INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

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

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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, bronchitics); 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
• BNP
• • Human BNP binds to particulate guanylate cyclase receptors of vascular smooth muscle and endothelial cells. Binding to the receptors causes an increase in cyclic guanosine monophosphate (GMP), which serves as a secondary messenger to dilate veins and arteries. 
  • By measuring the BNP level, it was thought that the ability to differentiate between CHF and COPD exacerbations in blue bloaters would have become much easier. However, clinical observation and research demonstrated that, in the cases of mild CHF exacerbations, the ability to differentiate between CHF and COPD is still not straightforward. A mild elevation of a BNP level still must be taken in context with the overall clinical picture.

Imaging Studies

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

Other Tests

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

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

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

• Oxygen  
• • Adequate oxygen should be given to relieve hypoxia. A belief (ingrained from medical school) is held widely that too much oxygen causes significant respiratory depression. Multiple studies in the literature dispute this view. 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 to 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 for [intermittent positive pressure ventilation (IPPV)]."¹
  • 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.
• Bronchodilator  
• • In the prehospital setting, administer short-acting beta-agonist nebulizer therapy, which should be given as needed. In addition, short-acting anticholinergics, such as ipratropium, can be given.
  • 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 ED care may comprise bronchodilators, antibiotics, magnesium, CPAP or biphasic positive airway pressure (BiPAP), Heliox (ie, mixture of helium and oxygen), and definitive airway management via intubation. All of these should be considered in the context of the individual patient's condition.

For more information, please see either Medication or In/Out Patient Meds in the Follow-up section.

Consultations

• Consult a pulmonologist.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medicines available for ED treatment of COPD include beta2-adrenoceptor agonists, anticholinergics, oxygen, methylxanthines, corticosteroids, some newer experimental classes of medication, and, possibly magnesium.

• Terbutaline can be considered for patients with such significant exacerbations that they are not moving enough air to take full advantage of nebulizer therapy.
• Beta2-adrenoceptor agonists  
• • These agents are first-line therapy for COPD, both for acute exacerbations and for acute treatment. Bronchodilators are given on an as-needed basis or on a regular basis to prevent or reduce symptoms. Short-acting agents are usually used for immediate relief of symptoms, whereas long-acting inhaled agents are better for day-to-day mitigation of the disease. Even longer-acting agents, which would allow once-daily dosing, are in development.
  • Combinations of bronchodilators may improve efficacy and reduce risk of adverse effects rather than increasing the dose of a single agent. Keep in mind that, based on several studies, the acute response to short-acting agents does not predict the future response to long-acting agents. 
  • Most of the beta-agonists used are racemic compounds that contain both the R and S enantiomers of the agonist. Much of the pharmacologic activity seems to reside in the R enantiomer, with the S thought to induce the negative side effects. Recently, the R enantiomer of both the short-acting agent albuterol (levalbuterol) and the long-acting agent formoterol (aformoterol) were approved for use in COPD. However, the cost effectiveness of these agents, in light of marginal observed clinical differences, remains controversial and needs further exploration.
  • Although the major action of beta2-agonists is relaxation of airway smooth muscles, they have also been shown to have several other potential effects. They seem to inhibit airway smooth muscle proliferation and inflammatory mediator release, as well as stimulation of mucociliary transport, cytoprotection of the mucosa, and attenuation of neutrophil recruitment and activation.
  • Multiple studies have demonstrated enhanced benefits of action when coadministered with inhaled anticholinergics and with corticosteroids.
  • The greatest single problem that persists in the acute phase is the under dosing of beta-agonists and the nonutilization 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.
  • Note that, in mild or moderate exacerbations, the use of MDIs with an aerosol chamber in higher doses (6-12 puffs) can achieve equivalent bronchodilation as the use of a nebulizer. This is particularly important in the office and prehospital setting.
• Anticholinergics 
• • Anticholinergics have an important role in the acute treatment of COPD exacerbations. The anticholinergics reduce airway tone and improve expiratory flow limitation, primarily by blocking parasympathetic activity in the large and medium-sized airways. They also block the release of acetylcholine, which has been linked to increased bronchial smooth muscle tone and mucus hypersecretion. 
  • Two anticholinergic agents are available at this time, a short-acting agent appropriate for management of acute exacerbations (ipratropium) and a long-acting agent (tiotropium).
• Methylxanthines: These agents increase collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive. Despite this, many questions exist as to their true efficacy, and they have no real role in the acute exacerbation of COPD, except to increase the risk of adverse effects.
• Phosphodiesterase inhibitors: In theory, phosphodiesterase inhibitors would work to selectively inhibit of phosphodiesterase to cause smooth muscle relaxation and anti-inflammatory effects. These agents would have a better safety profile than the methylxanthines, but they are all still in various stages of development.
• Antibiotics
• • 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.
  • The particular antibiotic chosen seems to have much less effect on outcome than the particular host factors of the patient in some studies, with other studies suggesting fluoroquinolones are the best strategy. This may really be a factor of the severity of the exacerbation and whether antibiotics are really indicated for minor exacerbations. 
  • If antibiotics are given, the choice should provide coverage against pneumococcus, H influenzae, Legionella species, and gram-negative enterics.
• Magnesium: Though controversial, administration of magnesium is thought to produce bronchodilation through the counteraction of calcium-mediated smooth muscle constriction. The addition of intravenous magnesium is now considered to have class B evidence supporting its use in difficult and life-threatening exacerbations.
• Heliox: Because of helium's low density, some class B evidence now exists for its use as the medium to drive nebulizer therapy. In theory, a mixture of helium and oxygen could improve gas exchange in patients who have an airway obstruction. In the realm of COPD exacerbations, however, the evidence is more slight, and more investigation is needed.
• Leukotriene receptor antagonists: Intravenous leukotriene receptor antagonists have been shown to have benefit in asthma in limited studies, but, at this time, they have no role in COPD exacerbations.

Drug Category: 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.

Drug Category: Corticosteroids

These agents have been shown to be effective in accelerating recovery from acute COPD exacerbations. Although they may not make a clinical difference in the ED, they have some effect by 6-8 h into therapy; therefore, early dosing is critical.

Some newer studies are suggesting that inhaled corticosteroids (eg, nebulized budesonide) may be equally effective as IV or PO steroids in the mild-to-moderate exacerbation. In addition, level B evidence suggests that the addition of inhaled corticosteroids to oral agents at discharge may be very beneficial.

Drug Category: Electrolyte supplements

Magnesium is used to replenish stores that become depleted in periods of adrenergic excess such as asthma attacks, COPD exacerbations, and diuretic use.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• In patients in extremis, CPAP or BiPAP may be attempted prior to intubation. This can be started in the ED and continued for several hours in the hospital. Usual recommended settings are an inspiratory positive airway pressure (IPAP) of 10 cm H₂O and an expiratory positive airway pressure (EPAP) of 2 cm H₂O, with further adjustments based on the individual. This is contingent on the patient's ability to withstand the mask. This treatment is not a substitute for intubation; rather, it is a means of trying to avoid intubation.
• Heliox is an additional strategy that can be attempted prior to intubation. Whether Heliox or CPAP is used will depend on the individual patient and local hospital availability. Again, like several other therapies mentioned in this article, study results both for and against Heliox have been published. The current summation of that literature indicates that Heliox may actually decrease the work of breathing while the patient is breathing the mixture, but its effects are not long lasting once it is removed. The proper mixture of the gases and the ability to deliver enough oxygen to the patient are also issues.
• Inhaled nitric oxide has been suggested, but at this point does not seem to have a role in acute treatment.
• Lung volume reduction surgery has also been touted as effective, but most recent studies demonstrate varying levels of success.

Further Outpatient Care

• Disposition from the ED depends on the clinical picture for each patient more than any single laboratory value or test. In general, the longer the exacerbation, the more airway edema and debris are present, making resolution in the ED increasingly more difficult. Patients who state that they "feel back to normal" and have no overt reason for admission can reasonably be discharged home with follow-up arrangements. The corollary to this is that patients who state they "do not feel comfortable," regardless of the numbers, are the best predictors of outcome and probably should be admitted. Data on risk factors for relapse and need for admission are limited at present.
• For patients who are sent home, nearly all should receive a short steroid burst and an increase in the frequency of inhaler therapy. Close follow-up should be arranged with the patient's regular care provider. Other therapies should be considered on a case-by-case basis.
• Patients with severe or unstable disease should be seen monthly.
• When their condition is stable, patients may be seen biannually.
• Check theophylline level with each dose adjustment, then every 6-12 months.
• For patients on home oxygen, check ABGs yearly or with any change in condition. Monitor oxygen saturation more frequently than ABGs.
  

In/Out Patient Meds

• Bronchodilators 
• • Beta2-adrenoceptor agonists
  • • See the Medication. Again, these agents are first-line therapy for COPD, both for acute exacerbations and for acute treatment. Bronchodilators are given on an as-needed basis or on a regular basis to prevent or reduce symptoms. Short-acting agents are usually used for immediate relief of symptoms, whereas long-acting inhaled agents are better for day-to-day mitigation of the disease.
    • Epinephrine or terbutaline can be administered subcutaneously when intravenous access is not possible or the patient is moving so little air that nebulizer therapy is ineffective. Terbutaline is thought to be safer in older patients, and it has shown to be more efficacious than epinephrine.
  • Methylxanthines: Theophylline increases collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive. Despite this, many questions exist as to its true efficacy. In general, if the patient is already on theophylline and has a subtherapeutic level, a mini-loading dose is appropriate. If the patient is not on theophylline, the delay before benefit of the oral form makes it not worth using. Intravenous aminophylline has a propensity to cause arrhythmias, especially in a population that already has cholinergic excess coupled with coronary disease.
  • Anticholinergics: These are as effective as beta-agonists in acute attacks, and they have synergistic properties with the beta-agonists. They act by antagonizing the vagal innervation of the tracheobronchial tree. Vagal tone can be increased by as much as 50% in patients with COPD.
• Corticosteroids: These also have bronchodilatory properties, although they primarily act by decreasing inflammation in the tracheobronchial tree. Although 8-12 hours are required for full effect, corticosteroids should be administered in the ED, as some mild improvements may be noted much earlier.
• Antibiotics
• • Antibiotics effectively reduce treatment failure and mortality rates in patients with severe COPD exacerbations. However, with mild or moderate exacerbations, antibiotics may or may not be indicated.
  • In cases of severe acute exacerbations of chronic bronchitis (AECB), recent guidelines suggest using fluoroquinolone antibiotics as first-line therapy. This suggestion is based on level I evidence from several trials that show clinical and microbial superiority of these agents.
  • Use of fluoroquinolones has also been shown to shorten hospital stay, reduce recurrences, and lower costs.
  • Fortunately, resistance to these agents is still very low, and reserving them for use in populations at risk should preserve their effectiveness for some time.
• Magnesium  
• • Although controversial, administration of magnesium is thought to produce bronchodilation through the counteraction of calcium-mediated smooth muscle constriction.
  • Magnesium depletion is known to occur in periods of adrenergic excess (eg, asthma exacerbations, diuretic use).
• CPAP and BiPAP
• • These devices help to decrease the work of breathing and maintain positive end-expiratory pressure (PEEP).
  • Patients must be alert with no excess secretions.
• Heliox
• • Heliox usually is a 60:40 mixture of helium and oxygen.
  • Helium is a smaller particle than oxygen and in small airways promotes laminar flow and facilitates both oxygen transport and carbon dioxide diffusion.
  • Many patients who seem to breathe better on Heliox return to a worsened respiratory state when removed from Heliox.

Deterrence/Prevention

• For the vast majority of patients, cessation of smoking is the only true means of prevention.

Complications

• Some complications that must be anticipated in COPD treatment include the following:
• • Incidence of pneumothorax due to bleb formation is relatively high; consider pneumothorax in all patients with COPD who have increased shortness of breath.
  • In patients who require long-term steroid use, the possibility of adrenal crisis is very real; at a minimum, patients with steroid-dependent COPD should receive stress dosing in the event of an exacerbation or any other stressor.
  • Infection (common)
  • Cor pulmonale
  • Secondary polycythemia
  • Bullous lung disease
  • Acute or chronic respiratory failure
  • Pulmonary hypertension
  • Malnutrition

Prognosis

• Patient's age and postbronchodilator FEV₁ are the most important predictors of prognosis. Young age and FEV₁ greater than 50% of predicted are associated with a good prognosis. Older patients and those with more severe lung disease do worse.
• Supplemental oxygen (when indicated) has been shown to increase survival rates.
• Smoking cessation improves the prognosis.
• Cor pulmonale, hypercapnia, tachycardia, and malnutrition indicate a poor prognosis.

Patient Education

• The best education comes in 2 forms.
• • Educate patients to the dangers of smoking and the improvement in quality of life attainable with smoking cessation.
  • Instruct patients with COPD to present early during an exacerbation and to not wait until they are in distress.
• This author's observation is that many people with respiratory disease do not know the basic ways to monitor their own disease fluctuations. In addition, they are frequently not taking/using their inhalers as prescribed. Spending the 5 minutes it takes to make sure they have an aero chamber, are using the right dosages, the right medicines, and know when to seek help can go a long way in preventing a respiratory disaster.
• Printed material is available from the National Jewish Hospital in Denver, Colorado, as well as the American Lung Association.
• Instruct patients about appropriate pulmonary toilet.
• For excellent patient education resources, visit eMedicine's Lung and Airway Center. Also, see eMedicine's patient education articles Chronic Obstructive Pulmonary Disease (COPD), Cigarette Smoking, Asthma, and Emphysema.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Be wary of discharging patients with exacerbations when they do not feel comfortable with their breathing, regardless of their oxygen saturation, ABG, or other test results.
• Always look for underlying cardiac ischemia with acute exacerbations. With hypoxia and distress, many of these patients can have unrecognized underlying ischemia.
• Administer as much oxygen as necessary to avoid hypoxia. If the patient retains excessive carbon dioxide, intubate.
• A common mistake is utilizing a high respiratory rate after intubation. The patient most likely is acidotic and has marginally normal or low potassium level due to diuretic and bronchodilator therapy. With a too-rapid respiratory rate, the patient will become alkalotic, causing an intracellular shift in potassium with potentially dangerous hypokalemia as a result.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Mar 13, 2008