§ Risk factors (Biomass fuel, smoking) sputum breathing à
• Results dyspnea
o LR. ORs associated with Infections Frequent Less frequent
§ 10-pack year increments PaCO2 Hypercapnea: Normal
§ 10-year age increments N= 35-40 50-60mmHg
o Relatively high prevalence/burden of COPD PaO2 êê45-60 ê65-75
in Metro Manila (Ranked 2nd among the 12 N = 80-100 Hypoxemic = blue Less hypoxemic
sites in male patients, 10th in females) due to high drive to
o Most patients in the study already have inhale & lesser
GOLD stage 2 to 3 severity sputum
• Conclusion Hct é =50-55 N = 35-45
o COPD is under diagnosed mainly due to the Compensation for Male: 36-44
underuse of spirometry as a diagnostic tool hypoxemia Female: 41-50
PH Pulmonary Mild pulmonary
Definitions of COPD Hypertension from hypertension
• 1995 Definition (old) hypoxemia
o Maximum respiratory flow reduction Cor pulmonale Common Rare
o Airway limitation is slowly progressive & Alveolar Normal êdue to destruction
irreversible (Asthma = reversible), this is elastic of elastic fibers à
probably the reason for the high burden of recoil airway narrowing
COPD DLCO Normal Decreased
• Pathophysiologic Definition *majority of COPD = Mixed!
o Chronic Obstructive Pulmonary Disease
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GOLD Definition
• Global Initiative For Obstructive Lung Disease
provides a global definition of COPD
• Latest guideline, this is what we follow
• A common, preventable and treatable disease
characterized by
o Progressive airflow limitation that is not fully
reversible
§ Bronchodilators will not fully reverse
airflow limitation.
§ In COPD <12% lang, sa asthma
>12% reversibility
o Enhanced chronic inflammatory response in
the airways & the lung to noxious particles or
gases
§ Cigarette smoking – most common
• Extrapulmonary effects – due spillage of
inflammatory reaction from the lungs to other organs
o Muscle wasting
o Osteoporosis
o CAD
• Exacerbations and comorbidities contribute to the
overall severity in individual patients
• Multicomponent disease: Systemic component à
Inflammation à Mucociliary dysfunction à
Structural changes àairflow limitation
Risk Factors
• Susceptibility genes
o Hereditary deficiency of Alpha-1 Anti-Trypsin
– presents as COPD in children
o Matrix Metalloproteinase 12 (MMP12) gene
mutation – related to decline in lung function
• Cumulative exposure to noxious inhaled
particles/gases – key risk factor for COPD
o Smoking – best studied COPD risk factor
o Indoor air pollution – from cooking/heating
with biomass in poorly-ventilated dwellings
o Outdoor air pollution
o Organic & inorganic occupational dusts
• Poor lung growth & development
o Any factor that affects lung growth during
gestation and childhood has the potential for
increasing an individual’s risk of developing
COPD
o “Childhood disadvantage factors”
§ There is a positive association
between birth weight and FEV1 in
adulthood
§ Lung infections
• Oxidative stress
• Female gender – more susceptible to the effects of
smoking
• Age – reflects the sum of cumulative exposures
throughout life
• Respiratory infections
• Low socioeconomic status
• Poor nutrition
• Comorbidities
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JMFV D2017
COPD Risk & Smoking Cessation
Fletcher Curve (1977)
• Axes
o y = FEV1 (% value at age 25)
o x = Age in years
• Non-smokers (Green area)
o After age 40, there is a physiologic 10%
decline in FEV1
o Non-smokers exemplify the normal aging
process
• Smokers (Red line)
o We see a rapid decline in FEV1
o At age ~60, he begins to have symptoms of
COPD due to a very low FEV1
o Before 75, patient dies = no more FEV1
o Smoking = Rapid decline in FEV1
• Quit smoking at 45 (dotted line)
o The decline in FEV1 simulates the
incremental decline of non-smokers
o Lesser decline vs current smokers
o At any point in time you stop smoking, you
protect your FEV1
• Quit smoking at 65 (dotted line)
o There still a protective effect to those who
quit smoking even at age 65
• Fletcher curve shows us that one of the best
treatment for COPD is not/to quit smoking
o Lost FEV1 can not be recovered
o We want to decrease the amount of decline
by advocating “NO/QUIT SMOKING”
COPD vs Asthma
• The inflammation in COPD is different from the
inflammation seen in Asthma
Asthma
• A chronic inflammatory disorder of the airways in
which many cells and cellular elements play a role.
• Chronic inflammation is associated with airway
hyper-responsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest
tightness and coughing, particularly at night or in
early morning.
Why is asthma particularly bad at night?
o Hypothesis: dominance of vagal
(parasympathetic) tone =
bronchoconstriction
• These episodes are usually associated with
widespread but variable airway obstruction within
the lung that is reversible with treatment.
• Clinical Diagnosis
o Episodic breathlessness, wheezing, cough,
chest tightness
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JMFV D2017

Precipitation by allergens or non-specific

o COPD
irritants e.g. smoke, fumes, strong smells, • Chronic bronchitis
exercise o Changes due to airway inflammation
o Nocturnal worsening of symptoms o Goblet cell hyperplasia, mucosal thickening
o Positive family history of asthma and atopic → chronic cough & mucous production
disease o REID Index – measures the normal airway
o Response to appropriate asthma therapy diameter over thickened airways
(reversible) • Emphysema
• Confirmatory Diagnosis o Changes due to destruction of parenchymal
o Via Spirometry structures
§ Reproducible but effort-dependent o Damage to elastic fibers à Airway distention
§ Pre and post tests lack sensitivity o There will be premature collapse of the
especially those on treatment, so alveolar wall à expiratory collapse à
repeated testing at different visits is premature closure of the airways
advised • COPD = Combine changes in both!
§ Proper instructions on maneuver o Dynamic airway narrowing & inflammation,
must be given decrease elastic recoil à airways lose their
o Degree of reversibility of FEV1 decline shape & become clogged with mucous à
should be ≥ 12% and ≥ 200 mL from pre- premature closure à air can not get out of
bronchodilator value the lungs à leading to
§ Failure to meet criteria may point to a § Airway trapping & hyperinflation
diagnosis of COPD § Increase in residual volume
o All these changes will lead to decrease the
COPD Asthma inspiratory capacity of the lungs (FRC) à
Onset Midlife, Early in life, dyspnea on minimal activity/rest
Childhood – often childhood
A1AT Typical Picture of COPD in practice
deficiency • Increase in AP Diameter of the lungs – due to
Trigger Noxious agent Sensitizing hyperinflation
agent • Muscle wasting/malnourished – due to increased
Inflammatory cells Neutrophils Eosinophils work of breathing
CD8+ T cells CD4+ T cells • Tripod position – maximizes use of diaphragm &
Macrophages Mast cells other muscles of respiration
Airflow limitation Not fully Reversible • Supraclavicular retractions
reversible (>12%) • Pursed lips – exerts a positive pressure on the
Ex-/Smoker Nearly all, long Possible airways
smoking history • Hoover’s Sign – inward displacement of the lower
Chronic productive Common Rare ribs during inspiration due to the action of the
cough diaphragm during inspiration
Variable –
night/early Signs & Symptoms
Symptoms Persistent & morning • Chronic productive cough
progressive (cholinergic • Dyspnea (clubbing is NOT seen in COPD)
release that • Wheezing
time) • Adaptive behavior
Nocturnal Uncommon Common • Chest pain, ankle swelling, anorexia, weight loss
awakening with due to muscle wasting, psychological distress &
breathlessness psychiatric morbidity
and/or wheezing • Normal PE or in Respiratory distress
Atopic S/S and Uncommon Common o Tachypnea, cyanosis, use of accessory
seasonal allergies muscles of respiration, pursed lip breathing,
barrel chest deformity, Hoover’s sign,
Diurnal variation Uncommon Common
• Percussion (hyperesonant) & palpation not very
Favorable response Inconsistent Consistent
useful
to inhaled
• Diminished breath sounds with adventitious sounds
glucocorticosteroids
CXR
Histopathologic Features of COPD

Normal Lung
• Has normal elastic recoil
o Maintains integrity of alveoli
o Inhale/exhale – airways are still open
• No hyperplasia, no mucosal thickening Normal Airway trapping
• Low set diaphragm
• Hyperinflation from air way trapping & decreased
lung elastic recoil – can be seen on CXR
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JMFV D2017

Disease Progression in COPD Treatment

GOLD Goals for COPD Treatment

• Main mechanisms that cause the symptoms of
COPD: Expiratory airflow limitation, air trapping &
hyperinflation à eventually leading to decline in
QoL à Disability, progression & death
Recognizing COPD
• Disease prevention is the ultimate goal of COPD
treatment
• Once COPD has been diagnosed, effective
management should be aimed at the following goals
o Relieve symptoms – dyspnea! Give
bronchodilators
o Prevent disease progression – stop smoking
o Improve exercise tolerance – pulmonary
rehabilitation programs
o Improve health status
o Prevent & treat complications
o Prevent & treat exacerbations
o Reduce mortality
Management Strategy
Assess degree of airflow limitation
• GOLD 2011 Stages
• Stages of COPD based on Spirometry

Diagnosis Stage of COPD Criteria

Clinical diagnosis of COPD should be considered in a 1. Mild FEV1/FVC < 0.70
patient with FEV1 ≥ 80% predicted
• Symptoms 2. Moderate FEV1/FVC < 0.70
o Cough 50% ≤ FEV1 < 80% predicted
o Sputum 3. Severe FEV1/FVC < 0.70
o Dyspnea 30% ≤ FEV1 < 50% predicted
• History of exposure to Risk Factors 4. Very severe FEV1/FVC < 0.70
o Tobacco FEV1 < 30% predicted or
o Occupational hazards FEV1 < 50% predicted plus
o Indoor & outdoor pollution Chronic respiratory failure
Then confirm your impression with
• Spirometry
o Standard confirmatory diagnostic tool & also
Assess symptoms
is used for classification of disease severity
• 2 scales
o Should be done after administration of short
o Modified British Medical Research Council
acting inhaled bronchodilator (400mcg
(mMRC) Breathlessness Scale
Salbutamol) to minimize variability
o COPD Assessment Test (CAT)
o Confirmation: post-bronchodilator FEV1/FVC
< 0.70 – means airflow limitation is not fully
mMRC Questionnaire
reversible
• Used to assess severity of breathlessness
o When possible, values should be compared
• Relates well to other measures of health status &
to age-related normal values to avoid
predicts future mortality risk
overdiagnosis of COPD in the elderly
Grade Description
o Any smoker with dyspnea à COPD!
0 Not troubled by breathlessness except in
• Why do we need Spirometry?
strenuous exercise
o Screen individuals at risk for pulmonary
1 Shortness of breath when hurrying up or
disease
walking up a slight hill
o Confirmation of COPD diagnosis
o Assess severity of pulmonary dysfunction 2 Walks slower than contemporaries on ground
o Guide to treatment selection level because of breathlessness, or has stop
o Assess effects of therapeutic intervention for breath when walking at own pace

3 Stops or breath after walking about 100m or

after a few minutes on level ground
4 Too breathless to leave the house, or
breathless when dressing or undressing

• Score > 2 = High symptom – patient is problematic!

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JMFV D2017

COPD Assessment Test Assess risk of Exacerbations

• Simple, validated 8-item patient-completed • Exacerbations
questionnaire developed to provide a reliable o GOLD Definition
measure of health status for COPD patients § An event in the natural course of the
• CAT enables patients to describe their symptoms disease characterized by a change in
more accurately to you the patient’s baseline dyspnea,
• CAT can be used to guide management decisions to cough, and/or sputum that is beyond
improve patient’s QoL normal day to day variations
§ Acute in onset
§ May warrant a change in regular
medication
o May be mild, moderate, or severe in nature.
More severe exacerbations can require
hospitalization and are associated with a
prolonged recovery period
o Commonly caused by bacterial/viral
infections of the lungs and airways.
o Associated with increasing markers of
inflammation
o Distressing for patients & loved ones
o Leads to
§ Accelerated lung function decline
§ Increased mortality
§ Increased economic costs
§ Impact on symptom & lung function
§ Negative impact on QoL
• BODE Index
o Body Mass Index, Obstruction, Dyspnea and
Exercise Capacity
o Useful for stratifying prognosis of patients for
risk of exacerbations, hospital admissions,
and mortality
o MMRC: Modified Medical Research Council
o Scores ranges from 0 to 10 and higher
• Scoring range of 0-40 scores correlate with a higher risk of death
o Higher the score = more impaired the patient • DOSE Index
is o Dyspnea (using MMRC score), Obstruction
o 5 – upper limit of normal in healthy non- (FEV1 % predicted), Smoking status,
smokers Exacerbation frequency
o >10 – poor QoL or troublesome symptoms o Score ranges from 0 to 8
o >15 – increased risk of death within 1y o ≥ 4 is associated with greater risk of hospital
o >25 – increased risk of re-admission to admission, respiratory failure, and future risk
hospital of exacerbation
• CAT scores of 10-20 identify patients mildly affected o Helps clinician to prioritize for intervention
by COPD:
o COPD is one of the person’s most important
problems HIGH RISK OF EXACERBATION
o Have only a few good days a week FEV1 <50%
o Have1-2 exacerbations a year > 2 exacerbations in the last year
o Wake up with breathlessness most days
o Walk up 1 flight of stairs only slowly
• EU study: in GOLD Stage I patients mean CAT
score was 16
• CAT score of >10 = HIGH SYMPTOMS! Assess Comorbidities
• Cardiovascular diseases
• Osteoporosis
HIGH COPD SYPMTOMS • Depression and anxiety
mMRC > 2 • Skeletal muscle dysfunction
• Metabolic syndrome
CAT > 10

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JMFV D2017

GOLD Combined Assessment Stategy Once classified, these are the treatment
• Uses the following recommendations
o GOLD Classification of airflow limitation
o mMRC Pharmacologic Management of COPD
o CAT Pharmacologic treatment is mainly for:
o Risk of Exacerbation 1. Symptom control
• Groups patients into 2. Improvement in quality of life
o A – Low risk. Less symptoms 3. Functional capacity
o B – Low risk. More symptoms 4. Decreasing exacerbation rates and severity
o C – High risk. Less symptoms
o D – High risk. More symptoms
• Important as per group has different treatment
strategy recommendations

*A à D = Less drugs à more drugs

How to use
• First assess symptoms with the CAT scale (or
dyspnea with the mMRC)
• Next assess the risk of exacerbations to determine if
the patient is low risk (lower boxes) or high risk
(upper boxes). This can be done by 1 of 3 methods
o Use spirometry to determine GOLD stage
§ GOLD 1 & 2 = Low risk
§ GOLD 3 & 4 High risk
o Assess the number of exacerbations the
patient has had within the previous 12
months (0 or 1 indicates Low Risk, while 2 or
more exacerbations High Risk)
o Determine whether the patient has had one
or more hospitalization in the year for a
COPD exacerbation
*There are no pharmacologic agents that have been
shown to retard the rate of lung function decline in
COPD
Actions of different Bronchodilators
• Beta 2 agonists
o Stimulate B2 receptors thus relaxing airway
smooth muscle
o Side effect: tremors
• Anticholinergics
o Block the effect of acetylcholine on M3
receptors thus relaxing airway smooth
muscle
o 1st choice in C & D
• Inhaled Corticosteroids
o Given starting class C – high risk of
exacerbation
o Not given in A & B = low risk of exacerbation
o In asthma, immediately give ICS, in COPD
wag ibibigay kagad, you need to make sure
that your patient is C or D
o Studies: ICS decreases the rate of
exacerbation
• PDE4 Antagonists
o Methylxanthines
o Antagonize bronchoconstriction by inhibiting
phosphodiesterase in smooth muscle
o PDE4 is pro-inflammatory so antagonize it!
o New in the market, can be used in class D

• In some patients, these three ways of assessing risk
of exacerbations will not lead to the same level of
risk; in this case, the risk should be determined by
the method indicating High Risk.
o Ex: Gold 1 but 3 exacerbations, patient is
High risk!
Antibiotics
• Given to those who have 3 cardinal symptoms –
increase in dyspnea, sputum volume, and sputum
purulence
• Have 2/3 of the cardinal symptoms if increased
purulence of sputum is one of the two symptoms
• Those who require mechanical ventilation

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JMFV D2017

Non-Pharmacologic Management of COPD

• Influenza Vaccination
o Reduces the risk of exacerbations in COPD
patients
o There is mild increase in transient local
adverse effects with vaccination, but no
evidence of increase in early exacerbations
• Pneumococcal Vaccination
o Protective in that it decreases the incidence
of infections à less exacerbations
• Smoking cessation
o Even a 3-min period of counseling to urge a
smoker to quit results in cessation rates of 5-
10%
§ Ask – identify all smokers at every
visit
§ Advise – strongly urge cessation
§ Assess – determine willingness to
quit
§ Assist – aid in quitting
§ Arrange – schedule follow-up
o Recall the Fletcher Curve for the benefits of
smoking cessation
o Single most effective & most cost-effective
intervention to reduce the risk of COPD and
stop its progression
• Pulmonary Rehabilitation
o All COPD patients benefit form PR,
maintenance of physical activity, improving
exercise tolerance & experiencing decreased
dyspnea & fatigue
• Long-term Oxygen therapy
o The only modality proven to improve survival
o Long-term administration of oxygen (>15
hours per day) to patients with chronic
respiratory failure has been shown to
increase survival in patients with severe
resting hypoxemia.
§ PaO2 below 55 mmHg or SaO2
below 88% with or without
hypercapnia confirmed twice over a
three week period
§ PaO2 between 55 mmHg and 60
mmHg or SaO2 of 88% if there is
evidence of pulmonary hypertension,
peripheral edema suggesting
congestive cardiac failure or
polycythemia (hematocrit > 55%)
o Not indicated in all patients
§ Subject to improper patient use
§ Not to be used in current smokers
§ Expert personnel required
§ Portable O2 needed for mobile
patients
o Supplemental oxygen should be titrated to
improve the patient’s hypoxemia with a
target saturation of 88-92%
• Ventilatory support

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