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The fourth leading cause of death in the United States is Chronic obstructive pulmonary disease (COPD), affecting approximately 16 million Americans each year.  About 100,000 deaths per year are directly attributable to COPD, and it is a contributing factor to many more.  Almost 90 percent of COPD is associated with smoking tobacco affecting at least 15 percent of those. Obviously, because more men smoke tobacco then women, they are affected more often.  COPD occurs predominantly in individuals older than 40 years. 

COPD has been recently defined by the National Heart, Lung, and Blood Institute and the World Health Organization due to increasing concern.  They formed the Global Initiative for Chronic Obstructive Lung Disease (GOLD).  In their 2001 report, Global strategy for the Diagnosis, Management and Prevention of COPD they define a new classification system for COPD that places less emphasis on the distinction between chronic bronchitis and emphysema than the previous statements.  The GOD report was also endorsed by the American Thoracic Society which defines COPD as “a disease state characterized by airflow limitation that is not fully reversible.  The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.”   

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. 

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

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."


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."


Initial Evaluation: 

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 (e.g., firefighters), and bronchiectasis, this is a disease process that is somewhat unique in its direct correlation to human activities.

Most often the consideration for COPD is in patients over age 50 that have dyspnea on exertion, chronic cough, and a history of significant smoking of more than 30 pack-years.  Breathing difficulty has often been described as an inability to get enough air or as “air hunger,” with a sensation that breathing requires more effort than normal.  Often patients describe wheezing or tightness in the chest.  A familial history of severe early-onset emphysema increases the possibilities of alpha1 antitrypsin deficiency.

Finally, smokers over age 50 are also at risk for coronary artery disease and lung cancer, which can yield similar symptoms and thus, it, is imperative to query the patient about chest pain, palpitations, hemoptysis, or weight loss, which would point to these conditions.  Many patients can point to occupational exposure to a variety of dusts and chemicals as the cause for both obstructive and restrictive lung disease, so an occupations history is mandatory rather than permissive.

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, “key” 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 ‘key” symptoms:

  • A long history of progressive dyspnea with late onset of nonproductive cough
  • Occasional mucopurulent relapses
  • Eventual cachexia and respiratory failure

Physical Examination: Depending on the type of COPD, physical examination may vary as follows:

Chronic bronchitis or the 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 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 or the 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.

Screening Examination for COPD: 

Forced expiratory time is a useful screening test for COPD (and asthma).  To perform this test, have the patient take a deep breath and then exhale as hard and long as possible, listening with a stethoscope placed over the trachea in the suprasternal notch until the last moment that sounds are audible.  A result of more than 6 seconds has a sensitivity of 75% to 92% in detecting obstructive disease, but a specificity of only 43% to75%

Sensitively can be increased up to 98% by using a cutoff value of 4 seconds, making this a useful screening maneuver, but only half of the patients identified will actually have obstructive airway disease. 

Always evaluate the suspected COPD patients for evidence of smoking related cardiovascular disease, such as carotid bruits, fine end-inspiratory rales, abdominal bruits, peripheral edema, and decreased peripheral pulses.  The oropharynx should be examined carefully for tobacco induced cancers.

Lab Studies:

     Arterial blood gas

  • Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity.
  • In general, renal compensation occurs even in chronic CO2 retainers (ie, bronchitis); thus, pH usually is near normal.
  • Generally, consider any pH below 7.3 a sign of acute respiratory compromise.

     Serum chemistry

  • These patients tend to retain sodium.
  • Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels; thus, serum potassium should be monitored carefully.
  • Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.

     CBC - Polycythemia

Imaging Studies:

     Chest x-ray

  • Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly.
  • Emphysema is associated with a small heart, hyperinflation, flat hemi diaphragms, and possible bullous changes.

Other Tests:

Pulse oximetry

  • Pulse oximetry does not offer as much information as ABG.
  • When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status.


  • The presence of underlying cardiac disease is highly likely.
  • Establish that hypoxia is not resulting in ischemia.
  • Establish that the underlying cause of respiratory difficulty is not cardiac in nature.

Pulmonary function tests

  • Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio
  • Poor/absent reversibility with bronchodilators
  • FVC normal or reduced
  • Normal or increased total lung capacity (TLC)
  • Increased residual volume (RV)
  • Normal or reduced diffusing capacity


The cornerstone of COPD prevention and care is avoidance of smoking. Early recognition and treatment of small airway disease in people, who smoke, combined with smoking cessation, may prevent progression of the disease.  All smoking must stop.  If your patient is smoking then it is imperative to help them to stop smoking, both to improve current function and to slow the deterioration of FEV1.  Either physician advocacy and/or referral to smoking cessation programs are extremely valuable.  The utility of nicotine patches, gum, or spray and bupropion (Zyban) increases the success of cessation labors.

Ipratropium bromide by metered dose inhaler (MDI) is used today for patients with continual or frequent symptoms.  A combined MDI containing ipratropium and Albuterol (Combivent) for patients using both medications.  Salmeterol (Serevent, a long acing beta 2 agonist), oral theophylline (With theophylline the serum level should be 5 to 12 mg/dL to minimize adverse effects such as nausea, palpitations, insomnia, tremor and seizures.), or sustained release oral Albuterol is added for more resistant cases.

Adverse effects due to corticosteroids have eliminated recommendation albeit COPD patients have a significant improvement when these agents have been used.  Thus, if stage II-B or III COPD has corticosteroid utility, performing PFTs and a symptoms assessment and a 6 to 12 week trial of medication, and then repeating the assessment to maximize clinical response has proven useful. 

Intravenous replacement therapy with alpha1-protease inhibitor (Prelisting) is given once per week for severe AAT deficiency.  If the patient has stopped smoking this care will stabilize the condition.

In severe COPD cases, continuous low-flow oxygen, non-invasive ventilation, or intubation may be needed. Surgery to remove parts of the disease lung has been shown to be helpful for some patients with COPD.

Specifically, the mainstays of therapy for acute exacerbations of COPD are oxygen, bronchodilators, and definitive airway management.


Oxygen Discussion:

·         Adequate oxygen should be given to relieve hypoxia.  With administration of oxygen, PO2 and PCO2 rise but not in proportion to the very minor changes in respiratory drive.

·         The need for intubation can be established quickly at the bedside by asking the patient hold the nebulizer in his or her hand. If the patient becomes so sleepy that the nebulizer starts to fall away, the patient should be intubated regardless of PCO2 level. The cause of increased CO2 production is not decreased respiratory drive but probably reversal of hypoxic arterial vasoconstriction in areas of less-ventilated lung tissue, which increases the extent of ventilation/perfusion defects and thus CO2. "Stated another way, there is probably no single value for arterial PCO2, pH, or PO2 that by itself constitutes and indication or [intermittent positive pressure ventilation (IPPV)]".

·         Occasionally, large increases in CO2 can lead to deterioration of mental status, causing stupor and obtundation. In such cases, decreasing O2 delivery is the wrong action. The CO2 narcosis inhibits respiratory drive to the point that decreasing O2 delivery leads only to worsening of hypoxia. The correct action is immediate intubation and oxygenation.

·         Supply the patient with enough oxygen to maintain a near normal saturation (above 90%) and do not be concerned about oxygen supplementation leading to clinical deterioration. If the patient's condition is that tenuous, intubation most likely is needed anyway.


·         In the prehospital setting, administer only beta-agonist nebulizer therapy, which should be given as needed.

·         If necessary and available, continuous positive airway pressure (CPAP) may be used.

·         Of course, in times of respiratory failure, patients may need intubation in the field.

Emergency Department Care:

In addition to oxygen, proper care may comprise bronchodilators, antibiotics, magnesium, CPAP or biphasic positive airway pressure (BiPAP), Heliox (ie, mixture of helium and oxygen), theophyline, corticosteroids, Terbutaline and antibiotics as well as definitive airway management via intubation. All of these should be considered in the context of the individual patient's condition.

Terbutaline can be considered for patients with such significant exacerbations that they are not moving enough air to take full advantage of nebulizer therapy.

The greatest single problem that persists in this area is the under dosing of beta agonists and the non utilization of anticholinergics. Although only a small subset of patients respond to beta agonists, a reasonable dose approaches continuous nebulization, as is seen in current asthma treatment.  Anticholinergics seem to have an important role in the acute treatment of COPD exacerbations.

The use of antibiotics is still controversial. These patients are almost uniformly heavily colonized with
Haemophilus influenzae, streptococcal pneumonia, and others; however, researchers have not proven these organisms to be the cause of the exacerbation. In fact, viruses are thought to be the instigating factor in as many as half of the cases. In addition, the particular antibiotic chosen seems to have much less effect on outcome than the particular host factors of the patient. Although some meta-analyses have suggested statistically significant improvement in outcome in those patients who receive empiric antibiotic coverage, the lack of quality studies and power leaves the subject open for debate. If antibiotics are given, the choice should provide coverage against pneumococcus, H influenzae, Legionella species, and gram-negative enterics.

ER Bronchodilators -- These agents act to decrease muscle tone in both small and large airways in the lungs, thus increasing ventilation. Category includes subcutaneous medications, beta-adrenergic agonists, methylxanthines, and anticholinergics. Note that only 10-15% of all patients with COPD have a true reversible (ie, bronchospastic) component; however, because predicting response is impossible on presentation, all patients should be treated with aggressive bronchodilator therapy.


Chronic Evaluation:

Smoking education is the most important fact in the care of COPD.  Further , in order to facilitate a superior collaborative partnership with the physician, the patient needs to demonstrate the proper use of inhalers, home management of medications, avoidance or respiratory irritations, and how and when to contact the patients physician.  Pulmonary rehabilitation programs, exercise programs tailored to the severity of disease, can improve the patient’s functional status, exercise tolerance, and the symptoms of breathlessness.  A well informed patient able to take charge of their health care team, will maintain the proper re-evaluation program, to ensure proper recording of disease and progress or success, as well as to maintain the most up to date cutting edge medical knowledge and care for the maintenance of a wonderful and carefree life.


Medical Text References:

  1. Dailey RH: Chronic obstructive pulmonary disease. In: Rosen P, et al, eds. Emergency Medicine Concepts and Clinical Practice. 3rd ed. Mosby-Year Book Inc; 1992:1093-1111
  2. Andreoli Thomas E et al, Cecil Essentials of Medicine, 4th Saunders, pages 145-150.
  3. Kasper Dennis L et al, Harrison’s Principles of Internal Medicine, 16th edition, Mc Graw Hill, pages 1547-1554
  4. Beers, Mark H et al, The Merc Manual of Diagnosis and Therapy, 17th Edition, Merck Research Laboratories, pages 568-582
  5. Sloane, Philip D et al, Essentials of Family Medicine, 4th Edition, Lippincott-Williams & Wilkins, pages 730-732
  6. Siedman JC: Chronic obstructive pulmonary disease. In: Tintinalli J, et al, eds. Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Com; 1992: 298-302.
  7. Brunton Laurence L et al, Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 11th edition, Mcgraw-Hill, pages 431-453
  8. Ibid, pages 253-254
  9. Ibid, 1608-1609



  • Alter HJ, Koepsell TD, Hilty WM: Intravenous magnesium as an adjuvant in acute bronchospasm: a meta-analysis. Ann Emerg Med 2000 Sep; 36(3): 191-7.
  • Balter MS, La Forge J, Low DE, et al: Canadian guidelines for the management of acute exacerbations of chronic bronchitis. Can Respir J 2003 Jul-Aug; 10 Suppl B: 3B-32B.
  • Cydulka RK, Emerman CL: Effects of combined treatment with glycopyrrolate and albuterol in acute exacerbation of chronic obstructive pulmonary disease. Ann Emerg Med 1995 Apr; 25(4): 470-3.
  • De Palo VA: Pulmonary disease: pneumonia, chronic obstructive pulmonary disease, asthma, and thromboembolic disease. J Am Podiatr Med Assoc 2004 Mar-Apr; 94(2): 157-67.
  • Dewan NA, Daniels A, Zieman G, Kramer T: The National Outcomes Management Project: a benchmarking collaborative. J Behav Health Serv Res 2000 Nov; 27(4): 431-6.
  • Ferguson GT, Cherniack RM: Management of chronic obstructive pulmonary disease. N Engl J Med 1993 Apr 8; 328(14): 1017-22.
  • Hirschmann JV: Do bacteria cause exacerbations of COPD?. Chest 2000 Jul; 118(1): 193-203.
  • Jaber S, Fodil R, Carlucci A, et al: Noninvasive ventilation with helium-oxygen in acute exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000 Apr; 161(4 Pt 1): 1191-200.
  • Lieberman D, Lieberman D, Ben-Yaakov M, et al: Infectious etiologies in acute exacerbation of COPD. Diagn Microbiol Infect Dis 2001 Jul; 40(3): 95-102.
  • Pierson DJ: Indications for mechanical ventilation in adults with acute respiratory failure. Respir Care 2002 Mar; 47(3): 249-62; discussion 262-5.
  • Schmidt GA, Hall JB: Acute chronic respiratory failure: Assessment and management of patients with COPD in the emergent setting. JAMA 1989; 261(23): 3444-3453.
  • Sclar DA, Legg RF, Skaer TL, et al: Ipratropium bromide in the management of chronic obstructive pulmonary disease: effect on health service expenditures. Clin Ther 1994 May-Jun; 16(3): 595-601; discussion 594.
  • Sohy C, Pilette C: Acute exacerbation of chronic obstructive pulmonary disease and antibiotics: what studies are still needed? Euorpean Respiratory Journal 2002; 19: 966-75.
  • Varkey B: Obstructive, occupational, and environmental diseases. Curr Opin Pulm Med 2004 Mar; 10(2): 97.
  • Whittle A: COPD guidelines. Thorax.

By Scott David Neff for INTERNAL MEDICINE DECEMBER 19th, 2010

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