Chronic Obstructive Pulmonary Disease, Chronic Bronchitis, and Emphysema

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Chronic Obstructive Pulmonary Disease, Chronic Bronchitis, and Emphysema

Chapter Objectives

After reading this chapter, you will be able to:

• Describe the American Thoracic Society (ATS) guidelines for chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema.

• Discuss the Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition of COPD.

• List the etiology and epidemiology and risk factors associated with COPD.

• Describe the GOLD global strategy for diagnosing COPD.

• Describe the key indicators for considering a COPD diagnosis.

• Dyspnea

• Chronic cough

• Chronic sputum production

• History of exposure to risk factors

• Describe the three main pulmonary function study measurements used to confirm the clinical suspicion of COPD:

• Forced vital capacity (FVC)

• Forced expiratory volume in 1 second (FEV1)

• Forced expiratory volume in 1 second/forced vital capacity ratio (FEV1/FVC ratio)

• Differentiate the following four stages of COPD as outlined by GOLD:

• Stage I: Mild COPD

• Stage II: Moderate COPD

• Stage III: Severe COPD

• Stage IV: Very severe COPD

• Identify additional diagnostic studies for patients identified as having Stage II, Stage III, or Stage IV COPD:

• Bronchodilator reversibility testing

• Chest x-ray examination

• Arterial blood gas measurement

• Alpha1-antitrypsin deficiency screening

• List the anatomic alterations of the lungs caused by both chronic bronchitis and emphysema.

• List the cardiopulmonary clinical manifestations caused by the anatomic alterations and pathophysiologic mechanisms associated with chronic bronchitis and emphysema.

• Identify the key distinctive differences between chronic bronchitis and emphysema—the “pink puffer” and the “blue bloater.”

• Describe the GOLD global strategy for the management and prevention of COPD.

• Describe additional treatment considerations for emphysema, including the following:

• Alpha1-antitrypsin replacement therapy

• Lung volume reduction surgery

• Lung transplantation

• Describe the clinical strategies and rationales of the SOAPs presented in the case studies.

• Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

Key Terms

Introduction

The American Thoracic Society (ATS) guidelines for chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema provide the following definitions:

Chronic obstructive pulmonary disease is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences.

Chronic bronchitis is defined clinically as chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of productive chronic cough have been excluded.

Emphysema is defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.

In patients with COPD either or both of those conditions may be present. However, the relative contribution of each to the disease process is often difficult to discern.

Note that the ATS’s definition for chronic bronchitis is based on the major clinical manifestations associated with the disease. Also note that the ATS’s definition for emphysema is based on the pathology, or the anatomic alterations of the lung, associated with the disorder.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) now provides the following working definition*:

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.

Note that the GOLD definition does not use the terms chronic bronchitis and emphysema. This is because, as GOLD explains, chronic bronchitis, which is defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years (i.e., clinical manifestations), is not necessarily associated with airflow limitation. GOLD further points out that emphysema, which is defined as destruction of the alveoli, is a pathologic term (i.e., anatomic alterations of the lung) that is sometimes—and incorrectly—used to describe only one of several structural abnormalities present in patients with COPD.

The bottom line is this: Even though chronic bronchitis and emphysema can each develop alone, they often occur together as one disease complex. When this happens, the disease entity is called chronic obstructive pulmonary disease. In other words, COPD is a term referring to two lung diseases—chronic bronchitis and emphysema—occurring simultaneously. Patients with COPD demonstrate a variety of clinical manifestations associated with both disorders—although the relative contribution of each respiratory disorder is often difficult to ascertain. This is why, in large part, the treatment of chronic bronchitis, emphysema, or a combination of both disorders (COPD) is essentially the same in the clinical setting.

Anatomic Alterations of the Lungs Associated with Chronic Bronchitis

The conducting airways (particularly the bronchi) are the primary structures that undergo change in chronic bronchitis. As a result of chronic inflammation the bronchial walls are narrowed by vasodilation, congestion, and mucosal edema. This condition is often accompanied by bronchial smooth muscle constriction. In addition, continued bronchial irritation causes the submucosal bronchial glands to enlarge and the number of goblet cells to increase, resulting in excessive mucous production. The number and function of cilia lining the tracheobronchial tree are diminished, and the peripheral bronchi are often partially or totally occluded by inflammation and mucous plugs, which in turn leads to hyperinflated alveoli (see Figure 11-1).

image
FIGURE 11-1 Chronic bronchitis, one of the most common airway diseases. AWO, Airway obstruction; ESG, enlarged submucosal gland; HALV, hyperinflation of alveoli (distal to airway obstruction); IEP, inflammation of epithelium; MA, mucous accumulation; MP, mucous plug.

The following major pathologic or structural changes are associated with chronic bronchitis:

Anatomic Alterations of the Lungs Associated with Emphysema

Emphysema is characterized by a weakening and permanent enlargement of the air spaces distal to the terminal bronchioles and by destruction of the alveolar walls. As these structures enlarge and the alveoli coalesce, many of the adjacent pulmonary capillaries also are affected, and this results in a decreased surface area for gas exchange. Furthermore, the distal airways, weakened in the process, collapse during expiration in response to increased intrapleural pressure. This traps gas in the alveoli. There are two major types of emphysema: panacinar (panlobular) emphysema and centriacinar (centrilobular) emphysema.

In panacinar emphysema, or panlobular emphysema, there is an abnormal weakening and enlargement of all alveoli distal to the terminal bronchioles, including the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli—the entire acinus is affected by dilatation and destruction. The alveolar-capillary surface area is significantly decreased (see Figure 11-2). Panlobular emphysema commonly is found in the lower parts of the lungs and often is associated with a deficiency of alpha1-antitrypsin. Panlobular emphysema is the most severe type of emphysema and therefore the most likely to produce significant clinical manifestations.

image
FIGURE 11-2 Panlobular emphysema. A, Normal alveoli for comparison purposes. B, Panlobular emphysema: abnormal weakening and enlargement of all air spaces distal to the terminal bronchioles. C, Excessive bronchial secretions from bronchitis, a common alteration of the lungs.

In centriacinar emphysema, or centrilobular emphysema, the pathology involves the respiratory bronchioles in the proximal portion of the acinus. The respiratory bronchiolar walls enlarge, become confluent, and are then destroyed. A rim of parenchyma remains relatively unaffected (see Figure 11-3). Centriacinar emphysema is the most common form of emphysema and is strongly associated with cigarette smoking and with chronic bronchitis.

The following are the major pathologic or structural changes associated with emphysema:

Etiology and Epidemiology

Although the precise incidence of COPD is not known, it is estimated that 10 to 15 million people in the United States have chronic bronchitis, emphysema, or a combination of both. Most authorities agree that COPD is underdiagnosed. It is felt that if you take into account the people who have not been “officially” diagnosed with COPD, the incidence would be over 20 million people in the United States. It is generally accepted that more people have chronic bronchitis than emphysema. For example, the National Center for Health Statistics estimates that in the United States about 9.5 million people have chronic bronchitis and 4.1 million people have emphysema. In 2004 the annual cost related to COPD in the United States was about $37.2 billion—including $20.9 billion in direct costs, $7.4 billion in morbidity costs, and $8.9 billion in indirect costs.

COPD is the fourth leading cause of death, claiming more that 100,000 Americans each year. It is estimated that COPD will become the third leading cause of death by 2020. Historically, more men than women have died from COPD each year. Since the year 2000, however, more women than men have died from COPD each year. In 2004, almost 61,000 women died of COPD compared with 57,000 men.

Risk Factors

According to GOLD, COPD risk factors are related to the total burden of inhaled particles a person encounters over his or her lifetime. GOLD recognizes the following as risk factors for COPD:

• Tobacco smoke—including smoke from cigarette, pipe, cigar, and other types of tobacco smoking popular in many countries, as well as environmental tobacco smoke. According to GOLD, cigarette smoking is the most commonly encountered risk factor for COPD worldwide.

• Occupational dusts and chemicals—vapors, irritants, and fumes, when the exposures are sufficiently intense or prolonged.

• Indoor air pollution—from biomass fuel used for cooking and heating in poorly vented dwellings, a risk factor that particularly affects women in developing countries.

• Outdoor air pollution—also contributes to the lungs’ total burden of inhaled particles and gases (e.g., silicates, sulfur dioxide, the nitrogen oxides, and ozone), although it appears to have a relatively small effect in causing COPD.

• Conditions that affect normal lung growth—any condition that affects lung growth during gestation and childhood (e.g., low birth weight, respiratory infections) has the potential for increasing an individual’s risk for developing COPD.

• Genetic predisposition (alpha1-antitrypsin deficiency)—in about 1 out of every 50 cases of emphysema, there is a specific hereditary basis for panlobular emphysema called alpha1 (or α1)-antitrypsin deficiency. Alpha1-antitrypsin is a major protein in the blood. It is produced by the liver. Alpha1-antitrypsin protects the lungs by blocking the effects of a powerful enzyme called elastase. Elastase is carried by the body’s white cells to help kill invading bacteria and to neutralize small particles inhaled into the lung. When old white cells are destroyed in the lungs, elastase is released. Under normal circumstances, alpha1-antitrypsin works to inactivate the released elastase. However, when the alpha1-antitrypsin level is low, the elastase is free to attack and destroy the elastic tissue of the lungs.

• The normal level of alpha1-antitrypsin is 200 to 400 mg/dL. Patients with normal levels of alpha1-antitrypsin are referred to genetically as having an MM phenotype or simply an M phenotype (homozygote). The phenotype associated with severely low serum concentrations is the ZZ phenotype, or simply Z. The heterozygous offspring of parents with the M and Z phenotypes have an MZ phenotype. The MZ phenotype results in an intermediate deficiency of alpha1-antitrypsin. The precise effect of the intermediate level of alpha1-antitrypsin is unclear. It is strongly recommended, however, that individuals with this phenotype not smoke or work in areas having significant environmental air pollution.

New on the list of risk factors is the notion that the remodeling of airways that occurs in asthma may be a harbinger of COPD. It will be interesting to see if this concern plays out.

Diagnosis of Chronic Obstructive Pulmonary Disease

According to GOLD, the diagnosis of COPD should be considered for any patient who is over 40 years of age and has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease, especially cigarette smoking. The key indicators for considering a COPD diagnosis are as follows:

Although these indicators are not diagnostic by themselves, the presence of multiple indicators significantly increases the probability of a diagnosis of COPD. When multiple key indicators are present, the diagnosis of COPD should be confirmed by a pulmonary function study.

Pulmonary Function Study in the Diagnosis of Chronic Obstructive Pulmonary Disease

The three main spirometry tests used to identify COPD are the forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and forced expiratory volume in 1 second/forced vital capacity ratio (FEV1/FVC ratio). Clinically, the FEV1/FVC ratio is also commonly called the forced expiratory volume 1 second percentage (FEV1%). Figure 11-4 illustrates a normal spirogram and a spirogram typical of patients with mild to moderate COPD.

image
FIGURE 11-4 Normal spirogram and spirogram typical of patients with mild to moderate chronic obstructive pulmonary disease.

image OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Chronic Bronchitis and Emphysema (COPD)a

The following clinical manifestations result from the pathophysiologic mechanisms caused (or activated) by Excessive Bronchial Secretions (see Figure 9-12) and Bronchospasm (see Figure 9-11)—the major anatomic alterations of the lungs associated with chronic bronchitis (see Figure 11-1); and the clinical manifestations activated by distal airway and alveolar weakening (see Figure 9-13)—the major anatomic alterations of the lungs associated with emphysema (see Figures 11-2 and 11-3).

image
FIGURE 11-3 Centrilobular emphysema. Abnormal weakening and enlargement of the respiratory bronchioles and alveoli in the proximal portion of the acinus.

image

Chest Assessment Findings Emphysema Chronic Bronchitis
Inspection    
General body build Thin, underweight Stocky, overweight
Altered sensorium—anxiety, irritability

Barrel chest Classic sign Occasionally Digital clubbing Late stage Common Cyanosis Uncommon—often reddish skin Common Peripheral edema and venous distention End-stage emphysema Use of accessory muscles Common, especially during exacerbations Common—severe stage Uncommon Pursed-lip breathing Common Uncommon Cough Sputum Palpation of the Chest Normal Percussion of the Chest Normal Auscultation of the Chest

image

CLINICAL DATE OBTAINED FROM LABORATORY AND SPECIAL PROCEDURES

Pulmonary Function Test Findings

Moderate to Severe Chronic Bronchitis and Emphysema (Obstructive Lung Pathophysiology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC FEVT FEV1/FVC ratio FEF25%-75%
↓ ↓ ↓ ↓
FEF50% FEF200-1200 PEFR MVV
↓ ↓ ↓ ↓

image

LUNG VOLUME AND CAPACITY FINDINGS

VT IRV ERV RVb  
N or ↑ N or ↓ N or ↓ ↑  
VC IC FRCb TLC RV/TLC ratio
↓ N or ↓ ↑ N or ↑ N or ↑

image

bAir trapping, and a subsequent increase in the RV and FRC, is uncommon in patients with only chronic bronchitis.

DIFFUSION CAPACITY (DLCO)c

Emphysema Chronic Bronchitis
Decreased
A decreased Dlco is a classic diagnostic sign of emphysema		 Normal

cThe most accurate way to express DLCO as the DLCO corrected for alveolar volume (DL/VA). This measure is always reduced in severe emphysema and reflects the loss of alveolar-capillary membrane.

Arterial Blood Gases

Chronic Bronchitis and Emphysema

dChronic ventilatory failure is more commonly seen in the patient with chronic bronchitis during the moderate and severe stages. Chronic ventilatory failure usually does not develop in emphysema until the severe stage.

Oxygenation Indicese for Chronic Bronchitis and Emphysema, Moderate to Severe Stages

eDO2, Total oxygen delivery; C(a-image)O2, arterial-venous oxygen difference; O2ER, oxygen extraction ratio; image, pulmonary shunt fraction; image, mixed venous oxygen saturation; image, oxygen consumption.

Hemodynamic Indicesg for Chronic Bronchitis and Emphysema, Moderate to Severe Stages

CVP RAP image PCWP CO SV
↑ ↑ ↑ N N N
SVI CI RVSWI LVSWI PVR SVR
N N ↑ N ↑ N

image

gCO, Cardiac output; CVP, central venous pressure; LVSWI, left ventricular stroke work index; image, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; RAP, right atrial pressure; RVSWI, right ventricular stroke work index; SV, stroke volume; SVI, stroke volume index; SVR, systemic vascular resistance.

image

RADIOLOGY FINDINGS

image
FIGURE 11-5 Chest x-ray film from a patient with chronic bronchitis. Note the translucent (dark) lung fields at the bases, depressed diaphragms, and long and narrow heart.
image
FIGURE 11-6 Chronic bronchitis. Bronchogram with localized view of left hilum. Rounded collections of contrast lie adjacent to bronchial walls and are particularly well demonstrated below the left main stem bronchus (arrow) in this film. They are caused by contrast in dilated mucous gland ducts. (From Hansel DM, Armstrong P, Lynch DA, McAdams HP, eds: Imaging of the diseases of the chest, ed 4, St Louis, 2005, Mosby.)
image
FIGURE 11-7 Chest x-ray film of a patient with emphysema. The heart often appears long and narrow as a result of being drawn downward by the descending diaphragm.
image
FIGURE 11-8 Emphysema. Lateral chest radiograph demonstrates a characteristically large retrosternal radiolucency with increased separation of the aorta and sternum measuring 4.6 cm, 3 cm below the angle of Louis and extending down to within 3 cm of the diaphragm anteriorly. Both costophrenic angles are obtuse, and both hemidiaphragms are flat. (From Hansel DM, Armstrong P, Lynch DA, McAdams HP, eds: Imaging of the diseases of the chest, ed 4, St Louis, 2005, Mosby.)
image
FIGURE 11-9 Cor pulmonale. A, A 50-year-old man with chronic airflow obstruction. Lungs are large in volume, the diaphragm is flat, and vascular attenuation is evident at the right apex. These features suggest emphysema, and this diagnosis was supported by a low carbon monoxide diffusion capacity. Lung “markings” are increased peripherally, particularly in the left midzone. B, The patient became chronically hypoxic and, with respiratory infections, hypercapnic. One of these episodes was associated with cor pulmonale when the patient became edematous, and the heart and hilar and pulmonary parenchymal vessels became enlarged. The emphysematous right upper zone shows fewer vascular markings and is relatively transradient. The diaphragm is less depressed and more curved than before. (From Hansell DM, Armstrong P, Lynch DA, McAdams HP, eds: Imaging of the diseases of the chest, ed 4, St Louis, 2005, Mosby.)

No radiographic abnormalities may be present in chronic bronchitis if only the large bronchi are affected. This often explains why the diagnosis is delayed. Although the situation is uncommon, if the more peripheral bronchi are involved, air trapping may occur. This is revealed on x-ray film as areas of translucency or areas that are darker in appearance. In addition, because of the increased functional residual capacity, the diaphragms may be depressed or flattened and are seen as such on the radiograph (Figure 11-5). Because bronchial wall thickening is common in chronic bronchitis, increased, diffuse, fibrotic-appearing lung markings are often seen. This is commonly referred to as a “dirty chest x-ray.” Finally, because right and left ventricular enlargement and failure are commonly associated with chronic bronchitis, in the late stage an enlarged heart may be seen on the chest radiograph. Bronchogram Small spikelike protrusions (“train tracks” appearance of airways) from the larger bronchi are often seen on bronchograms of patients with chronic bronchitis. It is believed that the spikes result from pooling of the radiopaque medium in the enlarged ducts of the mucous glands (Figure 11-6). Since the advent of the computed tomography (CT) examination, bronchograms are rarely done today on patients with chronic bronchitis. A “thin-section” CT exam is even more helpful.
  Emphysema
Chest Radiograph
Because of the decreased lung recoil and air trapping in emphysema, the functional residual capacity increases and the radiographic density of the lungs decreases. Consequently, the resistance to x-ray penetration is not as great, causing areas of translucency or areas that are darker in appearance. Because of the increased functional residual capacity, the diaphragm is depressed or flattened and the heart is often long and narrow (Figure 11-7). The lateral chest radiograph characteristically shows an increased retrosternal air space (more than 3.0 cm from the anterior surface of the aorta to the back of the sternum measured 3.0 cm below the manubriosternal junction) and flattened diaphragms (Figure 11-8).
Because right ventricular enlargement and failure sometimes develop as secondary problems during the advanced stages of emphysema, an enlarged heart may be seen on the chest radiograph (Figure 11-9).

image

aChronic bronchitis and emphysema frequently occur together as a disease complex referred to as chronic obstructive pulmonary disease (COPD). Patients with COPD typically demonstrate clinical manifestations of both chronic bronchitis and emphysema.

The presence of COPD is confirmed when the both FEV1 and FEV1/FVC ratio are decreased. A postbronchodilator FEV1 is recommended for both the diagnosis and assessment of the severity of COPD. Although the degree of spirometric abnormality usually determines the severity of COPD, the extent of the symptoms should also be considered when an individualized management program is developed for each patient.

Stages of chronic obstructive pulmonary disease.

GOLD now recognizes the following four stages of COPD:

Stage I, mild COPD, consists of mild airflow limitation (FEV1/FVC < 70%; FEV1 ≥ 80% predicted). At this stage the symptoms may be so mild that an individual may not recognize abnormal lung function.

Stage II, or moderate COPD consists of worsening airflow limitation (FEV1/FVC < 70%; FEV1 50% to <80% of predicted). The patient often complains of shortness of breath upon exertion. The patients usually will seek medical attention at this stage because of their symptoms.)

Stage III, severe COPD, includes further worsening of the airflow limitation (FEV1/FVC < 70%; FEV1 30% to <50% of predicted). At this stage the symptoms have an impact on the patient’s quality of life.

Stage IV, very severe COPD, includes severe airflow limitation (FEV1/FVC < 70%; FEV1 < 30% predicted, or FEV1 < 50% predicted, plus chronic ventilatory failure). Quality of life is very impaired and exacerbations may be life threatening.

Additional Diagnostic Studies for Chronic Obstructive Pulmonary Disease

In patients who are diagnosed with Stage II: Moderate COPD, Stage III: Severe COPD, and Stage IV: Very Severe COPD, GOLD also recommends the following additional tests for further assessments:

• Bronchodilator reversibility testing: To rule out a diagnosis of asthma, particularly in patients with an atypical history (e.g., asthma in childhood and regular nocturnal night waking with cough and wheeze).

• Chest x-ray examination: Seldom diagnostic in COPD but valuable to exclude alternative and/or additional diagnoses, such as pulmonary tuberculosis, and pneumonia, and to identify comorbidities such as cardiac failure.

• Arterial blood gas measurement: Perform in patients with FEV1 <50% predicted or with clinical signs suggestive of ventilatory failure or right-sided heart failure. The major clinical sign of ventilatory failure is cyanosis. Clinical signs of right-sided heart failure include ankle edema and an increase in the jugular venous pressure. Ventilatory failure is indicated by a Pao2 <60 mm Hg, with or without a Paco2 >50 mm Hg while breathing room air.

• Alpha1-antitrypsin deficiency screening: Perform when COPD develops in patients of Caucasian descent under 45 years of age or with a strong family history of COPD.

Key Distinguishing Features between Emphysema and Chronic Bronchitis

Even though chronic bronchitis and emphysema often occur as one disease complex (COPD), they can develop alone. A complete presentation of all the specific signs and symptoms associated with emphysema and chronic bronchitis are provided in the Overview section on pages 172 and 176. An abbreviated and handy overview of the key distinguishing features between emphysema and chronic bronchitis is provided as follows:

Clinically, the patient with emphysema is sometimes classified as a “pink puffer,” or a patient with type A COPD; and the patient with chronic bronchitis is sometimes classified as a “blue bloater,” or a patient with type B COPD. These general terms are primarily based on the clinical manifestations commonly associated with each respiratory disorder.

Pink Puffer (Type A Chronic Obstructive Pulmonary Disease)

The term pink puffer is derived from the reddish complexion and the “puffing” (pursed-lip breathing) commonly seen in the patient with emphysema. The major pathophysiologic mechanisms responsible for the red complexion and puffing are the following:

• Emphysema is caused by the progressive destruction of the distal airways and pulmonary capillaries.

• The progressive elimination of the pulmonary capillaries leads to a reduced pulmonary blood flow throughout the lungs—that is, an overall increased ventilation-perfusion ratio.

• To compensate for the increased ventilation-perfusion ratio in the patient who has emphysema hyperventilates.

• The increased respiratory rate, in turn, works to maintain a relatively normal arterial oxygenation level and causes a ruddy or flushed skin complexion. During the end stage of emphysema, however, the patient’s oxygenation status decreases and the carbon dioxide level increases.

• Thus, the patient with emphysema, who has both a red complexion and a rapid respiratory rate, is called a pink puffer.

In addition to the marked dyspnea and ruddy complexion, the pink puffer tends to be thin (because of the muscle wasting and weight loss associated with the increased work of breathing), has a barrel chest (because of overinflated lungs), uses accessory muscles of inspiration, and exhales through pursed lips.

Blue Bloater (Type B Chronic Obstructive Pulmonary Disease)

The term blue bloater is derived from the cyanosis—the bluish color of the lips and skin—commonly seen in the patient with chronic bronchitis. The bluish complexion is caused by the following:

• Unlike emphysema, the pulmonary capillaries in the patient with chronic bronchitis are not damaged. The patient with chronic bronchitis responds to the increased airway obstruction by decreasing ventilation and increasing cardiac output—that is, a decreased ventilation-perfusion ratio.

• The chronic hypoventilation and increased cardiac output (decreased ventilation-perfusion ratio) leads to a decreased arterial oxygen level, an increased arterial carbon dioxide level, and a compensated (normal) pH—or chronic ventilatory failure arterial blood gases (also called compensated respiratory acidosis). The respiratory drive is depressed in patients with chronic ventilatory failure.

• The persistent low ventilation-perfusion ratio and depressed respiratory drive both contribute to a chronically reduced arterial oxygenation level and polycythemia—which, in turn, causes cyanosis.

In addition, the blue bloater tends to be stocky and overweight, has a chronic productive cough, and frequently has swollen ankles and legs and distended neck veins as a result of right-sided heart failure (cor pulmonale).

Table 11-1 provide an overview of the more common distinguishing features between emphysema and chronic bronchitis.

TABLE 11-1

Key Features Distinguishing Emphysema from Chronic Bronchitis*

Clinical Manifestation Emphysema
(Type A COPD: Pink Puffer)		 Chronic Bronchitis
(Type B COPD: Blue Bloater)
Inspection
Body build Thin Stocky, overweight
Barrel chest Common—classic sign Normal
Respiratory pattern

Pursed-lip breathing Common Uncommon Cough Uncommon Common—classic sign Sputum Uncommon Cyanosis Uncommon (reddish skin) Common Peripheral edema Uncommon Neck vein distention Uncommon Use of accessory muscles Common Uncommon Auscultation Decreased breath sounds, decreased heart sounds, prolonged expiration Wheezes, crackles, rhonchi, depending on severity of disease Percussion Hyperresonance Normal Laboratory Tests Chest radiograph Hyperinflation, narrow mediastinum, normal or small vertical heart, low flat diaphragm, presence of blebs or bullae Congested lung fields, densities, increased bronchial vascular markings, enlarged horizontal heart Polycythemia Uncommon Common Infections Occasionally Common Pulmonary Function Study Dlco and Dlco/VA Decreased Often normal Other Pulmonary hypertension Uncommon Common Cor pulmonale Uncommon

image

The clinical features of emphysema and chronic bronchitis are not always clear-cut because many patients have a combined disease process (COPD—this is especially the case during the late stages of emphysema and chronic bronchitis).

General Management of Chronic Obstructive Pulmonary Disease

Global Initiative for Chronic Obstructive Lung Disease

In 1998, GOLD was created to increase the awareness of COPD among health professionals, public health authorities, and the general public and to improve prevention and management through worldwide efforts. GOLD prepares scientific reports on COPD, encourages dissemination and adoption of the reports, and promotes international collaboration on COPD research.

GOLD provides an outstanding COPD management program that includes the following goals: relieve symptoms, prevent disease progression, improve exercise tolerance, improve health status, prevent and treat complications and exacerbations, reduce mortality and to prevent or minimize side effects from treatment. A COPD management program should help to achieve these goals. The GOLD program consists of (1) assessing and monitoring the disease, (2) reducing risk factors, (3) managing stable COPD, and (4) managing exacerbations.

The first component of the COPD management program involves assessing and monitoring the disease. The following should be included in an assessment of a patient known or thought to have COPD:

The second component, reducing risk factors, is an important step in a COPD management program. Smoking cessation is the single most effective way to reduce the risk of developing COPD as well as slowing its progression. Preventing risks of occupational exposures is also important. Also, patients should avoid indoor and outdoor air pollution.

The third component is to manage the stable COPD patient. In order to achieve this you must determine the disease severity on an individual basis, implement a treatment plan that reflects the severity, and choose treatments according to national and cultural preferences, the patient’s abilities and preferences and the availability of medications. Patient education is important to improve skills and the patient’s ability to deal with the disease. Pharmacologic treatments used to control and prevent symptoms, reduce exacerbation, and improve exercise tolerance and quality of life can be found in Table 11-2. Bronchodilators are medications that are frequently used in symptom management of COPD. The inhaled method is preferred and these medications are given as needed to relieve and prevent worsening of symptoms. Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators.

TABLE 11-2

Medications Commonly Used in the Treatment of Chronic Obstructive Pulmonary Disease

Drug Inhaler (µg) Solution for Nebulizer (mg/mL) Oral Vials for Injection (mg) Duration of Action (hours)
Beta2-Agonists
Short-Acting Beta2-Agonists
Fenoterol 100-200 (MDI) 1 0.05% (syrup)   4-6
Levalbuterol       0.63, 1.25 4-6
Salbutamol (albuterol) 100, 200 (MDI and DPI) 5 5 mg (pill) syrup 0.024% 0.1, 0.5 4-6
Terbutaline 400, 500 (DPI)   2.5, 5 (pill) 0.2, 0.25 4-6
Long-Acting Beta2-Agonists
Formoterol 4.5-12 (MDI and DPI)       12+
Salmeterol 25-50 (MDI and DPI)       12+
Anticholinergics
Short-Acting Anticholinergics
Ipratropium bromide 20, 40 (MDI) 0.25-0.5     6-8
Oxitropium bromide 100 (MDI) 1.5     7-9
Long-Acting Anticholinergics
Tiotropium 18 (DPI)       24+
Combination Short-Acting Beta2-Agonists Plus Anticholinergic in One Inhaler
Fenoterol and ipratropium 200/80 (MDI) 1.25/0.5     6-8
Oxitropium bromide 75/15 (MDI) 0.75/4.5     6-8
Methylxanthines
Aminophylline     200-600 mg (pill) 240 mg Variable, up to 24
Theophylline (SR)     200-600 mg (pill)   Variable, up to 24
Inhaled Glucocorticosteroids
Beclomethasone 50-400 (MDI and DPI) 0.2-0.4      
Budesonide 100, 200, 400 (DPI) 0.20, 0.25, 0.5      
Fluticasone 50-500 (MDI and DPI)        
Triamcinolone 100 (MDI) 40   40  
Combination Long-Acting Beta2-Agonists Plus Glucocorticosteroids in One Inhaler
Formoterol and budesonide 4.5/160, 9/320 (DPI)        
Salmeterol and fluticasone 50/100, 250, 500 (DPI)
25/50, 125, 250 (MDI)		        
Systemic Glucocorticosteroids
Prednisone   5-60 mg (pill)      
Methyl-prednisolone   4, 8, 16 mg (pill)      

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Data from Global Initiative for Chronic Obstructive Lung Disease (GOLD): Pocket Guide to COPD Diagnosis, Management, and Prevention. A Guide for Health Care Professionals, 2007, GOLD, available at: www.goldcopd.org; and Gardenshire DS: Rau’s respiratory care pharmacology, ed 7, St. Louis, 2008, Elsevier.

The fourth component is management of exacerbations. An exacerbation is an event in the natural course of the disease that involves a change in the patient’s baseline dyspnea, cough or sputum and is beyond the normal day-to-day variations. An exacerbation is acute in onset and may be reason for change in a patient’s regular medication. The cause of about one third of severe exacerbations cannot be identified; however, the most common cause is an infection of the tracheobronchial tree and air pollution. In order to assess the severity of an exacerbation a patient must have his or her arterial blood gases measured, chest x-rays examined, and an electrocardiogram must be performed. Home management of an exacerbation consists of use of bronchodilators and glucocorticosteroids. If a patient has any of the following characteristics he or she should be hospitalized:

Figure 11-10 provides an overview of a chronic obstructive pulmonary disease (COPD) management algorithm recommended by GOLD.

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FIGURE 11-10 Chronic obstructive lung disease (COPD) management.

GOLD provides an excellent framework for the management of COPD that can be adapted to local health care systems and resources. Educational tools, such as laminated cards or computer-based learning programs, can be prepared that are tailored to these systems and resources. As of this writing, the GOLD program includes the following publications:

These publications are freely available on the Internet at www.goldcopd.org.

Respiratory Care Treatment Protocols

Oxygen Therapy Protocol

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in cystic fibrosis is caused by the pulmonary shunting associated with the disorder. When the patient demonstrates chronic ventilatory failure during the advanced stages of COPD, caution must be taken not to overoxygenate the patient (see Oxygen Therapy Protocol, Protocol 9-1).

CASE STUDY

Chronic Bronchitis

Admitting History and Physical Examination

This 66-year-old man has worked in a cotton mill in South Carolina for the past 37 years. He has a 120 pack/year (3 packs/day for 40 years) history of cigarette smoking, and he also chews tobacco regularly. He sought medical assistance in the chest clinic because of a chronic cough. He described it as a “smoker’s cough” and stated that it was present about 4 to 5 months of the year. For the past 3 years, his cough produced grayish-yellow sputum during the winter months. The sputum was thick and yellow. He stated that he was more short of breath during moderate exercise. He attributed this to “getting older.” The patient stated he had not been taking any pulmonary medications.

On physical examination the patient was in mild respiratory distress. He was obese (270 lb). He occasionally generated a strong productive cough during the visit. His sputum appeared grayish-yellow. Auscultation of the chest revealed moist rhonchi and scattered wheezes and crackles. An arterial blood gas assessment showed pH 7.36, Paco2 87, 48, and Pao2 64. The chest radiograph revealed increased markings in the lower lung fields bilaterally. No pulmonary hyperinflation was noticed. Spirometry showed a decrease in the FEV1/FVC ratio (55% of predicted) and a decreased FEV1 (35% of predicted). The respiratory care practitioner’s assessment at this time was documented in the patient’s chart as follows.

Respiratory Assessment and Plan

S “Smoker’s cough,” sputum production, dyspnea

O Strong productive cough. Sputum: Yellow-gray. Breath sounds: Rhonchi and crackles at lung bases. ABG: pH—7.36, Paco2—87, —48, Pao2—64. X-ray: increased markings at bases. PFTs: decreased FEV1/FVC ratio (55% of predicted), decreased FEV1 (35% of predicted).

A

P Bronchopulmonary Hygiene Therapy Protocol (cough and deep breathing, prn). Patient education on smoking. Refer to Smoking Cessation Clinic. Aerosolized Medication Protocol (med. neb. treatment with Levalbuterol q6h).

The patient was advised to stop smoking and seek medical assistance if his sputum became progressively more thick and yellow or his dyspnea became worse. The physician also prescribed a pneumococcal polysaccharide vaccine. Also prescribed was an inhaled glucocorticosteroid (beclomethasone) tid prn, and a formoterol inhaler twice a day. The Smoking Cessation Clinic prescribed slow-release nicotine patches, and the patient attended a week-long smoking cessation program. The patient did well, and at the 6-month follow-up visit he was no longer smoking. At this time, the patient stated that he had not had his “smoker’s cough” or produced any sputum in weeks.

A year later, however, the patient came to the emergency room and was clearly not doing well. He was back to his three-packs-per-day cigarette smoking habit, and he had been physically inactive and gained 30 pounds (to a weight of 300 lb) over the past year. He stated that he frequently coughed and it was more troublesome in the early morning. The patient also reported that his cough was now productive—about 3 to 4 tablespoons of thick yellow and green sputum daily. He complained of dyspnea during light exercise (e.g., stair climbing produced shortness of breath). On some days his increased work of breathing was more noticeable than on others. He denied hemoptysis, chest pain, orthopnea, fever, chills, or leg edema to the respiratory care team.

On observation, his ankles were swollen with pitting edema of 3+ and his neck veins were distended. He was cyanotic. Vital signs were as follows: blood pressure 165/90, heart rate 116 beats per minute, and a respiratory rate of 26 breaths per minute. His oral temperature was 98.4° F. Auscultation of the chest revealed bilateral posterior basilar rhonchi and crackles, which partially cleared with coughing. Expectorated sputum was copious, purulent, and yellow and green. A bedside spirometry showed an FEV1/FVC ratio of 55% and a FEV1 of 35%. On room air, his arterial blood gas values were pH 7.51, Paco2 51, image 39, Pao2 41. His resting Spo2 on room air was 83% and improved to 89% on 2 L of O2 per minute. His chest x-ray film showed diffuse, fibrotic-appearing lung markings and a moderately enlarged right side of the heart. His hemoglobin was 17.8 g%. At this time, the respiratory care practitioner reported the following SOAP note in the patient’s chart.

Respiratory Assessment and Plan

S Complains of productive cough and exertional dyspnea (history)

O Bibasilar crackles, wheezing, rhonchi, cyanosis, obesity. Vital signs: HR 116, BP 165/90, RR 26/min. Cough: productive with copious yellow green sputum. PFT: FEV1/FVC 55% and FEV1 of 35%. CXR: diffuse fibrotic lung markings and cor pulmonale. ABG: pH 7.51, Paco2 51, image 39, Pao2 41. Spo2 89% on 2 L/min O2. Hemoglobin 17.8 g%.

A

P Aerosolized Medication Therapy Protocol (MDI with combined albuterol and ipratropium, 2 puffs qid). Inhaled glucocorticosteroid (beclomethasone) qid. Bronchopulmonary Hygiene Therapy Protocol (cough and deep breathing under supervision qid, cautious trial of CPT with postural drainage to lower lobes, 3 times a day). Call physician about impending ventilatory failure and chest x-ray report of cor pulmonale. Also check to see whether the doctor wants to schedule complete pulmonary function test. Recheck Spo2 on room air. Again, advise and facilitate smoking cessation program.

Discussion

In the first portion of this case study, some of the clinical manifestations of chronic Excessive Airway Secretions (see Figure 9-11) were present. These findings were clearly documented in the first SOAP note when the therapist charted the presence of productive cough, rhonchi, and crackles sounds and pulmonary function findings that indicated airway obstruction.

The first part of this case also illustrates a definite role for the modern respiratory care practitioner. Such a professional may well be working in outpatient settings that necessitate the evaluation and treatment of patients such as this one. The history of productive cough and the findings of rhonchi and crackles in a smoker who is not seriously ill suggest a diagnosis of Stage III chronic bronchitis or COPD. The patient’s history, cough, sputum production, pulmonary function data, and chest x-ray examination confirm this suspicion. The physician’s prescription of pneumococcal polysaccharide vaccine and slow-release nicotine patches reflects the key elements of preventive therapy in chronic bronchitis—namely, avoidance of irritant fumes and particles; influenza and pneumococcal vaccines for prevention of those two common complicating diseases; and the need for continued follow-up.

In the second part of this case study, there were more of the classic clinical manifestations associated with chronic bronchitis. For example, the patient’s Excessive Bronchial Secretions (see Figure 9-11) not only resulted in hypoxia and cyanosis secondary to a decreased image ratio and pulmonary shunting but also produced increased airway resistance that resulted in rhonchi and crackles and a decreased FEV1/FVC ratio and FEV1. In addition, the second part of this case study started with the patient’s failure to stop smoking and with increased symptoms and worsening of his obstructive pulmonary disease (dyspnea and productive cough). The findings on the chest x-ray film also suggested cor pulmonale, which often occurs in bronchitis. His pulmonary function was worsening, and he had acute alveolar hyperventilation superimposed on chronic ventilatory failure with moderate to severe hypoxemia. Impending ventilatory failure was a serious concern.

In addition to treating the acute symptoms with a simple MDI bronchodilator regimen (see Protocol 9-4) and Bronchopulmonary Hygiene Therapy Protocol (see Protocol 9-2) in the form of cough and deep breathing, a cautious trial of chest physiotherapy, and postural drainage, the respiratory therapist does not give up on the longer-term but extremely important goal of modifying behavior (smoking cessation) in the patient. A complete pulmonary function test in the near future would further define the patient’s disease process, both in its nature and severity. Such data are often helpful to the patient’s understanding of just how ill he is and may constitute a “teachable moment” for the physician and therapist. Although the patient was discharged from the hospital 5 days later, he unfortunately died from another acute exacerbation of chronic bronchitis, ventilatory failure, and cardiac arrest 7 months later.

CASE STUDY

Emphysema

Admitting History and Physical Examination

This 27-year-old man was admitted to the hospital with the chief complaint of dyspnea on exertion. He had a 3-year history of recurrent respiratory problems that had necessitated several hospitalizations of several days’ duration in the past. Recently, his respiratory status had deteriorated to the point where he had to stop working. He had been employed for several years as a cook in a fast-food restaurant, where he was continuously exposed to a smoky environment. He had never smoked. On questioning, the patient related that he had been very short of breath for the past 6 weeks. He further stated that he was unable to walk up one flight of stairs without stopping, and his walking tolerance had decreased to about 100 yards.

On physical examination the patient appeared anxious. He was profusely sweating and was in moderate respiratory distress. He demonstrated a regular heart rate of 120 beats per minute, blood pressure of 140/70, respiratory rate of 32 breaths per minute, and an oral temperature of 100° F. Inspection of the chest revealed suprasternal notch retraction, with some use of the accessory muscles of inspiration. The lungs were hyperresonant to percussion, and breath sounds were diminished. His I : E ratio was 1 : 4. He had a barrel chest and his nail beds were moderately cyanotic. The patient was slightly confused—he was unable to concentrate well. The chest x-ray film showed moderate to severe hyperinflation of the lungs. Some infiltrates were present in the lower lung regions, and possible infiltrates were also noted in the right upper lobe. The radiology report suggested the presence of a pneumonic process superimposed on chronic lung disease.

Bedside spirometry revealed an FEV1/FVC ratio of 57% and an FEV1 of 40% of predicted. His arterial blood gases while on a 3 L/min O2 nasal cannula were pH 7.26, Paco2 82, image 36, and Pao2 of 48. The Sao2 was 75%. Laboratory studies revealed a hemoglobin of 16.5 g/dL and a white blood count of 15,000/mm3. Sputum cultures were positive for a variety of pathogenic and nonpathogenic organisms. The serum alpha1-antitrypsin level was 30 mg/dL (normal = 200 to 400 mg/dL). The remainder of the physical examination findings were not remarkable. The respiratory assessment read as follows.

Respiratory Assessment and Plan

S “I’m short of breath with any exercise at all.” Cough for past 6 weeks.

O HR 120, BP 140/70, RR 32, and temp 100° F. Use of accessory muscles of inspiration, increased AP diameter, cyanosis. Hyperresonant percussion note and diminished breath sounds. I:E ratio 1 : 4. Lower lung infiltrates, hyperinflation of lungs on CXR. PFT: FEV1/FVC ratio of 57% and FEV1 of 40%. ABGs: pH 7.26, Paco2 82, image 36, and Pao2 of 48. Sao2: 75%. Elevated WBC and gram-positive organisms in the sputum, alpha1-antitrypsin = 30 mg/dL.

A

P Notify doctor about acute ventilatory failure. Oxygen Therapy Protocol (HAFOE mask at Fio2 = 0.35). Place intubation equipment and ventilator on standby. Monitor and evaluate per ICU standing orders (Spo2, vital signs). Check ABG in 30 min.

The hospital course was relatively smooth. The HAFOE oxygen therapy was enough to increase the patient’s Pao2 to an acceptable level and correct the acute-on-chronic ventilatory failure. Within an hour the patient’s arterial blood gases were pH 7.36, Paco2 61, image 34, and Pao2 76. The patient’s heart rate, respiratory rate, and blood pressure returned to normal. Blood serologies suggested Mycoplasma pneumoniae infection. Intravenous antibiotics were prescribed. The patient was managed conservatively and improved steadily. When he appeared to have had the maximum benefit from the hospitalization, he was discharged with an oxygen concentrator, a portable “stroller,” and an oxygen-conserving device. He was to use O2 at 1 L/min at rest and 2.5 L/min with exercise for 18 to 24 hours a day. Arrangements were made to have him enroll in an alpha1-antitrypsin therapy trial and attend pulmonary rehabilitation classes. He was urged to secure employment elsewhere.

Discussion

This fascinating (but fortunately rare) form of emphysema is one in which “pure” emphysema is the dominant pathology. In patients with alpha1-antitrypsin deficiency, chronic bronchitis may be present, but it is much less common than is the usual, cigarette smoking–induced COPD. In this condition the patient’s deficiency of the protease inhibitor alpha1-antitrypsin resulted in WBC-mediated protease destruction of his pulmonary parenchyma. Note the slow, insidious onset of his symptoms.

The patient’s emphysema or Distal Airway and Alveolar Weakening (see Figure 9-12) was complicated by additional anatomic alterations of the lungs (i.e., Alveolar Consolidation [see Figure 9-8]). The alveolar consolidation was reflected in the patient’s immune-inflammatory response (fever and increased WBC), alveolar infiltrates (x-ray), low Pao2 (caused by a decreased image ratio and intrapulmonary shunting), and abnormal vital signs (see Figure 9-8).

The effects of distal airway and alveolar weakening were reflected in the patient’s increased AP diameter, use of accessory muscles of inspiration, hyperresonant percussion note, diminished breath sounds, PFT results, and the chest x-ray film, which showed alveolar hyperinflation (see Figure 9-12).

The selection of a good program of oxygen supplementation was certainly indicated. Note the selection of a HAFOE mask because of the patient’s initial significant CO2 retention. Pneumococcal and influenza prophylaxis were certainly indicated in this case. Frequent intravenous administration of alpha1-antitrypsin replacement represents modern therapy in the treatment of this unusual disease, as does counseling the patient that he should not knowingly expose himself to irritants such as those present in the smoky environment of his workplace.

Replacement alpha1-antitrypsin therapy does not repair the alveolar damage that has already occurred but is thought to stabilize the condition.

CASE STUDY

Chronic Obstructive Pulmonary Disease (COPD)

Admitting History and Physical Examination

This 73-year-old man was brought to this Chicago, Illinois emergency room by his adult son. The son stated that his father had a long history of cardiopulmonary problems with chronic productive cough and had been diagnosed as having COPD about 15 years ago. Over the past 10 years, the patient had been admitted to this hospital three different times for COPD exacerbations. The hospital’s electronic records showed that the patient had a long history of Stage III COPD. The patient required mechanical ventilation for 10 days during his last hospital stay. At the time of his last hospital discharge, his baseline FEV1/FVC ratio was 55% and his FEV1 was 35% of predicted. His Dlco was 60% of predicted. His baseline arterial blood gas values at his last hospital discharge were as follows: pH 7.37, Paco2 93, 53, and Pao2 63, Spo2 90%.

The patient had a long history of cigarette smoking, as well as working many long hours in smoke-filled rhythm-and-blues clubs throughout the Chicago area for over 40 years. The patient had been a rhythm and blues booking agent in the Chicago area since the late 1950s. He had worked with many of the greats—including, Muddy Waters, Buddy Guy, KoKo Taylor, Lonnie Brooks, and Candy Foster and the Shades of Blue. The patient stated that although he no longer worked in smoke-filled bars, he still smoked two to three packs of cigarettes per day. The patient’s son stated that when he checked in on his father earlier that day, he realized that his father was very confused and disoriented. The son immediately transported his father to the emergency room.

On examination the patient appeared to be in moderate to severe respiratory distress. He was anxious, confused, and disoriented. The patient stated that he could not take a deep enough breath. His vital signs were as follows: respiratory rate, 35 breaths per minute; heart rate, 145 beats per minute; blood pressure, 145/90; and temperature, 37° C. The patient was moderately overweight and had a barrel chest. His skin appeared cyanotic. He had a frequent weak cough. He produced a moderate amount of purulent, gray-yellow sputum with each cough. In an upright position, he used accessory muscles of inspiration. He had prolonged exhalations and he was pursed-lip breathing. He had 3+ pitting edema of his legs, ankles, and feet. His neck veins were distended. The patient had clubbing of his fingers and toes.

Palpation revealed decreased chest expansion. Hyperresonant percussion notes were present over both lung fields. Auscultation revealed diminished heart and breath sounds, with bilateral wheezes, rhonchi, and crackles heard over all lung fields. An x-ray film taken in the emergency room with a portable unit showed lung hyperinflation, depressed diaphragms, increased bronchial vascular markings, and an enlarged right side of the heart. Bedside spirometry was attempted, but the patient was too weak and confused to generate a good expiratory maneuver. Arterial blood gas values on a 2 L/min oxygen cannula were pH 7.24, Paco2 110, 55, Pao2 47, Spo2 77%. Laboratory results reveal a hemoglobin level of 19 g%. The respiratory therapist working in the emergency room documented the following assessment.

Respiratory Assessment and Plan

S:“I can’t take a deep breath.”

O:Moderate to severe respiratory distress. Vital signs: RR 35 bpm, HR: 145 bpm, BP: 145/90, T: 37° C. Barrel chest, cyanotic, frequent weak cough, moderate amount of purulent, gray-yellow sputum, using accessory muscles of inspiration, prolonged exhalation, pursed-lip breathing. 3+ pitting edema on legs, ankles, and feet. Distended neck veins, digital clubbing. Decreased chest expansion. Aus: diminished heart and breath sounds. Bilateral wheezes, rhonchi, and crackles could be heard over all lung fields. CXR: hyperinflation, depressed diaphragms, increased bronchial vascular markings, and an enlarged right heart. Arterial blood gas values on a 2 L/min O2 cannula were pH 7.24, Paco2 110, 55, Pao2 47, Spo2 77%. Hemoglobin level of 19 g%.

A:

P:Notify physician stat regarding acute ventilatory failure superimposed on chronic ventilatory failure. Also inform the physician about the clinical manifestations associated with cor pulmonale. Recommend Mechanical Ventilation Protocol and Oxygen Therapy Protocol. Start Bronchopulmonary Hygiene Therapy Protocol (chest physical therapy qid; suctioning prn). Start Aerosolized Medication Protocol (combination short-acting beta2-agonist plus long-acting anticholinergic—e.g., salbutamol/ipratropium). Supplement these agents with an inhaled glucocorticosteroid (beclomethasone tid).

Discussion

This case nicely demonstrates the clinical manifestations associated with both chronic bronchitis and emphysema—that is, COPD. The clinical manifestations of chronic bronchitis seen in this case include chronic productive cough, cor pulmonale (swollen lower extremities and distended neck veins), rhonchi, crackles and wheezing on auscultation, digital clubbing, and polycythemia (elevated hemoglobin level).

That the patient’s bronchitis was accompanied by emphysema was indicated by his lung hyperinflation (on inspection and on his chest x-ray film), his hyperresonant percussion note, and the presence of his pursed-lip breathing. The fact that he was in hypoxemic, hypercapnic respiratory failure—and that he required ventilator support—does not help to separate the two diagnoses. These arterial blood gas abnormalities can be seen in either condition. The clinical manifestations (clinical scenarios) in this case are caused by the anatomic alteration of the lungs associated with both chronic bronchitis and emphysema; these clinical scenarios are as follows:

Treatment in this case was first driven by the selection of a Ventilator Management Protocol. With this in place, the Oxygen Therapy Protocol and elements of the Bronchopulmonary Hygiene and Aerosolized Medication Protocols were begun with standard protocol specifics.

Determination of severe via the GOLD standards depend on spirometric demonstrations, which were not possible here. However, “respiratory failure” does qualify the patient as having Stage IV: Very Severe COPD, which raises the requirement for long-term oxygen therapy and consideration of surgical treatments “if applicable.” In this case, component 4 of the GOLD guidelines (Manage Exacerbations) was followed once the patient met the arterial blood gas criteria of respiratory acidosis and severe hypoxemia.

Unfortunately, this patient did not do well, and became ventilator-dependent. He died in a skilled nursing facility 3 months later, still “missing his smokes” and listening to rhythm and blues on his radio.

*GOLD (www.goldcopd.org) is recognized as a worldwide leading authority for the diagnosis, management, and prevention of COPD.

*The clinical features of emphysema and chronic bronchitis are not always clear-cut because many patients have a combined disease process (COPD—this is especially the case during the late stages of emphysema and chronic bronchitis).

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