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COPD 1
Chronic Obstructive Pulmonary Disease
 Definition
o COPD is a disease characterized by a progressive 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.
 Umbrella term – encompasses a number of pulmonary disease states
a) Bronchitis (pg 511 DiPiro)
-Condition with chronic or recurrent mucus secretion into the bronchial tree
with cough that occurs on most days
b) Emphysema
-Condition of the lung characterized by abnormal permanent enlargement of
the airspaces distal to the terminal bronchioles
-Destruction of their walls
-Without obvious fibrosis
 Epidemiology
o COPD currently affects ~16 million Americans
th
Rare blood test
confirms it. In
general, if pt.
presents with
obstructive lung
disease symptoms at
<35 years of age,
most likely have this.
o 4 leading cause of death in U.S.
o Burden on society (Annual cost to the nation for COPD is ~$31.9 billion)
 Risk factors
Major
Minor
o Smoking (#1 risk factor)
o Air pollution
o Increasing age
o Race (Caucasians at  risk)
o Male gender
o Nutrition status (Poor nutrition  risk)
o Existing impaired lung function
o Family History
o Alpha 1 antitrypsin deficiency
o Lower socioeconomic status
o Occupation
o Bronchial hyperreactivity
o Respiratory tract infections
Inhale particles that
(frequent)
aren’t normal to air
 Pathophysiology
o Proteolytic-antiproteolytic theory
 Alpha 1 antitrypsin
 Protease inhibitor that normally inhibits trypsin and other
proteases from destroying normal lung tissue
 Smoking is linked to a decreased activity of alpha 1 antitrypsin and
stimulation of proteases
 Oxidants from smoking inactivate anti-proteases (responsible for
protecting the lung)
Proteases
 Destroy PROTEINS that make up lung matrix
o Decrease cilia
o Impair T lymphocytes (make immunologic response )
o Increase neutrophil chemotaxis (neutrophils accumulate in respiratory tract)
o Increase levels IL-8 (more potentiation of inflammatory cascade)
Antiproteases
 Protect the lung by inhibiting proteases
 e.g. Alpha-1 antitrypsin
COPD 2
Pt. comes in with complaint of SOB.
 Clinical presentation (see table 27-2 pg 514 DiPiro)
Predominant
Predominant
emphysema
bronchitis
Age
60+
50+
Dyspnea
severe
less severe
Cough
After dyspnea
Before dyspnea
Sputum
Scanty, mucoid
Copius, purulent
Bronchial infection
Less frequent
More frequent
Cor pulmonale
Rare
Common
General appearance
Pink Puffer
Blue Bloater
Always tachypnic, expend
enormous amt. of calories per day
just breathing. Respiratory center
responds to CO2.
V/Q Mismatch
(V=ventilation,
Q= perfusion)
Retain a lot of CO2 b/c
respiratory center doesn’t
respond to a lot of CO2.
-
+
Poor ventilation (problem getting
air down)
Poor perfusion b/c alveolus and
capillary surrounding the alveolus
are destroyed
Poor ventilation but perfusion
is fine
Pt. usually comes in with
cough problem b/c
problem with upper
airway. Mucus
accumulation in airway.
Does not matter if pt. has
emphysema or bronchitis.
Both are treated the same.
Most pts. Have some
symptoms of both.
 DIAGNOSIS
 Should be considered in patients over the age of 35 who have a risk factor and who
present with one of more of the following symptoms:
o Exertional breathlessness
-Intermittently or everyday
-Present throughout the day
o Chronic cough
-Rarely only nocturnal
o Regular sputum production
o Frequent winter “bronchitis”
o Wheeze
o History of exposure to risk factors
-TOBACCO SMOKE!
o
Dyspnea
 Dyspnea scale (progressive and persistant)
GRADE DEGREE OF BREATHLESSNESS RELATED TO ACTIVITIES
1
Not troubled by breathlessness except on strenuous exercise
2
Short of breath when hurrying or walking up a slight hill
Walks slower than contemporaries on level ground b/c of
3
breathlessness, or has to stop for breath when walking at own pace
Stops for breath after walking about 100m or after a few minutes on
4
level ground
Too breathless to leave the house, or breathless when dressing or
5
undressing
 Spirometry (pulmonary function test)
 Should be performed:
o In all patients > 35y.o., current or ex-smokers, with a chronic cough
o At time of diagnosis
COPD 3
o To reconsider diagnosis if patient shows an exceptionally good Diagnostic Tests:
 Patients with COPD typically show:
response to treatment
-Decrease in FEV1 AND
o Follow disease progression (FEV1 q yr)
-Decrease in FVC
-FEV1/FVC <70% and
 Other tests at diagnosis
postbronchodilator FEV1 <80%
o Chest x ray (used to rule out pneumonia, lung cancer, TB)
predicted
o Full CBC (ID anemia / polycythemia)
o BMI (see if nutritionally stable)
o ?alpha 1 antitrypsin deficiency (screen; Do they have a family h/o of this?)
o ECG / echo (used to rule out CHF)
o Pulse oximetry
o Sputum Culture (used to rule out respiratory infection)
 (Bronchodilator) Reversibility testing
o No longer necessary (b/c a lot of times pt would be labeled as non-responsive,
but later may be responsive or chronically responsive)
 Differential List
o Asthma (easy to rule out in younger pt., reversible, more diurnal variation)
Pulmonary Fx Tests:
o CHF (have crackles, x-ray, echo, edema)
 FVC:
o Tuberculosis (around anyone recently infected with TB?)
 FEV1/FVC ratio
 Differential List for EXACERBATION
-Normal >80%
- <80% means obstruction
o Infection (flu, pneumonia)
 DL: diffusion capacity
o CHF exacerbation
 When DLCO reduced – means???
(DLCO = diffusion capacity of carbon monoxide)
o PE
-usually points to emphysema 2/2 diffusion
capacity diminished b/c of loss of surface area
available for gas exchange
 Disease ASSESSMENT
SEVERITY
Mild airflow obstruction
Moderate airflow obstruction
Severe airflow obstruction
#1 goal for
everyone with
COPD is to be a
non-smoker.
FEV1 (after b-agonist)
50-80% predicted
30-49% predicted
< 30% predicted
Example: Person
 Managing Stable COPD
who smokes 1
 SMOKING CESSATION
ppd for 20 yrs has
a 20 pack year
o Obtain smoking history
history
o Pack years
 Calculation NUMBER OF PACKS PER DAY X DURATION
o Counsel to quit AND offer assistance at each provider visit
o Only treatment that has been shown to prevent progression of the disease
When a person tries to quit
smoking, cough may
actually get worse. Make
sure to tell them that and that
it will eventually get better.
Cough might get worse b/c
smoking has killed all the
cilia. When stop smoking,
cilia try to come back alive.
More of a cough to clear the
lungs.
 Treatment
 INHALED BRONCHODILATOR THERAPY
 Short acting beta agonist: albuterol (Beta-2 agonist) (CENTRAL to sx management)
COPD 4
Never schedule
Albuterol for
asthma, but can
for COPD.
Albuterol stimulates
receptors on airway
smooth muscle, takes
effect relatively
quickly (within 1-2
min) and last s 4-6 hrs.
Cholinergic nerves
are going to be the
main neural
bronchoconstrictor
pathway in the
airways. Have
increased tone of
that in COPD pts.
so if have a drug
like ipratropium, it
will decreade tone
around the airways
(relaxes muscles)
Ipratropium has
favorable effects
on sleep. May
help people who
have trouble
sleeping b/c
cholinergic tone
peaks during
sleeping hours.
o MOA: Bronchodilation (stimulates B2-receptors on airway smooth muscle). Smooth
muscle relaxation following adenylate cyclase activation and increase in cyclic AMP
production
 Functional antagonism of bronchoconstriction
o Usual dose: 1-2 p q4 h prn SOB
o Max recommended dose in COPD: A little higher than what package insert says for
asthma b/c not getting a lot of good delivery of drug to site anyway b/c of  perfusion
and ventilation. 12 puffs a day for asthma (go a little higher for COPD) so 18-20 puffs
are ok if no signs of toxicity
o Place in therapy: Can be used as initial empirical treatment for relief of breathlessness
FIRST LINE. Appropriate to schedule around the clock
 Can be used ATC for symptomatic relief
Albuterol may help get some of the mucus out of
o Onset of effect: 1-3 minutes
the lungs ( mucocilliary clearance)
o Duration of action: 4-6 hours
o Reliever/rescue medication: PRN dosing
In general, long acting B-agonists are much more B2 selective than
o B2:B1 selectivity
short-acting. Short-acting will have more adverse effect like tachycardia,
 Albuterol = 1375:1
muscle tremor.
 Salmeterol = 85,000:1
o ADR: tachycardia, skeletal muscle tremor, H/A, anxiety
o Monitoring: Measure effectiveness by lung function, improvement in symptoms,
activities of daily living, exercise capacity, rapidity of symptom relief
o Education points: proper inhaler technique, carry with you
 Short acting anticholinergic: Ipratropium (Atrovent®)
o MOA: Anticholinergic; relaxes muscles around bronchial tree. (nonspecific muscarinic
receptor antagonist decreases airway smooth muscle tone)
-Scheduled
o Usual dose: 2-4 puffs q 4-6 hours prn SOB
ipratropium is
o Maintenance medication: 2-3 inhalations QID according to package insert
acceptable
(use around
o Max dose: 24 puffs / day
the clock)
o Place in therapy: Can be used as initial empiric treatment FIRST LINE
-Takes 30
min to kick in
 Symptomatic relief with anticholinergic ~80% will respond
 Symptomatic relief with SABA ~70%
o Onset of action: 20-30 minutes
Some say to start ipratropium even before
o Duration of action: 4-6 hours
albuterol. There was a study. Either will
be appropriate as first line.
o Usually used in combo with albuterol
o Combination product (Combivent®)
 Fixed dose combination of albuterol and ipratropium (ipratropium bromide and
albuterol sulfate)
 Onset of action:
 Albuterol: 1-3 minutes
 Ipratropium: 20-30 minutes
 Duration of action: 4-6 hrs
 Maintenance medication: 2-3 inhalations QID according to package insert
 Education: proper technique, carry with them
 Allergy alert: peanuts, soy lecithin
 Advantages:
COPD 5
 Cost (only need one inhaler)
  side effects b/c not maxing out on one drug
o ADR: dry mouth, dizziness
 Think anticholinergic side effects
 DON’T use in patients with
 Glaucoma
 Urinary retention
o Education points: proper inhaler technique
o Clinical pearls: ALLERGY ALERT! peanut allergy, soy lecithin
 Long acting beta agonist: salmeterol, formoterol (serevent, foradil)
o MOA: bronchodilator. Smooth muscle relaxation following adenylate cyclase
If pt. is still
activation and increase in cAMP production (stimulates B2-receptors on airway smooth
symptomatic when
muscle)
on combination of
Blister cap is refrigerated,
short acting agents,
o
Usual dose: salmeterol diskus 1 p BID, formoterol 1 blister cap BID more steps than salmeterol
move to longer
o Maintenance medication: 1 inhalation (discus) BID
acting agent.
o Place in therapy: used in patients who remain symptomatic despite
treatment with S.A.B.A.
o Use in those that experience >2 exacerbations/ year
o Onset of effect: 5 min (formoterol) 20 min (salmeterol)
o Duration of action: 12+ hours
o ADR: tachycardia, skeletal muscle tremor, anxiety, nervousness
o Education points: don’t over use (no added effects if take more hits, just more side
effects), NOT to be used for acute symptoms  don’t carry as a rescue inhaler
 Long acting anticholinergic: tiotropium (Spiriva)
o Will learn during in-service
o MOA:
o Usual dose:
o Duration of effect: 24+ hours
o Place in therapy:
o ADR: Dry mouth, problematic in glaucoma patients
o Education points: devise handihaler (new)
Be careful if pt.
has arrhythmias,
CHF, liver
problem, allergy
to caffeine or
chocolate
 Theophylline
o MOA: not fully understood. Thought to work on cAMP / PDE (increasing cAMP in
airway smooth muscle)
o Usual dose: Sustained release products
o Maintenance medication: qd to bid
o Place in therapy: only used after trial of SABA and LABA (NOT FIRST LINE)
 Pt unable to use inhaled therapy
o Duration of action: 12-24 hours
o Monitoring: plasma level
o Assess effectiveness by evaluating activities of daily living, improvement in symptoms,
exercise cap, and lung function
o Drug interactions (macrolides, FQ’s, smoking)
COPD 6
o Other clinical pearls (see asthma handout)
o Education points: limit caffeine use. Use as directed. Blood levels may be needed
o Side effects of theophylline and comparative concentrations
LEVEL
SIDE EFFECT
As level of theophylline
10-20
N/V
increases, so does the severity
>20
N/V/D irritable, insomnia
and adverse effect
>40
cardiac sx
>50
seizures
 Long Acting Bronchodilators: Oral B2
o Oral sustained-release B2-agonist
o Duration of action: 12 hrs.
o Side effects: tremor, tachycardia, palpitations
o Trade names: Volmax (albuterol sulfate), Proventil Repetabs (albuterol sulfate)
o Use limited by side effects
 CORTICOSTEROIDS
o INHALED
 MOA: anti-inflammatory
 Place in therapy:
Flovent, Pulmicort
 Patients with FEV1 <50% predicted
(same drugs as in
Asthma handout)
 Those who are having >2 exacerbations / year (that require treatment with
antibiotics or steroids)
 Moderate to sever COPD (d/c if no benefit after > 4 weeks)
 Goal: reduce exacerbation rates and slow decline in health status
 NICE guidelines: moderate to severe COPD (discontinue if no benefit > 4 weeks)
 Monitoring: risk of osteoporosis, cataracts
If need to keep
 Education points: importance of compliance, onset of effect
someone on oral
 Spacing device  Patient should use a spacer
corticosteroid,
use lowest dose
 Rinse mouth with water after use
possible and use
o ORAL
every other day.
 Maintenance use not generally recommended
 Maybe needed in those with severe dz, or those that can’t be withdrawn
Have role in
following an exacerbation
exacerbations
 Risks: osteoporosis, DM, cataracts, HTN, possible mood changes (these risks are
lower for inhaled corticosteroids)
 COMBINATION THERAPY 
In general, as the disease progresses, probably need add-ons.
 If patients remain symptomatic on monotherapy
 Effective combinations include
o Beta2 agonists + anticholinergic
o Beta 2 agonists + theophylline
o Anticholinergic and theophylline
o Long acting beta agonist and inhaled corticosteroid
o ?long acting beta agonist + long acting anticholinergic
 Clinical pearl
COPD 7
Not going to get
more drug from
nebulizer than
inhaler if used
correctly.
o patients on long acting inhalers, will still require a short acting agent for acute
symptoms of SOB/ cough
 Delivery Systems Inhalers (MDI, DPI (Turbuhaler, Diskus), Handihaler, Foradil blister caps
 Spacer (may use tidal breathing)
Phasing out metered dose inhalers (don’t want drug with
 Nebulizer
propellant anymore, too many fluorocarbons)
o Those with distressing or disabling breathlessness despite maximal therapy using
inhalers should be considered for neb therapy
 OXYGEN
o Long term oxygen therapy (LTOT) indicated in patients who have
decreased O2 sat and one of the following:
 Secondary polycythemia (increase in Hgb/Hct)
 Nocturnal hypoxemia
 Peripheral edema
Evidence of complication
 Pulmonary HTN
o To derive mortality benefits, need to use at least 15 hrs/day
o Ambulatory oxygen therapy
o Consider for those with exercise desaturation
o Show improvement in exercise capacity or dyspnea with oxygen
o Motivated to use it
 HEALTH MAINTENANCE
 Vaccinations
o Pneumovax
o Flu shot annually
 Mucolytics (water is the best mucolytic, may use Mucomyst or guaifenesin
o Considered for those with chronic cough production of sputum
 Anti-tussives
o Not recommended (don’t want to suppress cough b/c cough helps get gunk out of the
lungs)
 HOW TO CHOOSE WHICH
BRONCHODILATOR?
o PRN vs. scheduled
o Availability
o Individual Response
o Cost
o Long acting – convenient
o Combining bronchodilators
 Improve efficacy
 Decrease risk of ADR’s
Putting it all together
 OTHER THERAPIES
o Pulmonary rehabilitation
 Improve quality of life
 Physical wellbeing
 Emotional wellbeing
 Nutritional counseling
 Education
(Pulmonary rehabilitation is a multidisciplinary
group of physician, nurse, respiratory therapist,
pharmacist, intuitionalist, and social worker.)
COPD 8
1) Regular scheduled combo of SA bronchodilators (like combivent around the clock
or ipratropium around the clock)
2) Regular scheduled LA inhaled bronchodilator (like servent BID, tiotropium BID)
OR
3) Regularly scheduled combo of LA anticholinergic AND B-agonist
Combination LABA + ICS
-After trial of inhaled therapy
-Pt. can’t use inhalers
-Minimal drug interactions present
 MANAGING COMPLICATIONS OF COPD
Complications
 Exacerbations
 Pulmonary HTN
 Cor pulmonale
 Arrhythmias
 Polycythemia
 RTI
 Acute respiratory failure
 Exacerbations
o Definition
 Sustained worsening of symptoms from usual stable state which is beyond normal
day-to-day variations, and is acute in onset
o Etiology
 Infection (#1 cause), air pollution, unknown
o Conditions that may mimic:
 Pneumonia, CHF, PE, arrhythmia, pneumothroax
Staging Exacerbations:
o Diagnosis
Three symptoms:
o Usually associated with:
*Increased sputum purulence
*Increased sputum volume
 Worsening breathlessness
*Increased dypsnea
symptoms
MILD
ONE of three
MODERATE
SEVERE
symptoms present
TWO of the three
symptoms present
ALL THREE
symptoms present
COPD 9
 Increased sputum volume and purulence (sticky, thick)
 Changing sputum color
 Cough (worse)
For a couple days
o Treatment
 Initial
 Increase frequency of bronchodilator use – consider neb
 Oral antibiotics
 If purulent sputum
 Prednisone 30mg po qd for 7-14 days for all patients with significant
increase in breathlessness unless contraindicated
o Patients with FEV1 ≤ 50% and 2 or more exacerbations in a 12 month period are
candidates for ICS
 PULMONARY HTN
 Definition
o Disease in which blood pressure is abnormally high in the arteries between the heart
and lungs. This condition can ultimately lead to heart failure
o Mean pulmonary artery pressure (MPAP) via right heart catheterization
 >25mm Hg at rest
 >30mm Hg with exertion
 Etiology
o Primary PAH (idiopathic)
o Connective tissue disease (thickening / hardening of vessels leads to decreased
contractability)
o Medications (fenfluramine, phentermine)
o HIV
o Thromboembolic event
o
Chronic hypoxemia (chronic obstruction, not enough oxygen in the arteries btwn heart and lungs)
 Pathogenesis
o Pulmonary vasoconstriction
o Decrease flow in the pulmonary arterioles
o Reactive pulmonary hypertension
o Damaged pulmonary vasculature
o Increase in vascular injury with vicious cycle perpetuating pulmonary HTN
 Symptoms
o SOB, chest pain, syncope, fatigue, peripheral edema
 Diagnosis
o Of exclusion 2/2 non-specific symptoms
 Treatment
o CCB (standard of care)
 Diltiazem, nifedipine, amlodipine used most frequently
o Anticoagulation
 Warfarin target INR 2-3. Patients on warfarin showed increased survival
regardless of CCB efficacy
o Diuretics
 Evidence of peripheral edema, ascites
COPD 10
o Oxygen
 Maintain o2 sat > 90%
o Prostacyclin + analogs (epoprostenol, treprostinil, beraprost, iloprost
o Endothelin receptor antagonist (bosentan)
o Phosphodiesterase inhibit
 For more information on PPH see Chest supplement, July 2004
 COR PULMONALE
o Definition / etiology
 Enlargement of the right ventricle secondary to abnormalities of pulmonary
Chronic hypoxia

ventilation. Leads to right sided heart failure
Pulmonary HTN
 RetainNa/ H20 leads to development of edema

End stage  Cor pulmonale
o Pathogenesis
 Normally, flow through the pulmonary vascular bed depends not only on
pumping action of the RV, but also on respiratory movements and on the
filling and contraction of the left ventricle
o Diagnosis
 Subj: Peripheral edema
 Obj: Elevated systemic venous pressure (can cause hepatomegaly and ankle
edema)
 Heart sounds
 Gallup rhythm on auscultation
 Loud pulmonary second heart sound
 Pulmonary trunk may be enlarged on xray
 Echo may show enlargement of RV cavity
o Treatment
 Diuretics, Oxygen
 ARRYTHMIAS
o Etiology: decreased O2 delivered to heart
o Treatment (increase oxygen saturation (long term O2 therapy))
 Reverse cause: electrolyte changes, hypoxia, theophylline toxicity
 POLYCYTHEMIA 
 Definition
o Increase in circulating RBC above normal
 Etiology
o Erythropoeitin produced 2/2 kidneys sense hypoxemia. Increased production of RBC in
an effort to increase oxygen carrying capacity of blood. End result; increased risk of
clotting
 Signs / symptoms
o Elevated H/H (Hematocrit 55-60)
o Mental status changes (confused)
o Thrombotic stroke
 Treatment
o Chronic O2
COPD 11
o Phlebotomy (draining of the blood)
o ?anticoagulation
 RTI
 Signs/symptoms
o Changes in sputum color, quantity, consistency
o ? fever + WBC (usual signs of infection may not be present)
o increased breathlessness and cough
 Treatment
o antibiotic ? 7-10 days
 ACUTE RESPIRATORY FAILURE (take pt. to physician or ER)
 Definition
o Non COPD patient: paO2 < 50 or Pa CO2 > 50
o COPD ↓ PaO2 of 10-15 or ↑ PCO2 SO pH ≤ 7.3
o Signs/ symptoms
o Restlessness, tachycardia, cyanosis, irregular breathing, mental status changes,
diaphoresis (sweating), hypotension
End stage COPD
o Treatment
-Social worker
o Maximize bronchodilator
-do not
resuscitate order
o O2
-very difficult to
o Intubation
extubate pt w/
end-stage COPD
o Pulse steroids (pick a regimen, on 7 days, off 7 days)
b/c not too much
o Theophylline
lung fxn left
o Correct cause (infection, resp depressants)
Inhaled steroids. If pt has more than 2
exacerbations/year should have trial of
inhaled steroids
MONITORING
Smoking cessation
Improvement in status
Treatment / prevention of acute exacerbations
Reduction in rate of progression of the disease
Improvement of physical and psychological well-being of pt to maintain daily activities
Reduction in days lost from work, hospitalizations and mortality
FREQUENCY
MILD / MODERATE
At least annual
SEVERE
At least twice a year
COPD 12
Clinical
assessment
 Smoking status and desire to
quit 
 Adequacy of symptom control
 Breathlessness 
 Exercise tolerance
 Estimated exacerbation
frequency 
 Presence of complications
 Effects of each drug treatment
 Inhaler technique 
 Need for referral to specialist
and therapy services
 Need for pulm rehab (recommend
 Smoking status and desire to quit

 Adequacy of symptom control
 Breathlessness 
 Exercise tolerance 
 Estimated exacerbation
frequency 
 Presence of cor pulmonale
 Need for long-term oxygen
therapy
 Patient’s nutritional state
 Presence of depression
 Effects of each drug treatment
 Inhaler technique 
 Need for social services and
occupational therapy input
 Need for referral to specialist and
therapy services 
 Need for pulmonary rehab
 FEV1 and FVC
 BMI
 MRC dyspnea score




for anybody with moderate-severe)
Measurements
to make
FEV1 and FVC
BMI
MRC dysnea score
SaO2
 PATIENT EDUCATION
 Non pharmacologic therapy (smoking cessation)
 Inhaler / spacer / nebulizer technique
 Importance of compliance
 Disease progression
 Nutrition / exercise / psycho-social issues (anxiety or distress)
 Pulmonary rehabilitation ( hospitalizations,  severity of exacerbation)
 Maintenance of MDI / spacers
wash once every week in
soapy dish water
wash once every 2-4 weeks
 Prognosis
 Mortality rates
-FEV1 >50% predicted
 Comparable to general population
-FEV1 20% predicted
 Approximately 30% mortality at 1 year
 Approximately 95% at 10 years