COPD phenotypes
In the past, clinicians and researchers often distinguished two pathophysiologic types of COPD: type A and type B. These subtypes are no longer included in the definition of COPD, but the terms are embedded in older literature, so a brief discussion is given here. As originally conceived, type A (so-called “pink puffer”) physiology was associated with underlying emphysema, high minute ventilation, and relatively normal arterial PO2. Type B (so-called “blue bloater”) physiology was equated with chronic bronchitis, hypoxemia, hypercapnia, and cor pulmonale. These two types were thought to represent the two ends of the spectrum of COPD: “pure” emphysema or “pure” airways disease. It is now recognized that this framework is not useful in classifying patients, because the vast majority of patients with COPD have both aspects of the disease.
Currently, there is intense interest in developing a better understanding of COPD phenotypes, with the goal of identifying different clinically relevant classifications of the disease. An important current classification system, using categories A through D, relies upon an assessment of the patient’s symptoms as well as the risk for future exacerbations, based on the history of previous exacerbations (Fig. 6.8). Where the patient falls with respect to these two factors can then be used to personalize the approach to the patient’s therapeutic regimen.
FIGURE 6.8 Simplified depiction of the clinical classification scheme for COPD
defining phenotypes A to D based on the symptoms and history of exacerbations.
Source: (From the Global Strategy for Diagnosis, Management and Prevention of
COPD 2022, ©.)
Clinical features
Symptoms most commonly experienced by patients with COPD include dyspnea and cough, frequently with sputum production. Cough and sputum production may precede the development of dyspnea by many years. Most patients are symptomatic, but some are symptom-free, and the diagnosis of COPD is determined on the basis of pulmonary function tests.
Frequently, patients have a certain level of chronic symptoms, but their disease course is punctuated by periods of exacerbation. An exacerbation is defined as an acute event characterized by worsening of symptoms that requires a change in medication. The precipitating factor producing an exacerbation is often a respiratory tract infection of either viral or bacterial origin. A variety of bacteria are often chronically present in the tracheobronchial tree of patients with COPD, and an acute exacerbation can sometimes be due to the acquisition of a new strain of a colonizing bacterium. Other factors that cause acute deterioration in patients include exposure to a variety of air pollutants, bronchospasm (particularly if patients have a superimposed asthmatic component to their disease), and heart failure. However, in up to one-third of cases, the cause of an exacerbation cannot be identified. When exacerbations are severe, patients may develop frank respiratory failure, a complication discussed in Chapter 28.
The precipitating factor for an exacerbation of COPD is often either a viral or bacterial infection.
In addition to chronic symptoms of dyspnea, cough, or both, which may worsen during periods of acute exacerbation, patients may experience secondary cardiovascular complications of their lung disease (i.e., cor pulmonale). Patients with chronic hypoxemia and hypercarbia are particularly at increased risk for cor pulmonale.
Early in the course of the disease, physical examination may be normal or show only a prolonged expiratory time. As the process becomes more severe, characteristic findings are common. Breath sounds are generally decreased in intensity diffusely, and expiration is prolonged. Wheezing may be heard but does not necessarily reflect reversible bronchospasm. Some patients do not wheeze during normal tidal breathing, but do so when asked to give a forced exhalation. In patients with profuse airway secretions, coarse gurgling sounds labeled as rhonchi are frequently appreciated. Examination of the chest often discloses an increased anteroposterior diameter, indicating hyperinflation of the lungs. When diaphragmatic excursion is assessed by percussion of the lung bases during inspiration and expiration, diminished movement is noted.
In advanced COPD, patients may use accessory muscles of respiration (e.g., sternocleidomastoid and trapezius muscles), and the intercostal muscles may retract with each inspiration. The patient may assume a characteristic “tripod” position, leaning forward on straight arms allowing fixation of the clavicles and more effective use of accessory muscles. Pursed lip breathing may be observed. Severe disease may also be complicated by weight loss and muscle wasting. When cor pulmonale is present, with or without frank right ventricular failure, patients have the cardiac findings described in Chapter 14.
Smoking is not only the primary factor that initiates COPD but also a major risk factor that determines the prognosis of a patient’s illness. Patients who continue to smoke have the greatest progressive deterioration of pulmonary function over time. Exacerbations and respiratory tract infections frequently cause acute deterioration in lung function, but their effect on the long-term rate at which pulmonary function declines is not well established. Nonetheless, infections are the most important cause of acute mortality in patients with COPD, pointing to the need for influenza, COVID-19, and pneumococcal vaccination, as well as rapid appropriate treatment of bacterial respiratory infections and influenza.
Continuation of smoking is a major risk factor affecting the prognosis of COPD.
A wide spectrum of severity is characteristic of COPD, so morbidity from the disease varies tremendously among patients. Patients with mild disease are able to continue their usual work and lifestyle with minimal, if any, changes. Patients with severe disease are quite limited in their capacity for any exertion, are subject to frequent hospitalizations, and may have a life expectancy of less than 5 years.
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Diagnostic approach and assessment
In most cases, the diagnosis of COPD is suspected on the basis of history and physical examination, but spirometry with evidence of persistent airflow obstruction is still required to confirm the diagnosis in this clinical context. Chronic bronchitis is a clinical diagnosis, and the history is particularly crucial. Although emphysema is formally a pathologic diagnosis, a lung biopsy is not performed to make the diagnosis. Pathologic confirmation is generally obtained only at postmortem examination, if one is performed.
Chest radiographs have poor sensitivity in detecting COPD but are valuable in excluding other processes that cause dyspnea, such as heart failure, pulmonary fibrosis, or pleural disease. Patients with chronic bronchitis alone frequently have a normal chest radiograph. When present, chest radiographic findings suggestive of COPD include signs of hyperinflation, such as large lung volumes, flat diaphragms, an increased retrosternal air space, increased anteroposterior diameter (seen on the lateral view), and a paucity of vascular markings (Fig. 6.9). Hyperinflation associated with decreased vascular markings in the lungs results from the destruction of alveolar septa and enlargement of alveolar spaces, and has been called the arterial deficiency pattern of emphysema. In patients with α1-antitrypsin deficiency and early onset of emphysema, the arterial deficiency pattern is quite striking in the lower lobes, where there may be almost a complete loss of vascular markings.
FIGURE 6.9 Chest radiographs of a patient with severe chronic obstructive
pulmonary disease. The lungs are hyperinflated and the diaphragms are low and flat.
A, Posteroanterior view. B, Lateral view.
Characteristic radiographic findings in the more frequently recognized arterial deficiency pattern of COPD are as follows:
1.Large lung volumes
2.Flat diaphragms
3.Increased anteroposterior diameter
4.Loss of vascular markings
When cor pulmonale develops in patients with COPD, findings of pulmonary hypertension may be seen. These include enlargement of the proximal pulmonary arteries, pronounced tapering of the distal vessels, and cardiomegaly indicative of right ventricular hypertrophy or dilation.
High-resolution computed tomography (HRCT) is recognized as a more sensitive imaging method than plain chest radiography for detecting emphysema. Because it is expensive and rarely changes the management plan in this setting, it should not be considered part of the usual diagnostic evaluation for most patients with COPD. However, HRCT is an important step in characterizing the extent and distribution of emphysema in patients for whom lung volume reduction surgery is being considered.
The most useful physiologic adjuncts in evaluating patients with COPD are pulmonary function tests and arterial blood gas analysis. Spirometry demonstrates airflow obstruction, with decreases in FVC, FEV1, FEV1/FVC ratio, and MMFR. Measurements of lung volume generally give evidence of air trapping, with an elevation in RV. In patients whose lung compliance is increased (i.e., patients with emphysema), TLC is generally elevated. Measured FRC can be elevated as a result of either increased compliance (decreased elastic recoil) in emphysema or insufficient expiratory time in the face of significant airflow obstruction, leading to an elevation in end-expiratory lung volume. Whether emphysema is present can be indirectly assessed by measuring the diffusing capacity for carbon monoxide. In patients with emphysema, in whom the surface area for gas exchange is reduced, the diffusing capacity is decreased. In pure airway disease (e.g., chronic bronchitis without emphysema), the diffusing capacity is generally normal.
Pulmonary function tests in COPD show:
1.Airflow obstruction (decreased FVC, FEV1, FEV1/FVC, MMFR)
2.Air trapping and often hyperinflation (increased RV, FRC, and often TLC)
3.Diffusing capacity generally decreased in emphysema, normal in chronic bronchitis
Pulse oximetry is routinely used to evaluate patients with COPD, because supplemental oxygen is an important treatment in patients with hypoxemia (see later). If the clinician is concerned about CO2 retention or the accuracy of pulse oximetry, then measurement of arterial blood gases is necessary. Typically, patients with mild to moderate COPD have an increased alveolar-arterial oxygen gradient and mild hypoxemia. In more severe disease, hypoxemia worsens, and hypercarbia (CO2 retention) may develop. With chronic elevation in PCO2, the kidneys adjust bicarbonate excretion in an attempt to compensate and return the pH toward normal. With acute exacerbations of COPD, hypoxemia frequently worsens and CO2 retention becomes more pronounced, so the pH may drop from the stable compensated value.
In severe COPD, arterial blood gases typically show hypoxemia with or without hypercapnia.
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