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Chronic Obstructive Pulmonary Disease: Pathophysiology and Treatment

  • 7 minutes, 1 second
  • Pulmonology
  • 2020-08-19

Estimated read time is 7 minutes, 1 second

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Chronic Obstructive Pulmonary Disease is a set of lung diseases that limit airflow into the lungs by causing airflow obstruction and is not fully reversible. It is usually progressive and is associated with inflammation of the lungs as they respond to noxious particles or gases.

COPD patients report they are “hungry” for air

COPD is potentially preventable with proper precautions and avoidance of precipitating factors

This condition entails two major diseases :

Emphysema and chronic bronchitis. Asthma has also been included.


Emphysema is an abnormal permanent enlargement of the air space distal to the terminal bronchioles accompanied by destruction of bronchioles.

Chronic Bronchitis

Chronic bronchitis is the presence of chronic cough for 3 or more months in each of 2 successive years in a patient whom other causes of chronic cough have been excluded.

Signs and symptoms of chronic obstructive pulmonary disease

Features of Chronic Bronchitis and emphysema will be present such as:

  • Dyspnea that progresses in severity
  • The patient will first complain of dyspnea on exertion and progress to interfering with activities of daily living and rest
  • Minimal coughing with no to small amounts of sputum
  • Overdistention of alveoli causes the diaphragm to flatten and anteroposterior diameter to increase
  • The patient becomes chest breather, relying on accessory muscles
  • Ribs become fixed in inspiratory position
  • The patient is underweight (despite adequate calorie intake)

Epidemiology Of COPD

How common is COPD?

About 13.9% of the U.S. adult population (25+ years) have been diagnosed with COPD. An estimated 15-19% of COPD cases are work-related. 24 million other adults have evidence of troubled breathing, indicating COPD is under-diagnosed by up to 60%.

What can cause COPD?

Smoking is the primary risk factor. Long-term smoking is responsible for 80-90 % of cases. Nicotine stimulates the sympathetic nervous system resulting in increased heart rate, peripheral vasoconstriction, increases blood pressure and cardiac output.

How does cigarette smoking lead to COPD?

Cigarette smoking compounds problems in a person with CAD leading to reduced ciliary motility and possible loss of ciliated cells.

It also leads to abnormal dilation of the distal air spaces and alveolar wall destruction. This destruction may lead to carbon monoxide accumulation and reduced oxygen-carrying capacity.

Smoking also leads to cellular hyperplasia stimulating the production of more mucus reducing the airway diameter hence increasing difficulty in clearing secretions.

Smoker, compared to a non-smoker, is 10 times more likely to die of COPD

Prolonged exposures to harmful particles and gases from:

  • Second-hand smoke lowers pulmonary function and increases the risk of lung cancer.
  • Industrial smoke,
  • Chemical gases, vapors, mists & fumes
  • Dust from grains, minerals & other materials

Infection. Infection is a major contributing factor to the aggravation and progression of COPD

Heredity. Alpha antitrypsin deficiency (produced in the liver and found in the lungs) accounts for about 1% of the cases. Emphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages.

Other Risk Factors for COPD

  • History of childhood respiratory infections
  • Genetic makeup

Pathophysiology of chronic obstructive pulmonary disease

Emphysema is an abnormal permanent enlargement of the air space distal to the terminal bronchioles accompanied by destruction of bronchioles:

It starts with Hyperinflation of alveoli which then causes the destruction of alveolar walls and destruction of alveolar-capillary walls. Once the alveolar walls are destroyed there is  narrowing of the airways and loss of lung elasticity:

There are two types of emphysema:

  1. Centrilobular which affects the central part of the lobule and is the most common.
  2. Panlobular which is the destruction of a whole lobule and is usually associated with AAT deficiency

The structural changes in emphysema are:

  • Hyperinflation of the alveoli
  • Destruction of alveolar-capillary walls
  • Narrowed ,tortous small airways,
  • Loss of lung elasticity

Small bronchioles become obstructed as a result of

  • Mucus
  • Smooth muscle spasm
  • Inflammatory process
  • The collapse of bronchiolar walls

Recurrent infections lead to production and stimulation of neutrophils and macrophages which then release proteolytic enzymes. These enzymes cause alveolar destruction, inflammation, exudation and edema of the bronchioles.

Elastin and collagen are destroyed. Air then goes to the lungs but it is unable to come out on its own and remains in the lings causing bronchioles to collapse.

Trapped air causes hyperinflation and over distention of the alveoli. As more alveoli coalesce, blebs and bullae may develop destroying the alveolar walls and capillaries causing reduced surface area for O2 diffusion.

Compensation is done by increasing respiratory rate to increase alveolar ventilation. Hypoxemia usually develops late in the disease

Pathologic lung changes in chronic Bronchitis are;

  • Hyperplasia of mucus-secreting glands in trachea and bronchi.
  • Increase in goblet cells
  • Disappearance of cilia
  • Chronic inflammatory changes and narrowing of small airways
  • Altered function of alveolar macrophages leading to infections

In chronic inflammation, the primary pathologic mechanism causing changes that lead to narrow airway lumen and reduced airflow due to hyperplasia of mucous glands, Inflammatory swelling, excess, thick mucus production.

Greater resistance to airflow increases the work of breathing

Bronchioles are clogged with mucus  and pose a physical barrier to ventilation. Hypoxemia and hypercapnia due to lack of ventilation and O2 diffusion

The tendency to hypoventilate and retain CO2. Frequently patients require O2 both at rest and during exercise.

Cough is often ineffective to remove secretions because the person cannot breathe deeply enough to cause airflow distal to the secretions

Bronchospasm frequently develops more common with a history of smoking or asthma

Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema

Signs and symptoms of chronic bronchitis

Earliest symptoms are :

  • Frequent, productive cough during winter
  • Frequent respiratory infections
  • Bronchospasm at end of paroxysms of coughing
  • Cough
  • Dyspnea on exertion
  • History of smoking
  • Normal weight or heavyset
  • Ruddy (bluish-red) appearance d/t polycythemia (increased Hgb due to chronic hypoxemia)) cyanosis
  • Hypoxemia and hypercapnia results from hypoventilation and increased airway resistance + problems with alveolar gas exchange

Diagnosis and investigations

COPD Diagnostic Studies

st x-rays early in the disease may not show abnormalities

History and physical exam

Pulmonary function studies will indicate reduced FEV1/FVC and increased residual volume and total lung capacity

Arterial blood gas analysis

  • Reduced PaO2
  • Increased PaCO2 (especially in chronic bronchitis)
  • Reduced pH (especially in chronic bronchitis)
  • Increased Bicarbonate level found in late stages COPD

Ways to prevent or slow the progression of COPD

  • Stop smoking, if you smoke, to prevent further damage to your body. Smoking cessation is critical for all severities of COPD
  • Avoid or protect yourself from exposures to Second-hand smoke and other substances such as chemical vapors, fumes, mists, dust, and diesel exhaust fumes that irritate your lungs

Treatment of chronic obstructive pulmonary disease

Chronic Obstructive Pulmonary Disease can be managed, but not cured

Treatment is different for each individual and is based on the severity of the symptoms

 Early diagnosis and treatment can:

  • Slow progress of the disease
  • Relieve symptoms
  • Improve an individual’s ability to stay active
  • Prevent and treat complications
  • Improve the quality of life

What medications are used to treat symptoms?

Bronchodilators as maintenance therapy:

Beta-adrenergic agonists such as Ventolin(MDI or nebulizer is preferred).Anticholinergics eg Atrovent. These drugs work by relaxing muscles around airways

Steroids to reduce inflammation

Oxygen therapy to help with shortness of breath by raising PO2 in inspired air and treat hypoxemia

Respiratory therapy

  • Breathing retraining
  • Pursed-lip breathing prolongs exhalation and prevents bronchiolar collapse and air trapping
  • Diaphragmatic breathing Focuses on using diaphragm instead of accessory muscles to achieve maximum inhalation and slow respiratory rate


Chest physiotherapy – to bring secretions into larger, more central airways

  • Postural drainage
  • Percussion
  • Vibration

Encourage patient to remain as active as possible

Surgical Therapy

  • Lung volume reduction surgery
  • Lung transplant

Nutritional therapy

Full stomachs press on diaphragm causing dyspnea and discomfort

Difficulty eating and breathing at the same time leads to inadequate amounts being eaten

  • To decrease dyspnea and conserve energy
  • Rest at least 30 minutes prior to eating
  • Use bronchodilator before meals
  • Select foods that can be prepared in advance
  • 5-6 small meals to avoid bloating
  • Avoid foods that require a great deal of chewing
  • Avoid exercises and treatments 1 hour before and after eating
  • Avoid gas-forming foods
  • High-calorie, high-protein diet is recommended
  • Supplements
  • Avoid high carbohydrate diet to prevent increase in CO2 load

What medications are used to prevent complications?

The annual flu vaccine reduces the risk of flu and its complications
Pneumonia vaccine reduces the risk of the common cause of pneumonia


Pulmonary hypertension (pulmonary vessel constriction due to alveolar hypoxia and acidosis)

Cor pulmonale (Right heart hypertrophy + Right ventricular failure)


Acute Respiratory Failure

    National Institute for Health and Care Excellence. Chronic Obstructive Pulmonary Disease in Over 16s: Diagnosis and Management. Published in 2018. Available from: Health and Safety Executive. Chronic Obstructive Pulmonary Disease (COPD) Statistics in Great Britain. Published in 2019. Available from: National Institute for Health and Care Excellence. Quality Standards and Indicators: COPD. Published in 2015. Available from: Rabe KF and Watz H. Chronic Obstructive Pulmonary Disease. Published in

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