This document provides an overview of chronic obstructive pulmonary disease (COPD). It defines COPD as a progressive lung disease characterized by airflow limitation. The document discusses the causes of COPD, including cigarette smoking which is the primary cause in over 90% of patients. It also examines the pathophysiology of the two main types of COPD - chronic bronchitis and emphysema. The clinical evaluation and diagnostic tests used to diagnose COPD are outlined, including the use of spirometry to confirm airflow limitation. Treatment objectives for COPD and its management are briefly mentioned.

1. CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
(COPD)
RAHIL DALAL

2. Introduction:
•Definition:
According to Global Initiative for Chronic Obstructive Lung Disease
(GOLD),
“COPD is characterized by persistent airflow limitation that is usually
progressive and associated with an enhanced chronic inflammatory
response in the airways and the lung to noxious particles or gases.
Exacerbations and comorbidities contribute to the overall severity in
individual patients.”

3. Introduction:
• COPD includes emphysema, an anatomically defined condition
characterized by destruction and enlargement of the lung alveoli; chronic
bronchitis, a clinically defined condition with chronic cough (> 30 ml
sputum in 24 hours for atleast 3 months in a year for 2 consecutive years)
and phlegm; and small airways disease, a condition in which small
bronchioles are narrowed.
• COPD is present only if chronic airflow obstruction occurs; chronic
bronchitis without chronic airflow obstruction is not included within COPD.
•4th leading cause of death worldwide!!!!

4. Etiology / Cause:
•Cigarette smoking:
primary causal factor
Present in >90% patients
Components of tobacco smoke activate inflammatory cells, which produce
and release the inflammatory mediators characteristic of COPD.
• α1 – antitrypsin (AAT) deficiency:
A primary role of AAT is to protect cells, especially those in the lung, from
destruction by elastase released by neutrophils. In fact, AAT may be
responsible for 90% of the inhibition of this destructive enzyme

5. Etiology / Cause:
•Exposure to multiple environmental toxins increases the risk of COPD.
Thus, the total burden of inhaled particles (e.g., cigarette smoke as well as
occupational and environmental particles and pollutants) can play a
significant role in the development of COPD. In such cases, it is helpful to
assess an individual’s total burden of inhaled particles. For example, an
individual who smokes and works in a textile factory has a higher total
burden of inhaled particles than an individual who smokes and has no
occupational exposure.

7. Pathophysiology: Chronic Bronchitis
a. Respiratory tissue inflammation results in vasodilation, congestion, mucosal edema,
and goblet cell hypertrophy. These events trigger goblet cells to produce excessive
amounts of mucus.
b. Changes in tissue include increased smooth muscle, cartilage atrophy, infiltration of
neutrophils and other cells, and impairment of cilia.
c. Airways become blocked by thick, tenacious mucous secretions, which trigger a
productive cough.
d. Normally, sterile airways can become colonized with Streptococcus pneumoniae,
Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, and
Pseudomonas aeruginosa species. Recurrent lung infections (viral and bacterial) reduce
ciliary and phagocytic activity, increase mucus accumulation, weaken the body’s
defenses, and further destroy small bronchioles.

8. Pathophysiology: Chronic Bronchitis
e. As the airways degenerate, overall gas exchange is impaired, causing exertional
dyspnea.
f. Hypoxemia results from a V/Q imbalance and is reflected in an increasing arterial
carbon dioxide tension (i.e., increasing Paco2).
g. Sustained hypercapnia (increased Paco2) desensitizes the brain’s respiratory control
center and central chemoreceptors. As a result, compensatory action to correct
hypoxemia and hypercapnia (i.e., a respiratory rate or depth increase) does not occur.
Instead, hypoxemia serves as the stimulus for breathing. Use of narcotics or
benzodiazepines, especially in combination, should be done cautiously in these patients
to avoid respiratory failure.

9. Pathophysiology: Emphysema
a. Anatomical changes are the result of loss of tissue elasticity.
(1) Inflammation and excessive mucus secretion (as from long-standing chronic bronchitis)
cause air trapping in the alveoli. This contributes to breakdown of the bronchioles, alveolar
walls, and connective tissue.
(2) As clusters of alveoli merge, the number of alveoli diminishes, leading to increased space
available for air trapping.
(3) Destruction of alveolar walls causes collapse of small airways on exhalation and disruption of
the pulmonary capillary beds.
(4) These changes result in V/Q abnormalities; blood is shunted away from destroyed areas to
maintain a constant V/Q ratio, unlike the case in chronic bronchitis.
(5) Hypercapnia and respiratory acidosis are uncommon in emphysema because V/Q imbalance
is compensated for by an increased respiratory rate.

10. Pathophysiology: Emphysema
b. There are specific regions of the lung in which characteristic anatomical changes of
emphysema occur.
(1) In centrilobular (centriacinar) emphysema associated with cigarette smoking,
destruction is central, selectively involving respiratory bronchioles. Typically,
bronchioles and alveolar ducts become dilated and merge.
(2) In panlobular (panacinar) emphysema, all lung segments are involved. The alveoli
enlarge and atrophy, and the pulmonary vascular bed is destroyed. This form of
emphysema is associated with AAT deficiency.
(3) In paraseptal emphysema, the lung periphery adjacent to fibrotic regions is the site
of alveolar distention and alveolar wall destruction. This is associated with spontaneous
pneumothorax.

11. Clinical Evaluation – Physical findings
a. Predominant chronic bronchitis typically has an insidious onset after age 45.
(1) A chronic productive cough is the hallmark of chronic bronchitis. It occurs first in
winter, then progresses to year-round. It is usually worse in the morning. Smoking
cessation can help lessen the productive cough.
(2) Exertional dyspnea, the most common presenting symptom, is progressive.
However, the severity of this symptom may not reflect the severity of the disease.
(3) Other common findings include obesity, rhonchi and wheezes on auscultation,
prolonged expiration, and a normal respiratory rate. As the disease progresses, right
ventricular failure is common, which presents as jugular venous distention, peripheral
edema, hepatomegaly, and cardiomegaly. Because patients tend to develop cyanosis,
the term blue bloater is sometimes used to describe patients with chronic bronchitis.

12. Clinical Evaluation – Physical findings
b. Predominant emphysema has an insidious onset, and symptoms occur after age 55.
(1) The cough is chronic but less productive than in chronic bronchitis.
(2) Exertional dyspnea is progressive, constant, severe, more characteristic of
emphysema than chronic bronchitis.
(3) Other common findings include weight loss, tachypnea, pursed-lip breathing,
prolonged expiration, accessory chest muscle use, hyperresonance on percussion,
diaphragmatic excursion, and diminished breath sounds. Because patients are able to
maintain reasonably good oxygenation because of their tachypnea, the term pink puffer
is sometimes used to describe patients with emphysema.

13. Clinical Evaluation – Physical findings
c. Patients may have elements and physical findings from each of these disease
simultaneously.
Comorbidities such as CHF, CAD, stroke, DM, and depression are common in COPD
patients.

14. Clinical Evaluation – Diagnostic tests
a. COPD patients with characteristic symptoms of cough, dyspnea, sputum production,
and/or exposure to known risk factors (e.g., smoking) should be evaluated for a COPD
diagnosis.
If the patient has FEV1/FVC 70% and a postbronchodilator FEV1 80% predicted, he or
she has airflow limitation that is not fully reversible.
Patients with a smoking history (e.g., 20 pack/year history and 45 years old) should be
considered for the diagnosis.
Spirometry can be used to help make the diagnosis.

15. Clinical Evaluation – Diagnostic tests
b. Chronic bronchitis
(1) Blood analysis may reveal polycythemia as a result of to erythropoiesis secondary to
hypoxemia. With bacterial infection, the WBC count may be increased.
(2) Sputum inspection reveals thick purulent or mucopurulent sputum tinged yellow,
white, green, or gray; an acute change in color and/or quantity suggests infection.
(3) Arterial blood gas studies may show a markedly decreased Pao2 level (45 to 60 mm
Hg), reflecting hypoxemia, and a Paco2 level that is normal or elevated (50 to 60 mm
Hg), reflecting hypercapnia.

16. Clinical Evaluation – Diagnostic tests
b. Chronic bronchitis (contd.)
(4) Pulmonary function tests may be normal in the early disease stages. Later, they
show a reduced FEV1/FVC ratio, increased residual lung volume, a decreased vital
capacity, and a decreased FEV1. Unlike emphysema, chronic bronchitis patients tend to
have normal diffusing capacity, normal static lung compliance, and normal TLC.
(5) Chest radiograph typically identifi es lung hyperinfl ation, a barrel chest, and
increased bronchovascular markings.
(6) An ECG may reveal right ventricular hypertrophy and changes consistent with cor
pulmonale.

17. Clinical Evaluation – Diagnostic tests
c. Emphysema
(1) Sputum inspection reveals scanty sputum that is clear or mucoid. Infections are less
frequent than in chronic bronchitis.
(2) Arterial blood gas studies typically indicate a reduced or normal Pao2 level (65 to 75
mm Hg) and, in late disease stages, an increased Paco2 level (50 to 60 mm Hg).
(3) Pulmonary function tests show a reduced FEV1/FVC ratio, normal or increased static
lung compliance, reduced FEV1 and diff using capacity, and increased TLC and RV.
(4) Chest radiograph usually reveals bullae, blebs, a flattened diaphragm, lung
hyperinflation, vertical heart, enlarged anteroposterior chest diameter, decreased
vascular markings in the lung periphery, and a large retrosternal air space.

19. Treatment: Objectives

20. Treatment: Management