Year II Pulmonary System



Ahmet Baydur, MD (baydur@usc,edu) August 29 and September 5, 2019

Chronic Obstructive Pulmonary Disease (COPD)

Objectives:

By the end of the presentation the student should be able to:

1. Describe the up-to-date definition of chronic obstructive pulmonary disease as an inflammatory disease state.

2. List at least four factors which place a person at risk for developing COPD

3. Describe important clinical features of COPD. Be familiar with the overlapping pathophysiologic and clinical characteristics of individuals with features of emphysema and chronic bronchitis.

4. List key abnormalities of pulmonary function in a patient with COPD. Identify differences in flow-volume curve patterns in people with obstructive, restrictive, and extrathoracic obstructive respiratory disorders.

5. Describe the complications that affect quality of life and longevity in COPD.

6. Explain the pathogenesis of cor pulmonale and how it relates to chronic hypoxemia and structural changes in COPD.

7. Discuss key therapeutic modalities in the management of COPD, including pulmonary rehabilitation.

Strongly recommended reading material:

1. Weinberger SE, Cockrill BA, Mandel J. Principles of Pulmonary Medicine, 5th Edition (2008), Saunders, Philadelphia, PA, ch. 6, Chronic Obstructive Pulmonary Disease, pp. 90-109. Also available on-line: .

2. West JB, Pulmonary Pathophysiology: The Essentials (2013), ch. 4, Chronic Obstructive Pulmonary Disease, pp. 47-73. This reference has excellent study questions at the end of the chapter, and should be reviewed.

3. Global Strategy for the Diagnosis, Management, and Prevention of Chronic

Obstructive Pulmonary Disease (GOLD). Available from:

http//guidelines-global-strategy-for-diagnosis-

management.html (updated 2018).

Case presentation 1:

A 65-yr-old man with an 80-pack-year history of smoking complains of shortness of breath on exertion of several months’ duration. On inspection, there is increased anteroposterior diameter of the chest, pursed lips, and dyspnea during conversation. He is unable to complete more than 4 or 5 words at a time. On physical examination, the patient is noted to be tachycardic, have hyperresonant lungs with decreased breath sounds, no crepitations (râles), and no hepatomegaly or liver nodules on palpation. Which of the following conditions is the most likely diagnosis?

A. Alpha-1-antitrypsin deficiency

B. Asthma

C. Bronchiectasis

D. Centriacinar emphysema

E. Chronic bronchitis

F. Panacinar emphysema

Chronic Obstructive Pulmonary Disease (COPD)

I Synonymous Terms:

Chronic Obstructive Lung Disease (COLD), Chronic Airway Obstruction (CAO)

II Definitions

• Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.

• The chronic airflow limitation that is characteristic of COPD is caused by a mixture of small airways disease (e.g., obstructive bronchiolitis) and parenchymal destruction (emphysema), the relative contributions of which vary from person to person.

(GOLD definition, updated, 2017, ref. 3, above).

Most clinicians still use the following classifications to distinguish different forms of COPD based on symptoms, imaging and pathologic findings:

A. Chronic Bronchitis – chronic production of cough for 3 months in each of at least two successive years in a patient in whom all other causes of cough have been excluded.

B. Emphysema – abnormal permanent destructive enlargement of airspaces distal to the terminal bronchioles, accompanied by loss of alveolar attachments. The normal acinus loses its orderly appearance and may even become totally lost. Emphysema can now be precisely quantitated using high resolution CT scanning.

C. Small Airway Disease – Inflammation and narrowing of the peripheral airways, sometimes associated with cough and/or exertional shortness of breath. It can be detected by subtle changes in pulmonary function testing.

Most patients with COPD exhibit overlapping features of the above descriptions. Recent studies have further subdivided COPD into clinical phenotypes based on numbers of exacerbations, presence of plasma and intraalveolar inflammatory biomarkers, and imaging characteristics using high resolution CT scanning – this is still an area in flux and it may be years before consensus is reached on their usefulness in determining the best treatment for patients with specific features.

III Epidemiology

A. Prevalence --

1. About 12-14 million adults suffer from COPD in the U.S.

2. Women comprise about 52 % of that number (last 14 years).

3. Prevalence seems highest in Midwest and Southeast states.

B. Mortality

1. In 2011, there were approximately 135,000 deaths due to COPD in

the U.S. - third leading cause of death, behind cancer and heart disease .

2. Nearly 80% of COPD deaths are in non-Hispanic whites; Hispanics

exhibit the least number of deaths with approximately 3,700.

(Data from American Lung Association, Epidemiology and Statistics Unit, Research and Health Education Division, March 2013)

IV Risk Factors for COPD

1. Tobacco smoke is by far the most important cause of COPD:

a. Age of starting, total pack-years and current smoking status are all predictive of mortality.

b. It accounts for over 90% of all COPD risk factors in developed countries, and is of growing concern in developing nations.

2. Passive smoking (second hand smoke) — children of parents who smoke have more respiratory symptoms and disease than those of nonsmoking parents.

3. Ambient air pollution causes harm to persons with heart and lung disease. (fumes from gasoline engines and particulate matter from diesel exhaust increase respiratory symptoms and disease).

4. Inhalation of smoke from biomass fuels in developing countries is an important cause of COPD, particularly among women who cook in poorly ventilated homes.

5. Hyperresponsive airways

Asthma may progress to COPD through remodelling of airways.

6. Sex, race, socioeconomic status

a. Higher prevalence in women in recent years

b. Higher prevalence among lower levels of income and education.

7. Occupation – Exposure to inhaled environmental toxins is especially lethal

for smoking workers (petroleum products, pesticides, construction materials, cadmium and other heavy metal dusts)

8. Bacterial Infection and Pathogenesis of COPD.

a. Childhood infection and adult lung function

b. Vicious circle hypothesis (Fig.1)

c. Bacterial infection and chronic mucus hypersecretion

d. Bacterial infection and mucociliary clearance

e. Bacterial infection and airway epithelial injury ( Fig. 2 )

f. Bacterial infection and airway inflammation ( Fig. 2 )

g. Chronic bacterial infection of respiratory tissues ( Fig. 2 )

h. Intracellular Hemophilus influenza infection of respiratory tissues

i. Chronic Chlamydia Pneumoniae infection in COPD

9. Genetic / Molecular factors

COPD develops in only a minority of heavy smokers (10% to 20%), indicating that there are differences in individual susceptibility to the effects of tobacco smoking:

A. Alpha 1 – antitrypsin (anti-protease) deficiency –

A. a. The only definitely proven genetic abnormality leading to COPD.

B. Associated with lower lobe and panlobular emphysema.

C. b. Over 95% of persons with A1AT deficiency are homozygous for

D. the Z allele, i.e., PiZZ, but it is rare.

c. Those with heterozygous deficiency (PiMZ) may also become affected with increased airway hyperreactivity, but not all necessarily progress to COPD.

B. Genome studies have identified genetic links (polymorphisms) with specific clinical phenotypes of COPD, such as emphysema, chronic bronchitis (both with and without acute exacerbations), and asthma-COPD overlap syndrome (ACOS).

V. Clinical characteristics

A. History:

1. Smoking at least one pack of cigarettes daily for 20 years.

2. Cough with mucoid to mucopurulent sputum, seen especially with acute exacerbations. Most patients do not experience fever, chills or sweats – if they do, consider development of pneumonia complicating the COPD, particularly if sputum production increases and/or turns green, sometimes with blood streaking.

3. Dyspnea (breathlessness) – first with exertion then progressively at rest.

Exercise intolerance is due to many contributing factors:

a. Ventilatory limitation – due to hyperinflation, dead-space

ventilation, impaired gas exchange, deconditioning, peripheral

muscle dysfunction.

b. Gas exchange limitations – Hypoxemia, hypercarbia increase

ventilatory demands ( lactic acid production from fatiguing

respiratory muscles.

c. Cardiac dysfunction – right ventricular hypertrophy ( cor

pulmonale ( left ventricular dysfunction.

d. Skeletal muscle dysfunction – due to deconditioning, oxidative

stress, systemic inflammation, hypoxemia, chronic steroid use,

weight loss.

e. Respiratory muscle dysfunction – from chronic overload and

hyperinflation.

Important concept -- COPD is a systemic disease!

4. Increased frequency of respiratory illnesses, i.e., chest colds, upper respiratory infections (URI’s), “flu” episodes. These lead to exacerbations (cough, sputum production, shortness of breath).

5. May experience wheezing (seen in asthma/COPD overlap syndrome).

6. Patients with predominantly emphysematous features exhibit dyspnea, hyperinflated lungs, severe reduction in airflows, relatively normal blood gases. (“pink puffers”). Those with predominantly bronchitic characteristics exhibit productive cough, hypoxemia/hypercarbia, cor pulmonale and secondary erythrocytosis (“blue bloaters”). Most patients have overlapping features. Multiple phenotypes are now being recognized, with mix of different symptoms, physical and imaging findings.

B. Physical Exam

1. Thin, underweight (especially emphysema patients)

2. Barrel chest

3. Prolonged expiration with or without wheezes

4. Decreased breath sounds

5. Hyperresonance to percussion (indicates hyperinflated lungs)

6. Use of accessory muscles of respiration; abdominal muscles often tense

7. Cyanosis is a late finding (usually seen with PaO2 55 mm Hg or SpO2 > 88%. Long-term oxygen therapy improves quality of life and prolongs survival.

G. Good nutrition

H. Patient and caregiver education

I. Pulmonary rehabilitation in patients who are physically (and psychologically, with depression and anxiety) impaired

J. Mechanical ventilators during episodes of respiratory failure (invasive and non-invasive)

K. Lung volume reduction surgery or transplantation, in selected cases, for emphysema

Remember again, COPD is a systemic condition!

The NHLBI/WHO Workshop summary on the Global Initiative for COPD (GOLD) (ref. 3) is a current review of the state of the art on all aspects of COPD, and is recommended for those who wish to read more on this subject – contains practical aspects of definition, classification of severity, epidemiology, risk factors, and the 4 components of COPD management (assess and monitor disease, reduce risk factors, pharmacologic and nonpharmacologic treatment of stable COPD, and management of exacerbations). It is update periodically (latest update 2017).

Case revisited:

A 65-yr-old man with an 80-pack-year history of smoking complains of shortness of breath on exertion of several months’ duration. On inspection, there is increased anteroposterior diameter of the chest, pursed lips, and dyspnea during conversation. He is unable to complete more than 4 or 5 words at a time. On physical examination, the patient is noted to be tachycardic, have hyperresonant lungs with decreased breath sounds, no crepitations (râles), and no hepatomegaly or liver nodules on palpation. Which of the following conditions is the most likely diagnosis?

G. Alpha-1-antitrypsin deficiency

H. Asthma

I. Bronchiectasis

J. Centriacinar emphysema

K. Chronic bronchitis

L. Panacinar emphysema

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Fig. 1: Schematic diagram of the vicious circle hypothesis of the role of bacterial colonization in the progression of COPD (from Sethi Chest 2000;117:286S-291S).

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Fig. 3: Flow-volume curve patterns in different conditions (dashed curve normal). Expiration is that portion of the curve above the zero flow line, inspiration is below the line.

Fig. 4 A, B: Assessment tools for severity of COPD.

A. The CAT Assessment tool

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B. The GOLD ABCD Assessment Tool:

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Fig. 4: In the refined assessment scheme, patients should undergo spirometry to determine the severity of airflow limitation (i.e., spirometric grade). They should then undergo assessment of either dyspnea, using the mMRC, or symptoms using the CATTM. Finally, their history of exacerbations (including prior hospitalizations) should be recorded (GOLD 2017).

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Fig. 5: Step-wise management of COPD based on severity of functional loss (modified from ref. 3). Note: inhaled glucocorticoids are gradually being replaced by long-acting antimuscarinic agents in the management of more advanced stages of COPD.

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