Management of COPD .Chronic Obstructive pulmonary Diseases

1. COPD: Management
..updated
Pratap Sagar Tiwari, MD, Internal medicine
Note: this is for MBBS lecture class

2. Making a diagnosis
•A clinical diagnosis of COPD should be considered in
any patient who has dyspnea, chronic cough or
sputum production and a history of exposure to risk
factors of the disease.
•Spirometry is required to make the diagnosis in this
clinical context; the presence of a post
bronchodilator FEV1/FVC <0.70 confirms the
presence of persistent airflow limitation and thus
of COPD.
• FEV1:the volume of air forcefully expired during the 1st sec after taking a full breath
• Forced vital capacity (FVC):the total volume of air expired with maximal force

3. Treatment line begins after assessment of
severity of the condition
Postbronchodilator FEV1/FVC <0.7 defines Airflow limitation
Low
risk
High
Risk
3 yr mortality =24%

4. Mmrc : Assess severity of breathlessness
• 0-1 = less
breathlessnes
s
• >2= more
breathlessnes
s

5. BODE INDEX
Variable 0 1 2 3
FEV1 O
≥ 65 50-64 36-49 ≤ 35
Dist walked in 6
min (m) E
≥ 350 250-349 150-249 ≤ 149
MRC Dyspnoea
scale*
0-1 2 3 4
Body mass index > 21 ≤ 21
BODE score 0-2 =mortality rate of around 10% at 52 mnths,
BODE score 7-10=mortality rate of around 80% at 52 mnths.

6. Management of COPD
• Chronic stable phase COPD
• COPD on Acute exacerbation

7. Chronic Stable phase COPD
•Only three interventions- smoking cessation,
oxygen therapy in chronically hypoxemic
patients, and lung volume reduction surgery
in selected patients with emphysema—have
been demonstrated to influence the natural
history of patients with COPD.
•All other current therapies are directed at
improving symptoms and decreasing the
frequency and severity of exacerbations.

8. Pharmacotherapy
•Smoking cessation
•Bronchodilators

9. Smoking Cessation
There are 4 principal pharmacologic approaches to the problem:
1. Bupropion.
2. Nicotine replacement therapy available as
gum, transdermal patch, inhaler, and nasal
spray; and
3. Varenicline, a nicotinic acid receptor
agonist/antagonist.
4. Nortriptyline

10. Bronchodilators
•Anticholinergics
•B2 Agonists
Inhaled bronchodilators are the
mainstay of COPD management
Note:
•However no evidence that regular bronchodilator
use slows deterioration of lung function.
•Anticholinergics have a greater bronchodilating
effect than b2 agonists.

11. B Agonists
• Side effects: tremor and tachycardia
SABA Inhaler /mdi For nebuliser DOA (hr)
Salbutamol 100,200 mcg 5 mg/ml 4-6
Levalbuterol
Albuterol
Pirbuterol
Terbutaline
LABA Inhaler (mcg) Oral DOA (hr)
Salmeterol 25-50 12
Formeterol
Bambuterol
Indacarterol
10-20 mg od

12. Anticholinergics
• Side effects: urinary retention, and dry mouth,tremor and
tachycardia
SAA Inhaler For nebuliser
mg/ml
DOA (HR)
Ipratropium 20,40
MDI
0.25-0.5 6-8
Oxitropium 100
MDI
1.5 7-9
LAA Inhaler
(mcg)
Oral DOA (hr)
Tiotropium 18 DPI 24

13. Steroids in Stable Copd
• Inhaled Glucocorticoids
• Oral Glucocorticoids
•In COPD, inhaled GCs are used as part of a
combined regimen, but should NOT be used as sole
therapy for COPD (ie, without long-acting BDs).
•Regular Rx improves symptoms, lung function and
quality of life and reduce frequency of
exacerbations in COPD with FEV1 <60% but
however does not modify long term decline of
FEV1 nor mortality .

14. Inhaled Glucocorticoids
•Their use has been A/W ↑ rates of
oropharyngeal candidiasis & an ↑ rate of loss
of bone density.
•A trial of inhaled GC should be considered in
patients with frequent exacerbations,
defined as ≥2/yr, and in pts who
demonstrate a significant amount of acute
reversibility in response to inhaled BD.

15. Oral Glucocorticoids
•The chronic use of oral GCs for Rx of COPD is
not recommended because of an
unfavorable benefit/risk ratio.
•The chronic use of oral GCs is a/W significant
side effects, including osteoporosis, weight
gain, cataracts, glucose intolerance, & ↑ risk
of infection.

16. Theophylline(methylxanthine)
•Theophylline produces modest improvements in
expiratory flow rates and vital capacity and a slight
improvement in arterial o2 and Co2 levels in
patients with moderate to severe COPD.
•Nausea is a common SE; tachycardia and tremor
have also been reported.
•MX are less effective and less well tolerated than
long acting inhaled bronchodilators and is not
recommended if others r available & affordable.
•Addition of low dose slow release theophylline
may be given along with long acting BDs.

17. Phosphodiesterase 4 inhibitors
•Once a day dosage :No direct bronchodilator
activity but has shown to improve FEV1 in pts
treated with salmeterol or tiotropium.
•Roflumilast ↓ moderate to severe exacerbations
treated with CSs by 15-20 % in pts with ch
bronchitis, severe and very severe COPD and a
Hx of A/E.
•S/e: nausea, pain abodmen, diarrhea, insomnia
•Note: Roflumilast & Theophylline shouldnot be given
together.

18. Vaccination
•All Patients with COPD should receive the
influenza vaccine annually.
•Polyvalent pneumococcal vaccine is also
recommended, (in pt ≥65 yrs old or <65 +
Fev1 <40 %)

19. Others
Not recommended in stable copd by ATS, BTS,
ETS,GOLD
1. Mucokinetics and antioxidants (n-
acetylcysteine)
2. Antitussive
3. vasodilators like nitric oxide
4. Drugs to treat pulmonary hypertension (ETA)
5. Nedochromil (mast cell stabilizer)
6. Monteleukast (leukotriene modifier)
7. Antibiotics

20. Others
•Specific treatment in the form of IV a1AT
augmentation therapy is available for
individuals with severe a1AT deficiency.
•Eligibility for a1AT augmentation therapy
requires a serum a1AT level <11 uM
(approximately 50 mg/dL).

21. Oxygen (>15 hrs /day)
• Supplemental O2 is the only pharmacologic therapy demonstrated
to unequivocally decrease mortality rates in patients with COPD.
1. PaO2 ≤ 7.3 kPa (55 mmhg) or SaO2 <88%, with or without
hypercapnia confirmed twice over a 3 week period.
2. PaO2 :7.3 -8.0 kPa (55-60 mmhg) or SaO2 of 88%, if there is
evidence of pulmonary HTN, peripheral edema s/o CCF, or
polycythemia (HCT>55%).

22. Lung Volume Reduction Surgery (LVRS)
• Sx to reduce the vol of lung in pts with emphysema was first
introduced with minimal success in 1950s and was
reintroduced in the 1990s.
• Patients are excluded if they have significant pleural disease,
a pulmonary artery systolic pressure >45 mmHg, extreme
deconditioning, congestive heart failure, or other severe
comorbid conditions. Patients with an FEV1 <20% of
predicted and either diffusely distributed emphysema on CT
scan have an increased mortality rate after the procedure
and thus are not candidates for LVRS.
• Patients with upper lobe–predominant emphysema and a
low postrehabilitation exercise capacity are most likely to
benefit from LVRS.

23. Lung Transplantation
•Current recommendations are that
candidates for lung transplantation should be
<65 years; have severe disability despite
maximal medical therapy; and be free of
comorbid conditions such as liver, renal, or
cardiac disease.

24. Treatment line begins after assessment of
severity of the condition
Postbronchodilator FEV1/FVC <0.7 defines Airflow limitation
Low
risk
High
Risk
3 yr mortality =24%

25. Final: Steps in management
Clinical diagnosis
Spirometry
Gold severity stage
Drugs a/t stages

26. Stage Management
All - Avoidance of risk factor(s)
- Influenza vaccination
- Pneumococcal vaccination
Stage 1 Short-acting bronchodilator when needed
Stage 2 Short-acting bronchodilator when needed
Regular treatment with one or more long-acting bronchodilators
Stage 3 Short-acting bronchodilator when needed
Regular treatment with one or more long-acting bronchodilators
Inhaled glucocorticoids if significant symptoms, lung function response, or if
repeated exacerbations
Stage 4 Short-acting bronchodilator when needed
Regular treatment with one or more long-acting bronchodilators
Inhaled glucocorticoids if significant symptoms, lung function response, or if
repeated exacerbations
Treatment of complications
Long-term oxygen therapy if chronic respiratory failure
Consider surgical treatments

27. Important questions for MBBS
• Define COPD and mention its components ?
• Pathophysiology of Emphysema and mention the types of
emphysema?
• Bed side examination findings of Emphysema ?
• List Differential diagnosis of Acute onset of Dyspnea ?
• Define Dyspnea and list Modified MRC Dyspnea scale.
• List the muscles used for Normal and forceful respiration.
• Mention GOLD staging ,the spirometric classification of COPD .
• What are the four variables used in BODE index?
• Management of Stable phase of COPD.
• Management of COPD on Exacerbation.

28. Terms
• Dyspnea: Dyspnea is a term used to characterize a subjective
experience of breathing discomfort that is comprised of qualitatively
distinct sensations that vary in intensity.
• Orthopnea: Dyspnea that worsens in lying flat position and gets
relieved by sitting position.
• Platypnea: Dyspnea that is relieved when lying down, and worsens
when sitting or standing up.
• Trepopnia: Dyspnea while lying on one side but not on the other
(lateral recumbent position)
• Tachypnea: refers to abnormally fast breathing rate.
• Bradypnea: refers to abnormally slow breathing rate.

29. General appearance:
• On GE , my patient who is in upright position (sitting by the
edge of the bed),appears to be thinly built ,his bmi is …..kg/m2..
• He is conscious and well oriented to person place and time. His
speech is normal can complete a full sentence in one breath
and there is no hoarseness in voice.
• Patient is on oxygen therapy via nasal prongs. And there are
sputum cup and inhalers by his side.
• There is flaring of ala nasae and purse lip breathing and
accessory muscle like sternocledomastoid are active.
• There is supraclavicular hollowing and Tracheal tug is present.
• There is also indrawing of intercostal muscles (or retraction of
lowermost intercostal spaces are evident) but however audible
noises like wheeze or stridor are not heard from the end of the
bed.

30. General appearance:…continue
• The respiration is regular but labored and the rate is 22/m and FET is more than 6
sec.
(Respiration : comment on :rate ,rhythm, depth and effort ,If Normal: Respiration is quiet and
regular with normal depth and effortless. Rate is 14 /m and FET is less than 6 seconds.)
• There is no pallor, no icterus and no cyanosis and oral cavity seems normal. There
is no lymphadenopathy and JVP is not raised .
• His bp 120/80 mmhg ,axillary temperature is…and pulse is 80/m seems normal in
volume and character. All peripheral pulses are present and the condition of arterial
wall seems normal.
• On examination of Hands
• There is no clubbing , no peripheral cyanosis, and no palmar erythema.
• There is fine tremors when examined on outstretch hands but there is no flapping
tremors.
• (note: palmar erythema and a course flapping tremor , Warm hands with dilated veins ,
bounding pulses ,are signs of of CO2 retention. And a fine tremor is associated with beta 2
agonist use. Also look for other points like, wasting of the small muscles of the hand (Pancoast
tumour) and nicotine stains.
• Pain and/or swelling of hands/wrists suggesting possible hypertrophic pulmonary
osteoarthropathy.)

31. COPD on AE
• The goal of treatment in COPD AE is minimize the impact of current
exacerbation and to prevent the development of subsequent
exacerbations.
Signs of Severity

32. Exacerbation of COPD
• The Global Initiative for COPD(GOLD), a report produced by the
National Heart, Lung, and Blood Institute (NHLBI) and the WHO,
defines an exacerbation of COPD as an acute increase in symptoms
beyond normal day-to-day variation. This generally includes an acute
increase in one or more of the following cardinal symptoms:
1. Cough increases in frequency and severity
2. Sputum production increases in volume and/or changes character
3. Dyspnea increases

33. Common bacteria are;
• Haemophilus influenzae
• Moraxella catarrhalis
• Streptococcus pneumoniae
• Pseudomonas aeruginosa
• Enterobacteriaceae
• Haemophilus parainfluenzae
• Staphylococcus aureus
(Note: Despite the frequent implication of bacterial infection, chronic
suppressive or "rotating" antibiotics are not beneficial in patients with
COPD and is not recommended.)
Most common cause is viral upper RTI

34. Criteria for hospitalization
American Thoracic Society/European Respiratory Society (ATS/ERS)
• Inadequate response of symptoms to outpatient management
• Marked increase in dyspnea
• Inability to eat or sleep due to symptoms
• Worsening hypoxemia
• Worsening hypercapnia
• Changes in mental status
• Inability to care for oneself (ie, lack of home support)
• Uncertain diagnosis
• High risk comorbidities including pneumonia, cardiac arrhythmia, heart
failure, diabetes mellitus, renal failure, or liver failure
• In addition, there is general consensus that acute respiratory acidosis
justifies hospitalization.

35. Bronchodilators
•Typically, patients are treated with an
inhaled b-agonist, often with the
addition of an anticholinergic agent.
•Patients are often treated initially with
nebulized therapy, as such treatment is
often easier to administer in older
patients or to those in respiratory
distress.

36. Antibiotics
• Inexpensive common oral antibiotics usually adequate .Broader
spectrum if not responsive.
Glucocorticoids
• Among patients admitted to the hospital, the use of glucocorticoids
has been demonstrated to reduce the length of stay, hasten recovery,
and reduce the chance of subsequent exacerbation or relapse for a
period of up to 6 months.
• The GOLD guidelines recommend 30–40 mg of oral prednisolone or
its equivalent for a period of 10–14 days.

37. Oxygen
•Target Pao2: 60-70 mmhg
•Nasal cannulae can provide flow rates up to 6 L
/min with an associated FiO2 of approximately 40 %
•Simple facemasks can provide an FiO2 up to 55 %
using flow rates of 6 to 10 L per minute.
•Venturi masks can deliver an FiO2 of 24, 28, 31, 35,
40, or 60 percent.
•Non-rebreathing masks with a reservoir, one-way
valves, and a tight face seal can deliver an inspired
oxygen concentration up to 90 %.

39. Noninvasive Mechanical Ventilatory Support

40. Contraindications to NIPPV
• cardiovascular instability,
• impaired mental status or inability to cooperate,
• copious secretions or the inability to clear secretions,
• craniofacial abnormalities
• extreme obesity,
• or significant burns.

41. Causes of Chronic cough
A chronic cough is usually defined as a cough that lasts for eight weeks or longer.

42. ECG changes in COPD
• P pulmonale (right atrial enlargement)
• Low voltage QRS
• Right axis deviation
• Right bundle branch block (usually due to RVH)
• Poor progression of R waves in precordial leads

43. References
1. Global strategy for the diagnosis, management,
and prevention of copd . Updated 2014
2. Harrison's Principles of Internal medicine .18th
edition
3. Davidson's Principles and practice of Medicine
.21st edition.
4. Uptodate version 20.3
5. Mercksmannual