eMedicine Specialties > Emergency Medicine > Pulmonary

Chronic Obstructive Pulmonary Disease and Emphysema

Author: Paul Kleinschmidt, MD, Consulting Staff, Department of Emergency Medicine, Womack Army Medical Center
Contributor Information and Disclosures

Updated: Mar 13, 2008

Introduction

Background

Chronic obstructive pulmonary disease (COPD) is estimated to affect 32 million persons in the United States and is the fourth leading cause of death in this country. Patients typically have symptoms of both chronic bronchitis and emphysema, but the classic triad also includes asthma. Most of the time COPD is secondary to tobacco abuse, although cystic fibrosis, alpha-1 antitrypsin deficiency, bronchiectasis, and some rare forms of bullous lung diseases may be causes as well. 

Patients with COPD are susceptible to many insults that can lead rapidly to an acute deterioration superimposed on chronic disease. COPD exacerbation is an important but occasionally overlooked parameter. COPD exacerbations are very common, affecting about 20% of patients with moderate-to-severe COPD (1.3 events per year in patients with 40-45% predicted FEV1). Quick and accurate recognition of these patients along with aggressive and prompt intervention may be the only action that prevents frank respiratory failure.

For more information, see Medscape's COPD Resource Center.

For related CME activities, see New Data on Chronic Obstructive Pulmonary Disease, An Elderly Man With Dyspnea, CHEST 2007: Pulmonary Disease, and Practice Report Updated for COPD.

Pathophysiology

COPD is a mixture of 3 separate disease processes that together form the complete clinical and pathophysiological picture. These processes are chronic bronchitis, emphysema and, to a lesser extent, asthma. Progression of COPD is characterized by the accumulation of inflammatory mucous exudates in the lumens of small airways and the thickening of their walls. These walls become infiltrated by adaptive and innate inflammatory immune cells. Infiltration of the airways with substances such as polynuclear and mononuclear phagocytes and CD4 T cells increases with each stage of disease progression. This is also true for B cells and CD8 T cells, which organize into lymphoid follicles. This chronic inflammatory process is associated with tissue repair and remodeling that ultimately determines the pathologic type of COPD. 

It appears that smoking may overcome the body's natural mechanisms for limiting this immune response. This process can continue in susceptible individuals even after smoking cessation. Even if the original noxious insults are removed, COPD is still characterized by progressive accumulation of cells of the immune system, fibrosis, and mucus hypersecretion. The molecular basis for the lung inflammation seen in COPD is still an area of great research and debate, with the potential roles of cytokines, complex autoimmune processes, and immune modulation from chronic infection all under investigation.

The defining feature of COPD is irreversible airflow limitation during forced expiration. This may be a result of a loss of elastic recoil due to lung tissue destruction or an increase in the resistance of the conducting airways. The standard measure of COPD is the measure of forced expiratory volume in 1 second (FEV1) and its ratio to forced vital capacity (FVC), FEV1/FVC.

Each case of COPD is unique in the blend of processes; however, 2 main types of the disease are recognized.

Chronic bronchitis

In this type, chronic bronchitis plays the major role. Chronic bronchitis is defined by excessive mucus production with airway obstruction and notable hyperplasia of mucus-producing glands.

Damage to the endothelium impairs the mucociliary response that clears bacteria and mucus. Inflammation and secretions provide the obstructive component of chronic bronchitis. In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed. Emphysema is present to a variable degree but usually is centrilobular rather than panlobular. The body responds by decreasing ventilation and increasing cardiac output. This V/Q mismatch results in rapid circulation in a poorly ventilated lung, leading to hypoxemia and polycythemia.

Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary artery vasoconstriction and cor pulmonale. With the ensuing hypoxemia, polycythemia, and increased CO2 retention, these patients have signs of right heart failure and are known as "blue bloaters."

Emphysema

The second major type is that in which emphysema is the primary underlying process. Emphysema is defined by destruction of airways distal to the terminal bronchiole.

Physiology of emphysema involves gradual destruction of alveolar septae and of the pulmonary capillary bed, leading to decreased ability to oxygenate blood. The body compensates with lowered cardiac output and hyperventilation. This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in blue bloaters. Because of low cardiac output, however, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as "pink puffers."

Frequency

United States

Two thirds of men and one fourth of women have emphysema at death. Approximately 8 million people have chronic bronchitis and 2 million have emphysema.

Mortality/Morbidity

COPD is the fourth leading cause of death in the United States, affecting 32 million adults. It is also the fifth leading cause of death worldwide.

Sex

Men are more likely to have COPD than women.

Age

COPD occurs predominantly in individuals older than 40 years.

Clinical

History

Patients with COPD present with a combination of signs and symptoms of chronic bronchitis, emphysema, and asthma. Symptoms include worsening dyspnea, progressive exercise intolerance, and alteration in mental status. In addition, some important clinical and historical differences can exist between the types of COPD.

  • In the chronic bronchitis group, classic symptoms include the following:
    • Productive cough, with progression over time to intermittent dyspnea
    • Frequent and recurrent pulmonary infections
    • Progressive cardiac/respiratory failure over time, with edema and weight gain
  • In the emphysema group, the history is somewhat different and may include the following set of classic symptoms:
    • A long history of progressive dyspnea with late onset of nonproductive cough
    • Occasional mucopurulent relapses
    • Eventual cachexia and respiratory failure

Physical

Depending on the type of COPD, physical examination may vary.

  • Chronic bronchitis (blue bloaters)  
    • Patients may be obese.
    • Frequent cough and expectoration are typical.
    • Use of accessory muscles of respiration is common.
    • Coarse rhonchi and wheezing may be heard on auscultation.
    • Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis.
    • Because they share many of the same physical signs, COPD may be difficult to distinguish from congestive heart failure (CHF). One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation.
  • Emphysema (pink puffers)  
    • Patients may be very thin with a barrel chest.
    • They typically have little or no cough or expectoration.
    • Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position.
    • The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant.
    • Overall appearance is more like classic COPD exacerbation.

Causes

In general, the vast majority of COPD cases are the direct result of tobacco abuse. While other causes are known, such as alpha-1 antitrypsin deficiency, cystic fibrosis, air pollution, occupational exposure (eg, firefighters), and bronchiectasis, this is a disease process that is somewhat unique in its direct correlation to a human activity.

More on Chronic Obstructive Pulmonary Disease and Emphysema

Overview: Chronic Obstructive Pulmonary Disease and Emphysema
Differential Diagnoses & Workup: Chronic Obstructive Pulmonary Disease and Emphysema
Treatment & Medication: Chronic Obstructive Pulmonary Disease and Emphysema
Follow-up: Chronic Obstructive Pulmonary Disease and Emphysema
References
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Further Reading

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Keywords

COPD, chronic bronchitis, cough, dyspnea, pulmonary infections, cardiac failure, respiratory failure, edema, weight gain, obesity, mucopurulent relapses, cachexia, blue bloater, pink puffer, asthma, wheeze, wheezing, emphysema, tobacco abuse, cystic fibrosis, alpha-1 antitrypsin deficiency, bronchiectasis, bullous lung disease, excessive mucus production, hyperplasia of mucus-producing glands, hypoxemia, polycythemia, hypercapnia, respiratory acidosis, cor pulmonale, hypoxemia, right heart failure, progressive exercise intolerance, recurrent pulmonary infections, progressive cardiac failure, progressive respiratory failure, progressive dyspnea, coarse rhonchi, wheezing, cyanosis, barrel chest, air pollution

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Contributor Information and Disclosures

Author

Paul Kleinschmidt, MD, Consulting Staff, Department of Emergency Medicine, Womack Army Medical Center
Paul Kleinschmidt, MD is a member of the following medical societies: American Academy of Emergency Medicine and Special Operations Medical Association
Disclosure: Nothing to disclose.

Medical Editor

David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Paul Blackburn, DO, FACOEP, FACEP, Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona
Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Program Director, Department of Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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