Chronic obstructive pulmonary disease (COPD) is a common lung disease characterized by airflow limitation and tissue destruction due to chronic inflammation from smoke exposure. Symptoms include cough, dyspnea, and sputum production that worsen over time. The diagnosis is confirmed by spirometry showing airflow limitation that is not fully reversible with treatment. Management includes smoking cessation, pulmonary rehabilitation, inhaled bronchodilators and corticosteroids to control symptoms and reduce exacerbations.

1. Chronic Obstructive
Pulmonary Disease
(COPD)
KRVS Chaitanya

2. Introduction
• Chronic obstructive pulmonary disease (COPD) is a
common and treatable disease characterized by
progressive airflow limitation and tissue destruction.
• It is associated with structural lung changes due to
chronic inflammation from prolonged exposure to
noxious particles or gases most commonly cigarette
smoke.

3. • Chronic inflammation causes airway narrowing and
decreased lung recoil.
• The disease often presents with symptoms of
cough, dyspnoea, and sputum production.
• Symptoms can range from being asymptomatic
to respiratory failure

5. Epidemiology
• COPD is primarily present in smokers and those greater age 40.
• Prevalence increases with age and it is currently the third most
common cause of morbidity and mortality worldwide.
• In 2015, the prevalence of COPD was 174 million and there
were approximately 3.2 million deaths due to COPD worldwide.
• However, the prevalence is likely to be underestimated due to
the under diagnosis of COPD.

6. Etiologic
• COPD is caused by prolonged exposure to harmful particles or
gases.
• Cigarette smoking is the most common cause of COPD
worldwide.
• Other causes may include second-hand smoke, environmental
and occupational exposures, and alpha-1 antitrypsin deficiency
(AATD).

8. Mechanism of Injury / Pathological
Process
• COPD is an inflammatory condition involving the
airways, lung parenchyma, and pulmonary vasculature.
• Emphysema describes one of the structural changes seen in
COPD where there is destruction of the alveolar air sacs (gas-
exchanging surfaces of the lungs) leading to obstructive
physiology.

10. • The process is thought to involve oxidative stress and protease-anti
protease imbalances.
• In emphysema, an irritant (e.g., smoking) causes
an inflammatory response.
• Neutrophils and macrophages are recruited and release multiple
inflammatory mediators.
• Oxidants and excess proteases lead to the destruction of the air sacs.
• The protease-mediated destruction of elastin leads to a loss of elastic
recoil and results in airway collapse during exhalation.

11. • The inflammatory response and obstruction of the airways
cause a decrease in the forced expiratory volume(FEV1) and
tissue destruction leads to airflow limitation and impaired gas
exchange.
• Hyperinflation of the lungs is often seen on imaging studies
and occurs due to air trapping from airway collapse during
exhalation.
• The inability to fully exhale also causes elevations in carbon
dioxide (CO2) levels.

12. • With disease progression the reduction in ventilation or
increase in physiologic dead space leads to CO2 retention.
• Acute exacerbations of COPD are common and usually occur
due to a trigger (e.g., bacterial or viral pneumonia ,
environmental irritants).
• There is an increase in inflammation and air trapping often
requiring corticosteroid and bronchodilator treatment.

13. Clinical Presentation
• COPD will typically present in adulthood and often during the
winter months.
• Patients usually present with complaints of chronic and
progressive dyspnoea, cough, and sputum production.
• Patients may also have wheezing and chest tightness.
• While a smoking history is present in most cases, there are
many without such history.

14. • They should be questioned on exposure to second-hand
smoke, occupational and environmental exposures, and family
history.
• COPD is a complex interaction between asthma, chronic
bronchitis, and emphysema.

15. Evaluation
• COPD is often evaluated in patients with relevant
symptoms and risk factors.
• The diagnosis is confirmed by Spirometry.
• Other tests may include a
– 6-minute Walk Test
– Laboratory Testing
– Radiographic Imaging.

16. Spirometry

17. • Assessment - A diagnosis of COPD should be
considered in patients over the age of 35 who have a
risk factor (generally smoking) and who present with
exertional breathlessness, chronic cough, regular
sputum production, frequent winter ‘bronchitis’ or
wheeze.
• X-Ray - An x-ray of the chest may show an over-
expanded lung (hyperinflation) and can be useful to
help exclude other lung diseases.

19. 3. Pulmonary function tests - Essential in the
diagnosis, staging, and monitoring of COPD.
– Spirometry is performed before and after
administering an inhaled bronchodilator.
– Inhaled bronchodilators may be a short-acting
beta2-agonist (SABA), short-acting
anticholinergic, or a combination of both.

20. • A ratio of the forced expiratory volume in one second to
forced vital capacity (FEV1/FVC) less than 0.7 confirms the
diagnosis of COPD.
• Patients with a significantly reduced FEV1 and signs of
dyspnea should be evaluated for oxygenation with
pulse oximetry or arterial blood gas analysis.

21. 4. Blood tests -
• A blood sample taken from an artery can be tested for blood
gas levels which may show low oxygen levels (hypoxemia)
and/or high carbon dioxide levels (respiratory acidosis).
• A blood sample taken from a vein may show a
high blood count (reactive polycythemia), a reaction to long-
term hypoxemia.

23. Outcome Measures
• There can be a different number of ways of measuring the
impact or change of someone's COPD, examples being from
lung function, lung volumes and exercise capacity.
• A cross-sectional study recommends cardiopulmonary
exercise testing (CPET) as an efficient tool in assessing
functional capacity and prognosis in Heart Failure and COPD
patients.

24. Other outcome measures include:
• Bleep Test; Shuttle Walk Test; Ergometry; BORG RPE; 6-
minute walk test is commonly performed to assess the
submaximal functional capacity of a patient.
• This test is performed indoors on a flat and straight surface.
• The length of the hallway is usually 100 feet and the test
measures the distance the patient walks over a period of 6
minutes; Grip Strength; 30 second Sit to stand.

25. • According to a longitudinal study, changes in frailty status of
COPD patients were associated with significant clinical
outcomes related to: dyspnea; mobility; physical activity;
handgrip and quadriceps strength.
• It was found that five-times sit-to-stand and exacerbations
were independent predictors of the improvement in frailty
status.

26. Management / Interventions
• The primary goals of treatment are to control symptoms,
improve the quality of life, and reduce exacerbations and
mortality.
• The non-pharmacological approach includes smoking
cessation and pulmonary rehabilitation.
• Annual influenza vaccination is recommended in all patients
with COPD.

27. Treatment options
PHARMACOLOGICAL THERAPY NON PHARMACOLOGICAL THERAPY
Bronchodilators Pulmonary rehabilitation
Corticosteroids (Inhalations/systemic) Patient education
Phosphodiesterase 4 inhibitors Nutrition management
Antibiotics Oxygen therapy
Methylxanthines Ventilatory support
Surgical treatment, endoscopic treatment

28. The classes of commonly used medications in COPD include:
1. Bronchodilators (beta2-agonists, antimuscarinics,
methylxanthines),
2. Inhaled corticosteroids (ICS) and systemic glucocorticoids,
3. Phosphodiesterase-4 (PDE4) inhibitors,
4. Antibiotics.

30. Management of stable COPD

31. Pharmacological therapy

33. Exercise
• Exercise prescription is a key component of pulmonary rehabilitation
programmes, which are part of the non-pharmacological approach to
managing COPD.
• There is a high level of evidence for the benefits of pulmonary
rehabilitation for people with COPD Strength and endurance exercise are
endorsed for people with COPD.
• Use of protein supplements, in combination with exercise, could also be
beneficial, refer to dietician.

34. • Muscles that are required for arm exercise are also involved in
movement of the chest wall during respiration and thus the
need to breathe often compromises the individual’s ability to
undertake daily activities, therefore exercise prescription
involving arm exercise needs to be carefully prescribed.

35. Promote Effective Inhaled Therapy
• In people with stable COPD who remain breathless or have exacerbations
despite use of short-acting bronchodilators as required, offer the following as
maintenance therapy:
– If forced expiratory volume in 1 second (FEV1)≥50% predicted: either
long-acting beta2 agonist (LABA) or long-acting muscarinic antagonist
(LAMA)
– If FEV1<50% predicted: either LABA with an inhaled corticosteroid (ICS)
in a combination inhaler, or LAMA
• Offer LAMA in addition to LABA + ICS to people with COPD who remain
breathless or have exacerbations despite taking LABA + ICS, irrespective of
their FEV1.

36. Provide Pulmonary Rehabilitation
• Pulmonary rehabilitation (PR) should be made available to all
appropriate people with COPD including those who have had a
recent hospitalisation for an acute exacerbation.
• A randomised study suggests positive outcomes with functional
electro stimulation in patients with severe chronic obstructive
pulmonary disease hospitalized for acute exacerbation.
• A study suggests that patients affected with COPD and pulmonary
hypertension experience a lower exercise capacity and quality of
life.

37. • Another randomized controlled trial examining the effects of virtual
training (VR) and exercise training on the rehabilitation of patients with
COPD suggests that pulmonary rehabilitation program supplemented with
VR training has positive outcomes in improving physical fitness in patients
with COPD.
• Studies suggest PR was useful in patients with moderate to severe COPD.
• A prospective, multisite, randomised controlled trial will determine whether
an 8-week PR programme (exercise training will comprise: over ground or
treadmill walking, lower limb stationary cycling, lower and upper limb
strengthening exercises) is equivalent to a 12-week PR programme in
people with COPD.

38. Palliative Setting
• Opioids should be used when appropriate for the palliation of
breathlessness in people with end-stage COPD unresponsive to
other medical therapy
• Use benzodiazepines, Tricyclic antidepressants, major
tranquillisers and oxygen to treat breathlessness
• Provide access to multidisciplinary palliative care teams and
hospices

39. Thank You