GOLD 2020 Loss of small airways + mucociliary dysfunction
—feature of the disease
2011- ABCD Assessment Tool-- Multimodality
assessment, symptom burden and importance
of exacerbation in the prevention of
management of COPD, pharmacotherapy
implications
Does not predict mortality and other important
health outcomes (can be done w spirometric
grading)
2017- separate it from spirometric grade
FEV1- cannot influence therapeutic decision
making, needs symptoms and exacerbation risk
Spirometry- diagnosis, prognosis, treatment
with non pharmacologic strategy
No more ACO, but different disorder sharing the
some common traits and clinical features
2019- Different treatment pre and post (follow
up)
Blood eosinophil as a marker of efficacy of
inhaled corticosteroids
Clarify diagnosis of exacerbations with different
alternative diagnosis
First program 1998
First report- 2001
FEV1- unreliable for breathlessness, exercise
limitation, health status impairment
COPD- 4th leading cause of death, 3rd by 2020
3 million died 2012- 6% death globally
Preventable and treatable
Major cause of chronic M and M
Die prematurely
COPD- persistent symptoms and airflow
abnormalities, airway or alveolar abnormalities,
exposure to noxious gas and particles
+ host factors
+lung pathology with no airflow limitation
Comorbidities may impact M and M
Symptoms may be underreported by patients
Airflow limitation= airway + lung parenchyma
abnormalities- evolution at different rates
Chronic inflammation- structural changes,
narrow airway, destroy lung parenchyma,
alveolar detachment, decreased elastic recoil
Decreased airway openness during expiration
Airflow limitation- measured by spirometry
Chronic bronchitis- old age + gas exposure
Symptoms precede airflow limitation
OR with normal spirometry findings (+airway
abnormalities)
Burden of COPD
Leading cause of M and M
Will continue to increase due to longevity and
exposure to risk factors
Exposure + host factors
Prevalence- vary
<6%- under reported
Increase with age
PLATINO- 7.8% to 19%, >60 y/o post
bronchodilator
BOLD- use spiro + risk factors (questionnaires),
>40 y/o- worse lung fxn
2010- 384 million
3 million deaths annually
2060- 5.6 million deaths 
M and M
Inc with age- younger age if with comorbities
OR with chronic conditions
Impair health status, interfere management
Death is underestimated, reliability is
problematic
Inc mortality- inc smoking, inc aging of the
population, decrease death from others, lack of
effective disease modifying agents
Economic and social burden
Inc economic burden- 6% of total annual
healthcare benefits
Greatest proportion is exacerbations
Inc cost with increase severity
Home based care underestimates true cost
Threat to economy by influencing human
productivity
Social burden- use of DALY- 2015- 5 th cause
US- 2nd cause of DALY
Mortality- limited perspective on burden
Factors influencing disease development and
progression
Associations rather than relationships
Non smokers with COPD- less symptoms, mild,
lower burden
Non smoker + chronic airflow limitation- less CA
and CVS comorbidities > (-) chronic airflow
limitation—but with inc pneumonia and mort
from respiratory failure
Current understanding of risk factors is
incomplete
No studies have monitored its entire course
Interactions between genes and environment
Sex, economic status, exposures, life
expectancy
Genetics
Deficiency in A1 antitrypsin
Inc serine protease- mucus secretagogue
Problem with genes encoding MMP 12 and
glutathione S transferase- related to decline in
lung function
Age and Sex
Healthy aging and cumulative exposure
Aging mimics structural changes in lungs
associated with COPD
Men = women (patterns of smoking)
Women more susceptible to smoke than men
More disease with same amount of smoke
consumed
Greater burden of small airway disease in
women
Lung growth and development
Processes affecting lung growth
Dec lung fxn via spirometry leads to COPD
Presence of childhood disadvantage factors
(infection)= important as heavy smoking
50% FEV1 problem
50% abnormal lung fxn and growth
Synergistic interaction between smoking,
respiratory infant infection + overcrowding by
age 43 y/o
Exposure to particles
Smokers have higher symptoms, greater
abnormalities, greater decline in FEV1, and
greater mortality
Other factors: cigars, marijuana, passive
cigarette exposure, ETS (inc lung burden of
inhaled gases and particles)
Affects fetus growth and immunity
Occupational exposure like organic or inorganic
dust, chemicals and fumes
Different occupations- gardeners, sculptors,
warehouse workers (more of emphysema and
gas trapping (CT scan) + symptoms + airflow
limitation) + dust M=F
19.2 %, 31% in non smokers
Accounted for 10-20% of COPD
Higher in less regulated areas
Indoor air pollution- affects women- 3M
worldwide
Urban air pollution- affects person with heart
and lung problems
Role of outdoor air is small compare to smoking
Association with PM 2.5/10
Impair lung growth in children- PM <2.5 and inc
NO2 (FEV1 <80%)
Exposure effects still unresolved
Socioeconomic status- poverty = COPD risk inc
Not sure if related to exposure also
Asthma and airway hyperreactivity
+ asthma- 12x risk
20% irreversible airflow obstruction
Self reported asthma- excess FEV1 loss
11% lung growth decline
1st risk factor- smoking- 39% attributable risk
2nd risk factor- airway hyperresponsiveness-
15%, independent of asthma- inc COPD and
mortality
Different pathology bet asthma and non asthma
COPD
Chronic bronchitis- + associated with decline in
FEV1 and in mucus hypersecretion
Inc COPD in young adults who smoke
Inc total # of exacerbations severity
Infection
Dec lung fxn, inc symptoms
Pseudomonas- inc mortality and
hospitalizations for exacerbations
Infections- effect on disease development is less
clear
HIV inc risk
TB- risk and potential comorbidity and
differential diagnosis
Pathology, pathogenesis and pathobiology
Lung inflammation- modified response in COPD
(emphysema and airway fibrosis), gas trapping
and airflow limitation
Pathology- inc inflammation and structural
changes, inc with disease severity and persist
even with smoking cessation
Affects airways, parenchyma and lung
vasculature
Inc inflammatory cells
Pathogenesis
Modified inflammatory response not yet
understood or genetically determined
Pertubations in lung microbiome
1. Oxidative stress- inc biomarkers- H2O2,
8 isoprostane, inc exacerbations, dec
Nrf2- anti oxidants
2. Protease and antiprotease imbalance-
inc protease (breakdown connective tx
compartment)- destroy elastin- features
of emphysema
3. Inflammatory cells- release mediators,
IgA deficiency associated with bacterial
translocation, small airway
inflammation and airway remodeling
(neutrophils, macrophages and
lymphocytes)
4. Inflammatory mediators- chemotactic
factors, mediators and cytokines
5. Peribronchiolar and interstitial fibrosis-
asymptomatic smokers and growth
factors, inflammation first, airway
limitation and obliteration—
emphysema
Pathophysiology
Inflammation and airway narrowing- dec
FEV1
Emphysema and airway narrowing- airway
limitation and dec gas transfer
1. Airway limitation and gas trapping-
inflammation, fibrosis and exudates-
spirometric abnormalities, peripheral
airways trapped gas causing
hyperinflation—impair contractile
properties of respiratory muscles—
exertional dyspnea, tx: bronchodilators
2. Gas exchange abnormalities-
hypoxemia and hypercapnia, dec
ventilator drive, inc dead space
ventilation—CO2 retention—
hyperinflation—inc effort to breath—
ventilatory muscle impairment—V/Q
mismatch
3. Mucus hypersecretion—chronic
bronchitis not airflow limitation—inc
goblet cells and enlarged glands
(chronic irritation from noxious agents)
eGFR, mediators and proteases also
stimulate mucus hypersecretion
4. PHTN- late in the course, due to hypoxic
vasoconstriction, intimal hyperplasia
and smooth muscle hyperplasia and
hypertrophy, loss of pulmonary
capillary bed in emphysema,
inflammation and endothelial
dysfunction—inc exacerbations and R
heart dysfunction
5. Exacerbations- from infection, noxious
chemicals, unknown factors
Inc inflammation, gas trapping, reduced
expiratory flow, V/Q mismatch—
hypoxemia
6. Systemic features- +chronic diseases
Affects cardiac and gas exchange fxn—
hyperinflation
Inflammation- skeletal muscle wasting
and cachexia, worsen comorbidities
Diagnosis and Initial Assessment
Spirometry- post bronchodilator FEV1/FVC
<0.70
Goal- determine airflow limitation, impact of
disease on health status, future risk of events-
to guide therapy
Treat concomitant chronic diseases
Dyspnea, cough, sputum production, hx of
infection, exposure to risk factors
If you consider COPD- perform spirometry- age
>40 y/o
Indicators are not diagnostic but they inc the
probability
Symptoms- most common characteristic
symptom- chronic progressive dyspnea
30%- cough and sputum production
Vary day to day
Precedes airflow limitation x years
Help develop appropriate interventions
Search underlying cause- if w COPD risk factors
+/- airflow limitation, +/- dyspnea
Seek help- impact of symptoms on functional
status, rather than basis of airflow limitation
Dyspnea- cardinal symptom- disability and
anxiety, effort to breath, chest heaviness, air
hunger, chest tightness
Cough- first symptom
Expected consequences acc to patient from
smoking etc
Initially intermittent—then daily
Can be productive/ non productive
+airflow limitation even without cough
Sputum production
Small quantities of tenacious sputum
Difficult to evaluate bec px swallow it rather
than expectorate
Intermittent
Can have flare up and remissions
Large quantities- bronchiectasis
Purulent- inc inflammatory markers, bacterial
infection- weak association
Wheezing and chest tightness
Vary, laryngeal
Widespread intrathoracic and extrathoracic
wheeze
Chest tightness follows exertion- poorly
localized, muscular, isometric contraction of
intercoastal muscles
Fatigue, weight loss and anorexia
Prognostic importance
Sign of other disease
Cough syncope, rib fractures- asymptomatic
Ankle swelling- cor pulmonale
Depression and anxiety- inc exacerbations and
poor health status
Medical History- exposure to risk factor, PMHx,
FHx, pattern of symptom development (adult
life, conscious of breathlessness, social
restrictions), hx of exacerbations and
hospitalizations, impact of disease, social family
support, reducing risk factors
Physical Examination
Rarely diagnostic
Low sensi and specificity
Spirometry
Most reproducible and most objective
measurement of airflow limitation
Non invasive and readily available
PEFR- not specific
FEV1/VC rather than FEV1/FVC- lower ratio
values
Decrease in both FEV1 and FVC
Using fixed ratio- greater dx in elderly, less dx if
<45 y/o and mild disease > cut off using lower
limit lower 5%
Not inferior regarding prognosis
GOLD favors fixed ratio over LLN even if it
causes over diagnosis and mistreatment due to
diagnostic simplicity and consistency
Should repeat if value is between 0.6 to 0.8
Post broncho dilator is required for diagnosis
and assessment, but reversibility on therapeutic
decision is no longer recommended
Cannot augment diagnosis, differentiate from
asthma, and predict response to treatment

Role of screening spirometry is controversial
Screen only those who are high risk
Method of early case finding
FEV1/FVC predict all cause mortality
A subgroup of patient also increases lung cancer
Cost effective based on risk based score
Not effective in directing management decisions
or improving outcomes (presymptomatic)
Do not screen, but rather do active case finding
Values in asia and Africa are lower than Europe
and US
Based on appropriate reference values
Severity score are always overestimated unless
predicted value are used
Assessment
1. Determine airflow limitation
2. Impact on patients health
3. Risk of future exacerbations
4. Guide therapy
Consider the ff aspects of the disease
1. Severity of spirometric abnormality
(table) FEV1 severity
2. Current nature and magnitude of
symptoms—mMrc
a. Measure breathlessness
b. Measure health status
c. Predict future mortality risk
CAT test and CCQ- less complicated
than others
Symptomatic impact- do not categorize
patients
CAT- 8 item 0-40 score
SGRQ >/=25- +COPD (consider
treatment) CAT cut off point is 10
mMrc >/=2- separate less
breathlessness from more
breathlessness
3. Hx of exacerbations/ risk- mild
moderate and severe (ARF)
Best predictor- earlier treated patients
FEV1- lack precision as predictor of
exacerbation and mortality in patients
with COPD
Hospitalization- poor prognosis and inc
risk of death
Spirometric relationship between death
and exacerbation
4. Presence of comorbidities
Multifactorial
Inc risk of the diseases
Combined COPD Assessment
2011 ABCD Assessment Tool
Incorporate px outcomes, highlight importance
of exacerbations prevention
NOT for mortality prediction or other important
health outcomes
Separate from spirometric grade
Symptoms + exacerbations
FEV1- for mortality outcomes and
hospitalizations, and consideration of non
pharmacologic therapies (LT LVRS), cannot
determine all therapeutic options 
Clinical parameters are more clear
Do spiro first—assess airflow limitation—assess
symptom and exacerbation
Group B- do surgery
Group D- treat exacerbations
*discordance between symptoms and
spirometric findings—do CT scan, check co
morbidities that may impact symptoms
Symptoms may be underestimated
May do exercise test 
Spirometry- for prognosis and identify rapid
decline
What to screen?
AATD- panlobular basal empysema <45 y/o
<20% normal- homozygous deficiency
Older- centrilobular apical
Additional investigations:
1. Imaging- CXR- not diagnostic and useful,
for other diagnosis only
Hyperinflation, hyperlucency, tapering
of vascular markings
CT scan- bronchiectasis and lung cancer
assessment
Inc emphysema- inc lung CA
 Evaluated for surgery and lung
transplantation- distribution of
emphysema
2. LV and diffusing capacity
Inc residual volume and total lung
capacity
Not essential for management
DLCO- impact of emphysema, helpful in
patients with breathlessness out of
proportion to spirometry
3. Spo2 and ABG
For clinical signs of respiratory failure
and right heart failure
Spo2 <92%, do ABG
4. Exercise testing and physical activity
Fall in a year before death
Indicator of health status impairment
Predictor of prognosis
Assess disability and risk of mortality
5. Composite scores
Inc mort- exercise, FEV1, weight loss,
peak O2 consumption, O2 sats
BODE index- composite score on
survival
6. D/D- difficult to distinguish from asthma
7. Biomarkers- CRP and procal- for
restricting antibiotics during
exacerbations, weak association, not
reproducible (SUMMIT study)
Sputum color- inc S/S
8. Other considerations- those with N
spiro but w symptoms, needs tx on
chronic basis

CHF- volume restriction, NOT flow limitation

OB- young age, exposure to fumes, RA, after
lung transplant, hypodense areas on expiratory
CT scan
Diffuse panbronchiolitis- Asian, males, non
smoker, chronic sinusitis, diffuse small
centrilobular nodular opacities and
hyperinflation
Prevention and Maintenance Therapy
1. Smoking Cessation- influence natural
history of COPD, if effective- success
rate 25% can be achieved
Pharmacotherapy- nicotine
replacement products—CI: MI and CVD,
can be started >2 wks after MI
Secretions are swallowed- nausea
Acidic beverages interfere with
absorption
E cig- controversial- can cause lung
injury (eosinophic pneumonia, AH,
respiratory bronchiolitis)
Vaping- THC, CBD, oils, vitamin E
THC- associated with lung illness
No infection, only inflammation and
injury
Other products- supportive intervention
Check smoking relapse and failure
5 step program
3 min counselling
Counselling intensity= cessation success
Give financial incentives
Pharmacotherapy + behavioral support
2. Vaccinations
Influenza- dec incidence of LRTI
Dec serious illness (LRTI, hospitalization,
death), dec exacerbation- live or killed-
dec IHD in elderly, ADR- mild and
transient
Pneumococcal- dec LRTI
Px >65 y/o
PPSV 23- younger w co morbidities
(cardiac)
Only significant protection, does not
reduced risk of pneumonia
Dec exacerbation
PPSV 23- dec incidence of CAP in COPD
<65 y/o, FEV <40 + cardiac
comorbidities
PCV 13- same or greater
immunogenicity up to 2 yrs after
vaccination
RCT- PCV 13- prevent CAP and invasive
pneumonia >65 y/o- lasted 4 yrs
+bacteremia
Pharmacotherapy in stable COPD
Dec symptoms
Dec exacerbations
Improve exercise tolerance and health status
CANNOT modify decline in lung function 
Treatment regimen needs to be individualized
1. Bronchodilators
Inc FEV1 and other spirometric values
Improve expiratory flow
Alter smooth muscle tone
Widen airways
DOES NOT alter elasic recoil
Improve exercise performance
Reduce dynamic hyperinflation during
rest and exercise
Changes difficult to predict
Use of short acting are not
recommended
Given regular basis to prevent and
reduce symptoms
FEV1 change is flat
Inc dose provides subjective benefit in
acute episodes, NOT in stable disease
Beta agonist + anti cholinergics
a) Beta Agonist
Relax smooth muscle
Inc cAMP
Wears off within 4 to 6 hrs
SABA- improve FEV1 and symptoms
(regular and prn)
LABA- no additional benefit
LABA- no benefit in mortality and
lung function, +benefit on other
effects
Indacaterol- LABA OD- +cough-
improve breathlessness,
exacerbation rate and health status
Others- improve lung fxn and
symptoms
AE: cardiac problems, arrhythmias,
tremors in older pxs any route
Low K - + thiazide
Inc O2 consumption under resting
condition in pxs w CHD
Dec O2
+tachyphylaxis
 No effect on COPD in contrast to
asthma
2. Anti muscarinic
Block bronchoconstrictor effect of
acetylcholine on M3 muscarinic
receptors
SAMA- also block M2- vagal induced
bronchoconstriction
LAMA- prolong M3 binding- faster
dissolution from M2, prolong
bronchodilator effect
SAMA> SABA- lung fxn, health status,
oral steroid requirement
LAMA- improve rehab (Tiotropium)
Improve symptoms and health status
Dec exacerbations and hospitalizations
LAMA > LABA
Inc FEV1 in mild to mod COPD
Attenuate post bronchodilator therapy
AE: poor absorption: +atropine effects
Dry mouth, urinary symptoms (no
causal relationship)
+CVD event tx w ipratropium
Bitter metallic taste
Tiotropium- no difference bet respimat
and dry powder
Glaucoma- if FM contact with eyes
Less safety data on other LAMA
3. Methylxanthines
Controversial
Non selective phosphodiesterase
inhibitor
Non bronchodilator action
Data on duration are lacking
Theophylline- clearance varies with age
Metabolized in cytochrome P450
oxidase
Small bronchodilator effect
Dec gas trapping
Inc respiratory muscle function
Modest bronchodilator effect
Studies are all in standard release
preparations
Greater symptom and FEV1
improvement than Salmeterol
Effects of low dose theophylline on
exacerbation rates - contradictory
evidence
AE: toxicity is dose related, therapeutic
ratio is small, +benefit on near toxic
doses
Arrhythmias and convulsions
HA, insomnia, nausea and heartburn
Prone to overdose
+ effect with Coumadin and digitalis
4. Combination
SAMA + SABA= improve FEV1 and
symptoms, as well as LABA + LAMA
LAMA + LABA- lung fxn, dyspnea, health
status, dec exacerbation rates, greater
QOL
Formoterol + tiotropium- impact on
FEV1
Less effect than individual component
Greater impact on patient related
outcomes
Better w long acting
Better w lower dose and twice daily
regimen
Better in patient reported outcomes
LAMA- dec hospitalization and
exacerbation
Tiotropium- improve rehab and exercise
performance
ICS/LABA- if w high eo count
5. Anti inflammatory agents
END POINT- exacerbation rates
a. Inhaled ICS
Limited response of the drug
Other drugs facilitate corticosteroid
sensitivity in COPD
Long term response are unclear
Modulated with the use of
bronchodilators
Does not modify FEV1 and mortality
TORCH trial- higher mort in fluticasone
alone in comparison to fluticasone +
combi
Not the same in SUMMIT trial
Moderate COPD- slower decline in FEV1
(9ml/year)
UK- If moderate to severe- better ICS +
LABA, no effect on survival, better CAT,
no effect on pneumonia, heterogenous
group, 8.4% reduction
ICS- inc pneumonia esp those with
severe disease
*blood eo count- predict magnitude of
effect of steroids + bronchodilators to
prevent exacerbations
No effect if eo <100
>300- + benefit
Estimates- not precise cut off points
Use as decision regarding steroid use
Always check exacerbation risk >/=
exacerbations or 1 hospitalizations in
the prev yr (higher effect of ICS)
Mechanism of high eo is ??
Other factors needs to be explored
COPD exacerbation and blood eo= ??
relationship
ICS= +candida, hoarseness, skin
bruising, pneumonia
Even at low doses
Factors for the AE: smoking,
+pneumonia, BMI <25, age >/=55, poor
MRC grade, eo <2%, severe airflow
limitation
Mod COPD= ICS + LABA- no inc risk of
PNA
RCT- dec bone density and fractures
Observational study- DM cataract and
TB- no RCT- difficult to conclude
Withdrawal of ICS- different results,
modest dec in FEV1 prob inc eo level
(greatest if blood eo level >300)
Triple therapy improve lung fxn, health
status, dec exacerbations
Greater benefit if symptomatic, FEV
<50, +hx of exacerbations
Dec mortality also (42.1% reduction)-
CVS respi at COPD mort
Survival not endpoint
Oral steroids- no benefit, + health
problems, muscle weakess, respiratory
failure
Acute exacerbations
Chronically lack benefit
b. PDE4 Inhibitor- chronic bronchitis,
severe to very severe COPD,
improve lung function, reduce
moderate to severe exacerbations,
esp those on fixed those ICS/LABA
Inc CAMP, dec inflammation
Roflumikast, OD, no
bronchodilator activity
Inc effect if w exacerbation and
hospitalization
AE: more effect than inhaled
GI, sleep, HA, reversible, early
course of treatment
Caution w depression and
underweight pxs
c. Long term azith/ erythromycin dec
exacerbation x 1 yr, inc bacterial
resistance, prolong QT and hearing
impairment
less benefit in smokers
moxi no effect
d. Mucolytics- decreased risk of
exacerbation, modest improvement
in health status
No target population
e. Immunoregulator- long term
effects?
Mepolizumab, benralizumab- ok to
replace oral steroids, w
exacerbation and eosinophilic
inflammation
No effect on FEV and QOL
XX- nedocromil
xx- infliximab- inc CA and
pneumonia
f. Statins- increased risk of
exacerbation
+ effects on outcomes on CVS and
metabolic patients
Vitamin D- dec exacerbation for
those w low vitamin D
Issued Related to Inhaled Delivery
Particle size should be 2-5 microm
Extra fine particles <2.5 more peripheral
deposition
Adherence rate DPI 23%
2/3- 1 mistake
Poor inhaler- + symptom
Determinants of poor inhalation- old age,
multiple devices, no education
Not all pxs will improve
Change device
Use placebo or bring the device
Nebulization not superior to inhaler if done
correctly
Other Therapies
1. Alpha 1 antitrypsin- IV slow down
emphysema, most effective in FEV1 35-
49%
Most suitable- non or ex smokers with
FEV1 35-60%
Evidence of lung disease after optimal
therapy
Preserve it after smoking cessation-
expensive
AATD FEV1 <65%
Recent- extensive lung dse, FEV >65,
AATD
2. Vasodilators- worsen oxygenation, no
outcome improvement
No improvement in rehab, exercise
capacity, health status, PAP
CI: stable COPD
3. Antitussives- no evidence
Rehab, education and Self Management
Rehab- optimal benefits 6-8 wks
No benefit if extended to 12 weeks
Supervised training 2x weekly is recommended
Maximize personal gains
Improve physical psychological impact
Improve health status, SOB and exercise
tolerance, health related QOL, all COPD grades
Moderate severe disease
Hypercapnic patients
?? acute exacerbations (</=4 weeks)- dec
hospitalizations
Exacerbations </=2 wks- dec readmission and
mortality (meta analysis)
Don’t do it before dc- compromise survival
with unknown mechanism
Cost effective treatment
Dec anxiety and depression
Challenge is ignorance, sustaining the activity
Inc activity, dec sedentary
Home exercise less effective
Benefits wane over time
Target pxs behavior
Education, integrative care, self management
Only self management with personalized
education has benefit
Improve status, dec hospitalization and ER visits
Others no benefit
Self management- Dephi process- intervention,
structured, multi component and interactive
Improve COPD outcomes – action plans
Inc mortality?? Vs no impact- COMET PIC-COPD-
tx exacerbations early
Heterogenous, difficult to assess real life
Proper health coaching- dec hospitalization and
ER (exacerbation)
Integrative care program
Needs to be structured
Multiple care providers
Did not improve mortality
Telemedicine- no effect
Do not need to be structured, should be
individualized
Supportive and Palliative, End of Life Care
Control symptoms
Manage px close to death
Support QOL, prevent suffering
Less in COPD than in CA
Provide spiritual emotional support, enhance
QOL, optimize function
Hospice/end of life- <6 months
Can be consulted, OPD- less common
Palliative therapies- dyspnea- opiates, CWV,
NMES, fan blowing, morphine- inc exercise
endurance (?px characteristics), rehab, NIV, O2
if spo2 <92%,
No effect- benzodiaz, music, relaxation,
counselling, support, psychotherapy
Nutritional support- vitamin C E Zinc, Selenium-
improve anti oxidant deficits, quadriceps
strength, protein, no effect on endurance
Low BMI, low fat free mass- worse outcomes
12 month intervention- higher physical activity
than capacity
Malnourished- improve with 6 min walk
Panic Anxiety and Depression
Multifactorial
Improve with rehab
Antidepressants- inconclusive
Ok w cognitive therapy and mind body
intervention
Fatigue- rehab, self management, mind and
body intervention, nutritional support
End of Life Care/ Hospice Care
Mort rate vary 28-80%
Cause of death- CVS, respi failure and
malignancy
High symptom burden- families need to
understand the disease
Views directives and death preferences
6 month survival prediction is diificult
Early discussion is important
Follow wish of patient
Hospice care- additional benefit- home/
hospital bed
Focus on disability and symptom burden
Other treatments:
A: O2 therapy/ Ventilatory support
Long term >15 hrs- inc survival in chronic
arterial hypoxemia (severe resting)
No effect sa mild or moderate (stable resting or
exercise)
Breathlessness is relieved if mild or non
hypoxemic
Air travel is ok, basta PO2 50, inc NC 3lpm or
venture 31%
May travel without O2- Spo2 >95, 6MWT >84%
Not sure when hypoxemia will develop even at
air/ sea
Check comorbidities
Walking the aisle- can aggravate hypoxemia
NIV- dec M/M- hospitalized, exacerbation of
COPD, ARF- hospital free survival
CPAP- COPD + OSA- with benefit
Prolong time of death/ hospitalization x 12
months (hypercapnia) PCo2 >52 mmHg
Interventional Therapy
1. LVRS- inc muscle and mechanical
efficiency
Inc elastic recoil pressure of the lung
Improve expiratory flow rate and
reduce exacerbations
Most benefit- upper lobe, low post
rehab exercise capacity
High post rehab- no difference in
survival, but with improve health and
exercise status
High mortality- homogenous,
FEV1/DLCO <20%
Costly > without surgery
2. Bullectomy- in selected patients- dec
dyspnea, improve lung function and
exercise tolerance
CI: pulmo HPN, hypercapnia, severe
emphysema
3. Lung transplantation- in selected pxs-
no effect on prolong survival- improve
health status and functional capacity
Bilateral 70%- longer survival age <60
y/o
7 years, 5 yrs if single
4. Bronch intervention- improvement 6-
12 months following treatment
Less M and M
Dec thoracic volume, improve muscle
NO to stent and sealant- inc M and M
Endobronchial valve- improve FEV1 and
6 min walk test x 6 months
Better if no interlobar collateral
ventilation (AE: PTX, valve removal)
Better if heterogenous
PTX- occur 72 hrs after procedure-
means successful procedure, rapid
 ipsilateral non target lobe expansion
(intact fissure, no collateral ventilation)
MDs needs expertise in management of
complications
Less exacerbation and respiratory
failure
Less complications than LVRS
5. Vapor ablation- no need fissure/
collateral circulation
Improve after 6 months
+ exacerbation at 12 months
Therapy is limited
6. Coils- inc 6 min WT and FEV1 and QOL
Inc PNA, PTX, exacerbations,
hemoptysis
Limited
Management of Stable COPD 
Assess symptoms and future risk of
exacerbations
Pharmacologic and non pharmacologic
NO smoking
Let patient understand the disease and risk
factors and the role they play
Assess, decreased risk factors
Pharmacotherapy is based on initial GOLD
group
Review ABCD
Tx effects
No more ACO, tx asthma
Common risk factor: smoke exposure
Dec smoke, dec air pollution and occupational
exposures
Policy making
Tobacco cessation- cost effective
Pharmacologic Treatments:
1. Correct use of inhaler
2. Theophylline is not recommended
unless long term therapy is
unaffordable or not available
3. Inhaled > oral
4. Short acting- occ dyspnea and relief
only
5. Mucolytics in selected pxs only
6. Long term steroids not recommended
(monotherapy)
7. Ok if w LABA
8. Roflumilast- chronic bronchitis, severe
or very severe airflow limitation
9. Former smoker + exacerbations-
macrolides
10. Opioids- dyspnea w severe disease
Review
Assess
Adjust
Follow up (base on dyspnea/ exacerbation), not
ABCD
Group B- has comorbidities that should be
investigated
Group D- LABA+LAMA- w if w symptoms
If both- do exacerbation algorithm
Dyspnea- LABA+LAMA—step down to 1 if
persistent or switch device
Dc or shift ICS if there is no response
r/o other causes of dyspnea
Exacerbations- LABA--- LABA+LAMA, LABA+ICS
(asthma), when ICS will respond
Eo >300 + 1 exacerbation
Eo >100 + >/=2 exacerbation
Na persistent- give triple therapy
(see figure)
Treatment: non pharmacologic
Rehab- for group B C D
Self management education and coaching
Goal: motivate engage and coach patient
Patient is also a partner
Not education alone
Offer end of life care
Pulmo rehab for breathlessness
Pulmo rehab- inc physical activity- internet
intervetions lack details
Time points to refer to rehab: at diagnosis, at
discharge, during deterioration
Structured program
Rehab Goal 2030- make rehab accessible
Exercise + counselling- constant load or interval
training
Physical activity- predictor of mortality
Exercise up to 60-80% of the symptom limited
maximum work or heart rate, borg rate 4-6
Endurance- continuous/ intermittent (divide it
with high intensity exercise)- comorbidities
limiting performance
Optimize exercise with bronchodilators
Add strength training and whole body vibration
technique
Inspiratory muscle technique- not consistent
Outcomes should be specific
Check exercise tolerance- ergo or treadmill
Shuttle walk- complete info than self paced,
easier to perform
Walking test- need practice session
Use questionnaires
Palliative care
Nutritional support- amount and duration not
established
Long term O2 therapy- should be re evaluated
60-90 days
Ventilatory support
OSA- CPAP
NIV- daytime hypercapnia, recent
hospitalization
Bronchoscopic technique
Vapor ablation- segmental > lobar
No contralateral ventilation or + fissure
integrity- pwede ang valve
Homogenous- not candidate of LVRS, but
pwede sa bronchoscopic technique
LVRS- upper lobe empysema
Bronch therapy- improve FEV1, exercise
tolerance, QOL, lung fxn at 6-12 months after
treatment
Criteria for transplant
Criteria for listing
Palliative care- effective in symptom control
Do ff up on these patients
Measure functional capacity, O2 and FEV1
Check symptoms exacerbations and sputum
type
Do imaging and smoking status
Check comorbidities
Check post op complications- impt predictor-
surgical site- inc risk as incision approaches
diaphragm
Lower risk w epidural/ spinal anes > gen anes
Tx COPD before surgery
Major risk of complications- FEV <30-40%, VO2
<10 or 35 predicted
Multidisciplinary
Don’t do it if w exacerbation
Management of Exacerbations
- Worsening of symptoms
- Needs additional therapy
- Negative impact
- Airway inflammation, inc mucus
production, gas trapping
- Inc dyspnea and other symptoms
- Not specific, needs D/D
- Most common precipitations-
respiratory tract infections
- Dec negative impact
- Dec subsequent events
- SAMA and SABA initial
- LAMA and LABA- before hospital
discharge
- Steroids- 5-7 days only- improve FEV1,
oxygenation, shorten recovery time and
hospitalization
- Antibiotics- 5-7 days- shorten recovery
time, shorten risk of early relapse,
treatment failure, hospitalization
duration
- Methylxanthines- xx- in SE
- NIV- dec hospitalization, improve
survival, dec WOB and intubation,
improve gas exchange
- Do prevention after exacerbation
1. Mild- short acting
2. Moderate- short acting + antibiotics +
steroids
3. Severe- ER/ hospitalization/ ARF
need to seek professional help
Rhinovirus- longer, more severe- winter
months, 1 wk after exacerbation onset
PM 2.5- inc hospitalization and mortality
Inc bacteria in sputum, inc eo and
neutrophils
Triggers- pollution, infection, ambient
temperature
Symptoms last 7 to 10 days, some may last
even longer
20%- no recovery
Contribute to disease progression
Cluster in time, progression to another
event
Frequent (>/=2) exacerbations- worse
outcome and morbidity
Any disease severity groups
Susceptibility- ??- greater perception of
breathlessness
Greatest predictor- # of exacerbation in the
previous yr, moderate stable phenotype
Change their frequency with change in FEV1
Greater empysema/ bronchitis
Pulmonary artery: aorta ratio >1
Check vitamin D deficiency
Treatment Options
80%- OPD basis tx
Check O2 and assess, NIV, meds
Exacerbation is heterogenous
Severity is based on clinical signs:
1. No respiratory failure- RR 20-30, no
muscle use, O2 improve, normal PCO2,
(28-35%)
2. ARF- non life threatening- RR >30,
+muscle use, +hypercapnia- PCO2 50-60
mmHg, O2 improve (28-35%)
3. ARF- life threatening- #2 + mental
status change, needs o2 fio2 >40%,
PCO2 >60, Ph <7.25
Poor prognosis
5 year mortality- 50%
Factors- old age, low BMI, comorbids, prev
exacerbation/ hospitalization, +clinical
severity, needs long term o2 at discharge,
poor lung fxn, poor exercise, low lung
density, inc bronchial wall
Inc mort during cold weather
+use of educational intervention
Pharmacologic Treatment
1. Bronchodilators
No high quality RCT
SABA w or wo SAMA
No different in FEV1 bet MDI and
nebulize (easier if sicker patients)
Do not use continuous nebulizer
Use of long acting, no study, but start it
before hospital discharge
Use air driven rather than O2 driven-
avoid inc PCO2
2. Steroids
40 mg x 5 days, >7 days- Pna and mort
Improve O2, risk of early relapse and
treatment failure
URTI- ICS/LABA x 10 days
Use only with significant exacerbation
Less effective if low eo, use steroid
sparing agent instead
3. Antibiotics
Use of antibiotics is controversial
Use clinical signs like sputum color
Dec mortality, treatment failure and
purulence- moderate COPD
Doxycycline 
Sputum cultures are not feasible
Give it if inc dyspnea, inc sputum
purulence and volume, needs MV
Give it 5-7 days
Oral is preferable
Co amox, macrolide tetracycline
Cover gram neg if on MV, severe airflow
limitation/ exacerbation
Use of procal protocol in ICU- higher
mort
4. Others- fluid balance, anticoagulants,
nutrition, tx comorbidities
5. Smoking cessation
Respiratory Support
1. O2- target 88-92%
Do ABG/ VBG (accurate)
 Venturi- more accurate than nasal
prongs
2. HFNC- 8l/min infants, 60lpm in adults
Alternative to NIV
Improve WOB, gas exchange, lung
volume, compliance, homogeneity
Dec intubation but not stat significant
No effect on mortality
Dec hypercapnia
3. Vent support/ICU
a. NIV-success rate 80-85%, preferred
initial, improve O2 and acidosis, dec
RR and WOB, dec HD and pna
Wean- if px able to tolerate 4 hrs off
NIV
b. IMV- inc M and M
Check complications
Lower mort than others- 17-49%
Further deaths in the nxt 12
months, or FEV <30%, other
comorbidities, housebound
Hospital discharge and FF up
Early and Late ff up
Introduce care bundles- ? cost effectiveness
Telemonitoring- no change but good practice
Ok w coaching
Early rehab (<4 weeks)- survival
Do CT scan if w recurrent exacerbations
COPD and Comorbidities (Stable)
COPD co exist with other disease
Has impact on the course
Its presence should not alter its treatment and
treat the comorbidities the usual way
Most frequent- lung ca
Most common mortality- lung cancer
Most common and important- CVS diseases
Underdiagnosed- osteoporosis and depression
and anxiety
GERD- poor health status, inc exacerbations
Simplify tx
Avoid polypharmacy
COPD + comorbidities- impact on prognosis
Different relationships
Link, sequelae of COPD itself
Should be identify and tx
Some are overlooked
Common at any stage
d/d is difficult
inc risk
Guidelines are not substitute for tx of individual
pxs
CVD- common and important
1. Heart failure- prevalence 20-70%,
incidence- 3-4%, significant, independent
predictor of all cause mortality
40% on MV has LV dysfunction (type 2
ARF)
Use selective B1 blocker
Tx the same way
Acute HF- NIV
2. IHD- check risk factor profile
30 days after exacerbation- inc
myocardial damage
+Trops- inc short and long term mort
3. Arrhythmias- common, afib is common
after exacerbation
COPD meds has acceptable safety
Caution: SABA and theophylline-
difficult rate response
4. PAD- impact QOL and functional activity
8.8% prevalence
Worse health status
5. HPN- most frequent, implications on
prognosis
Diastolic dysfunction from optimally tx
HPN- causes exercise intolerance,
exacerbations and hospitalizations
Treatment is the same
Selective beta blocker- less prominent
6. Osteoporosis- major comorbidity,
underdiagnosed, poor health status and
prognosis, dec BMI, + emphysema
+fractures, low bone mineral density
Systemic steroids should be avoided
repeatedly
7. Anxiety and depression-poor prognosis,
female, young smoking, low FEV1, cough,
higher SGRC score, +hx of CVD
Exercise and rehab are beneficial
1.9x commit suicide.
8. Lung cancer- stronger in emphysema than
airflow limitation
Greatest risk if w both findings
 Inc in inc age and smoker
Poor outcomes and post op
complications
LDCT- not every world does it
9. Metabolic syndrome and DM
More frequent
Affect prognosis
Prevalence 30%
Should be tx acc to guidelines
10. GERD
Independent risk factor
Worse health status (along w PAD)
PPI- dec exacerbations
Value remains controversial and needs to
be established
11. Bronchiectasis
Ct scan
Impact of dse is unknown
Inc mortality and longer exacerbations
12. OSA
Worse prognosis if overlap
More desat, low O2 and hypercapnia
More Pulmo HPN and arrhythmia
13. Multimorbidity
Usually in aging population
Complex, avoid polypharmacy, tx evidence
are from trials
Check anemia and vitamin D deficiency