|
| A) | reversible airway obstruction characterized by wheezing and dyspnea. | ||
| B) | a normal inflammatory response to inhaled noxious particles or gases. | ||
| C) | an enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. | ||
| D) | a cough with sputum production on most days for at least three months of a year for two consecutive years. |
Emphysema is an enlargement of the air spaces (alveoli) distal to the terminal bronchioles, with destruction of their walls [40]. The destruction of air space walls reduces elastic recoil and the surface area available for the exchange of oxygen and carbon dioxide during breathing. These airways can collapse, leading to further limitation in airflow. Emphysema can be classified by location as panacinar/panlobular and centriacinar/centrilobular [41].
| A) | Male sex | ||
| B) | Oxidative stress | ||
| C) | Respiratory infections | ||
| D) | Genetic predisposition |
RISK FACTORS FOR COPD
|
| A) | 5% | ||
| B) | 15% | ||
| C) | 30% | ||
| D) | 50% |
Cigarette smoking is the predominant and primary risk factor for COPD, and approximately 15% of all persons who smoke will develop clinically apparent COPD. Smokers of more than 40 pack-years exposure have a much higher likelihood of developing COPD than nonsmokers. The combined exposure to tobacco smoke and certain occupational dusts and chemicals magnifies the risk for COPD [6,7,8,9,10,11]. In developing countries, COPD has been attributed to chronic exposure to smoke from burning biomass fuels for indoor cooking and heating purposes. The COPD caused by smoking is associated with more rapid disease progression and more severe emphysema than COPD from biomass exposure, which is characterized primarily by airway-wall thickening and improved lung function in response to the use of bronchodilators [11]. Smokers with pre-existing airway reactivity also have a greater susceptibility to developing COPD.
| A) | Down syndrome | ||
| B) | Sickle cell disease | ||
| C) | Alpha-1 antitrypsin deficiency | ||
| D) | Adenosine deaminase deficiency |
It is believed that a variety of genes play an important role in COPD pathogenesis. A genetic disorder that causes alpha-1 antitrypsin deficiency is an important cause of emphysema in nonsmokers and increases susceptibility to disease in smokers. People with severe hereditary deficiency of alpha-1 antitrypsin are genetically predisposed to developing COPD. Alpha-1 antitrypsin deficiency stimulates neutrophil elastase activity, which leads to parenchymal destruction in the lungs and causes emphysema.
| A) | Thickening of intima | ||
| B) | Increase in goblet cells | ||
| C) | Destruction of alveolar wall | ||
| D) | Decrease in the number of macrophages |
INFLAMMATORY CELLS IN COPD
| Cell Type | Characteristic Changes |
|---|---|
| Neutrophils | Elevated levels of neutrophils in sputum of normal smokers, with greater levels in those with COPD related to disease severity. Few neutrophils are seen in tissue. They may be important in mucus hypersecretion and the release of proteases. |
| Macrophages | Greatly increased numbers of macrophages are seen in airway lumen, lung parenchyma, and bronchoalveolar lavage fluid. Derived from blood monocytes that differentiate within lung tissue, these cells produce increased inflammatory mediators and proteases in patients with COPD in response to cigarette smoke and may show defective phagocytosis. |
| T-lymphocytes (T-cells) | Both CD4+ and CD8+ cells are increased in the airway wall and lung parenchyma, with an increased CD8+:CD4+ ratio. Greater numbers of CD8+ T-cells (Tc1) and T helper 1 (Th1) cells, which secrete interferon-γ and express the chemokine receptor CXCR39. CD8+ cells may be cytotoxic to alveolar cells, contributing to their destruction. |
| B-lymphocytes (B-cells) | Elevated levels in peripheral airways and within lymphoid follicles, possibly as a response to chronic colonization and infection of the airways. |
| Eosinophils | Elevated levels of eosinophil proteins in sputum and increased eosinophils in airway wall during exacerbations. |
| Epithelial cells | May be activated by cigarette smoke to produce inflammatory mediators. |
| A) | the total T-cell count in decreased. | ||
| B) | the predominant T-cell subtype is CD4+. | ||
| C) | neutrophils play a primary role in the generation of mucous metaplasia. | ||
| D) | All of the above |
It is suggested that neutrophils play a primary role in the generation of mucous metaplasia in chronic bronchitis and the destruction of lung tissue in emphysema. The neutrophilic inflammatory response appears to account for the excessive mucus secretion observed in response to an acute secretagogue and for augmentation of the bronchial mucus-producing apparatus observed in these patients [34,35]. There is a strong correlation between peripheral airway dysfunction in COPD and sputum neutrophil counts [36].
Macrophages are the predominant inflammatory cells present in lavage fluid in patients with COPD [37]. Numerous studies have demonstrated a direct correlation between the number of alveolar macrophage in the lung tissue and the severity of lung destruction [38].
| A) | They attract T-lymphocytes. | ||
| B) | They attract neutrophils and monocytes. | ||
| C) | They may induce fibrosis in small airways. | ||
| D) | They suppress the inflammatory process and systemic reaction. |
INFLAMMATORY MEDIATORS INVOLVED IN COPD
| Cell Type | Action |
|---|---|
| Lipid mediators (e.g., leukotriene B4) | Attract neutrophils and T-lymphocytes |
| Chemokines (e.g., interleukin-8) | Attract neutrophils and monocytes |
| Proinflammatory cytokines (e.g., tumor necrosis factor-α, interleukin-1ß, and interleukin-6) | Amplify the inflammatory process and may contribute to some of the systemic effects of COPD |
| Growth factors (e.g., transforming growth factor-ß) | May induce fibrosis in small airways |
| A) | alveolar underinflation. | ||
| B) | air trapping during expiration. | ||
| C) | increased inspiratory capacity. | ||
| D) | decreased functional residual capacity. |
There is a direct correlation between degree of inflammation, fibrosis, and luminal exudates in small airways and the reduction in FEV1 and FEV1/forced vital capacity (FVC) ratio. The effect on airflow is pronounced in the smaller (<2 mm in diameter) conducting airways. The resultant peripheral airway obstruction produces alveolar hyperinflation and air trapping during expiration. Hyperinflation diminishes inspiratory capacity and increases functional residual capacity, which causes dyspnea and limitation of exercise capacity.
| A) | Xerostomia | ||
| B) | Breathlessness | ||
| C) | Chronic cough | ||
| D) | Limited exercise tolerance |
The cardinal signs and symptoms of COPD are chronic cough, sputum production, breathlessness (shortness of breath and dyspnea), and limited exercise tolerance. Other common signs that may be present in COPD include:
Tachypnea
Pursed lips breathing
Prolonged expiration phase of breathing (compared with inspiration)
Active use of neck muscles during breathing
Increased resonance of the chest (by percussion) caused by hyperaeration and emphysematous change
Increased anteroposterior (A-P) diameter of the chest ("barrel chest")
| A) | is diagnostic. | ||
| B) | is relatively common. | ||
| C) | is caused in part by chronic oxygen deprivation. | ||
| D) | None of the above |
Clubbing of the fingers may be present in patients with COPD, in part caused by chronic oxygen deprivation. However, it is relatively uncommon. Clubbing is more likely indicative of other chronic diseases such as congenital heart defect, bronchiectasis, infectious endocarditis, or cirrhosis of the liver.
| A) | FEV1 less than 80% predicted | ||
| B) | FEV1 more than 85% predicted | ||
| C) | Prebronchodilator FEV1/FVC more than 0.75 | ||
| D) | Postbronchodilator FEV1/FVC more than 0.75 |
A clinical diagnosis of COPD should be considered in the patient who presents with shortness of breath or dyspnea, chronic productive cough, and easy fatigue, especially if combined with a history of risk factor exposure (e.g., long-term exposure to tobacco or dust and chemicals, age, genetics). The diagnosis should then be confirmed by spirometry. The presence of a Tiffeneau index or postbronchodilator FEV1/FVC less than 0.70 and FEV1 less than 80% predicted confirms the presence of airflow limitation that is not fully reversible [199].
| A) | Pattern of symptoms of COPD | ||
| B) | Long-term exposure to risk factors | ||
| C) | Impact of the disease on the patient's life | ||
| D) | Family history of chronic cardiac conditions |
As with any illness, a careful history is critical in determining the correct diagnosis. The goals of history taking are to identify possible causes of dyspnea and other symptoms and to screen for COPD risk factors. An inadequate history may result in misdiagnosis or delayed diagnosis, with ramifications on disease course. A comprehensive medical history of an individual presenting with COPD symptoms should include:
Long-term exposure to risk factors, such as smoking or occupational and environmental exposures
Past medical history, including asthma, allergy, respiratory infections in the past (especially in childhood), sinusitis or nasal polyps, and other respiratory illnesses
Family history of COPD or other chronic respiratory disease
Pattern of symptoms of COPD (e.g., development in adulthood, increasing dyspnea or breathlessness, frequent "winter colds," restricted social life)
History of previous hospitalizations or exacerbations for respiratory illnesses
Presence of comorbid conditions, such as chronic heart disease, malignancy, musculoskeletal disorders, or osteoporosis
Medical treatments
Impact of the disease on the patient's life, including restricted activity, absenteeism at work, financial impact, and depression or anxiety
Family and social support available
Possibilities for COPD risk factor reduction, particularly smoking cessation
| A) | Lung infiltrate visible on chest x-ray | ||
| B) | Fine basilar crackles on auscultation | ||
| C) | Largely irreversible airflow limitation | ||
| D) | Presence of allergy, rhinitis, and/or eczema |
DIFFERENTIAL DIAGNOSIS OF COPD
| Diagnosis | Suggestive Featuresa | |||||
|---|---|---|---|---|---|---|
| COPD |
| |||||
| Asthma |
| |||||
| Bronchiectasis |
| |||||
| Congestive heart failure |
| |||||
| Tuberculosis |
| |||||
| Diffuse panbronchiolitis |
| |||||
| Obliterative bronchiolitis |
| |||||
| ||||||
| A) | 1. | ||
| B) | 2. | ||
| C) | 3. | ||
| D) | 4. |
SPIROMETRIC CLASSIFICATION OF COPD SEVERITY BASED ON POSTBRONCHODILATOR FEV1a
| GOLD Stage | Spirometric Finding | ||
|---|---|---|---|
| 1 (mild) | FEV1 ≥80% predicted | ||
| 2 (moderate) | 50% ≤ FEV1 <80% predicted | ||
| 3 (severe) | 30% ≤ FEV1 <50% predicted | ||
| 4 (very severe) | FEV1 <30% predicted | ||
| |||
| A) | Dyspnea | ||
| B) | Obstruction | ||
| C) | Body mass index | ||
| D) | Chest x-ray findings |
The BODE index is a multidimensional grading method used to assess clinical risk in patients with COPD based on four factors: body mass index (BMI), obstruction, dyspnea, and exercise (Table 10) [5,57]. It is a better prognostic marker of subsequent survival than any other component alone [5,57]. Each component of the BODE index is graded and a score out of 10 is obtained; higher scores are indicative of greater mortality risk. This method reflects the effect of both pulmonary and extrapulmonary factors on prognosis and survival in COPD.
| A) | Expiratory gas trapping | ||
| B) | Extent and pattern of emphysema | ||
| C) | Changes in small airway wall thickness | ||
| D) | All of the above |
Computed tomography (CT) of the chest has advanced understanding of COPD and has an important role in the clinical assessment of selected patients. Chest CT can identify the presence and extent of disease patterns that impact prognosis and influence the management of patients with COPD [10]. CT imaging features that are associated with adverse clinical outcomes include early interstitial lung abnormalities, bronchiectasis, presence and pattern of emphysema, airway wall thickness, and expiratory gas trapping [224]. The addition of expiratory CT scans has enabled measurement of small airway disease. Chest CT also may reveal extrapulmonary findings of importance, such as coronary artery calcification, cardiac chamber enlargement, and early-stage lung cancer. The presence of predominantly upper-lobe emphysema on CT imaging identifies the patient who is a good candidate for surgical lung-volume reduction [60].
| A) | who are black and older than 50 years of age. | ||
| B) | and without a positive family history of COPD. | ||
| C) | who are white and younger than 45 years of age. | ||
| D) | All of the above |
White patients who experience COPD at a young age (i.e., younger than 45 years) or who have a positive family history of COPD may be screened for alpha-1 antitrypsin deficiency. A serum concentration of alpha-1 antitrypsin less than 15% to 20% of the normal expected value indicates a high probability of homozygous alpha-1 antitrypsin deficiency.
| A) | There are few available options. | ||
| B) | They are ineffective and lack empirical support. | ||
| C) | Healthcare professionals cannot refer to smoking cessation clinics. | ||
| D) | Relatively few smokers (about 5%) are interested in attending classes. |
Behavioral interventions are nonpharmacologic treatments delivered directly to individual smokers [209]. The main disadvantage of this approach is that relatively few smokers (about 5%) are interested in attending specific classes at any given time [210]. Therefore, group sessions appear to be the most cost-effective approach to delivering smoking cessation interventions [211]. Although relatively few patients want to go to classes, healthcare professionals should still have a list of referral smoking cessation clinics in their area for those smokers who express an interest in attending them and for those who have failed to respond to other approaches. Simple computer-tailored cessation messages may also be an effective alternative for behavioral support, doubling the cessation rates. This concept has been incorporated into patient support programs provided by several manufacturers of smoking cessation products [210].
| A) | Bupropion | ||
| B) | Varenicline | ||
| C) | Nicotine replacement | ||
| D) | None of the above |
The first-line pharmacologic interventions for smoking cessation are NRT, bupropion, and varenicline [217,218]. However, no pharmacotherapy has been approved for use among pregnant or nursing women. The five forms of NRT available are the patch, gum, lozenge, nasal spray, and inhaler.
| A) | stage 3 (severe) COPD. | ||
| B) | stage 2 (moderate) COPD. | ||
| C) | stage 1 (mild) COPD. | ||
| D) | stage 0 (at risk) COPD. |
GOLD GUIDELINES FOR STEPWISE MANAGEMENT OF COPD BY SEVERITY
| Treatment Step | Symptom Grade | ||||
|---|---|---|---|---|---|
| Stage 0 (At Risk) | Stage 1/A (Mild) |
Stage 2/B (Moderate) | Stage 3/C (Severe) | Stage 4/D (Very Severe) | |
| Step 1 | Avoidance of risk factors | ||||
| Step 2 | Offer short-acting or long-acting bronchodilator to reduce breathlessness | ||||
| Step 3 |
Initiate regular treatment with one or a combination of long-acting bronchodilators Begin rehabilitation | ||||
| Step 4 |
Utilize single or combination long-acting bronchodilator Add inhaled corticosteroids if repeated exacerbations | ||||
| Step 5 |
Add macrolide in former smokers Consider roflumilast if patient has chronic bronchitis | ||||
| A) | Fenoterol | ||
| B) | Salmeterol | ||
| C) | Tulobuterol | ||
| D) | Arformoterol |
MEDICATIONS COMMONLY USED IN THE MANAGEMENT OF COPD
| Drug | Inhaler (mcg) | Solution for Nebulizer (mg/mL) | Oral | Vials for Injection (mg) | Duration of Action (hours) |
|---|---|---|---|---|---|
| Short-acting beta2-agonists | |||||
| Fenoterol | 100–200 (MDI) | 1 | 0.05% (syrup) | — | 4–6 |
| Levalbuterol | 45–90 (MDI) | 0.21, 0.42 | — | — | 6–8 |
| Salbutamol (albuterol) | 100, 200 (MDI & DPI) | 5 | 5 mg (pill), 0.024% (syrup) | 0.1, 0.5 | 4–6 |
| Terbutaline | 400, 500 (DPI) | — | 2.5 mg, 5 mg (pill) | — | 4–6 |
| Long-acting beta2-agonists | |||||
| Arformoterol | — | 0.0075 | — | — | 12 |
| Formoterol | 4.5–12 (MDI & DPI) | 0.01 | — | — | 12 |
| Indacaterol | 75–300 (DPI) | — | — | — | 24 |
| Olodaterol | 5 (SMI) | — | — | — | 24 |
| Salmeterol | 25–50 (MDI & DPI) | — | — | — | 12 |
| Tulobuterol | — | — | 2 mg (transdermal) | — | 24 |
| Short-acting muscarinic antagonists | |||||
| Ipratropium bromide | 20, 40 (MDI) | 0.25–0.5 | — | — | 6–8 |
| Oxitropium bromide | 100 (MDI) | 1.5 | — | — | 7–9 |
| Long-acting muscarinic antagonists | |||||
| Aclidinium bromide | 322 (DPI) | — | — | — | 12 |
| Glycopyrronium bromide | 44 (DPI) | — | — | — | 24 |
| Tiotropium | 18 (DPI), 5 (SMI) | — | — | — | 24 |
| Umeclidinium | 62.5 (DPI) | — | — | — | 24 |
| Combination short-acting beta2-agonist plus muscarinic antagonist in one inhaler | |||||
| Fenoterol/ipratropium | 200/80 (MDI) | 1.25/0.5 | — | — | 6–8 |
| Salbutamol/ipratropium | 100/20 (SMI) | — | — | — | 6–8 |
| Combination long-acting beta2-agonist plus muscarinic antagonist in one inhaler | |||||
| Formoterol/aclidinium | 12/340 (DPI) | — | — | — | 12 |
| Indacaterol/glycopyrronium | 85/43 (DPI) | — | — | — | 24 |
| Olodaterol/tiotropium | 5/5 (SMI) | — | — | — | 24 |
| Vilanterol/umeclidinium | 25/62.5 (DPI) | — | — | — | 24 |
| Methylxanthines | |||||
| Aminophylline | — | — | 200–600 mg (pill) | 240 | Variable, up to 24 |
| Theophylline (SR) | — | — | 100–600 mg (pill) | — | Variable, up to 24 |
| Inhaled corticosteroids | |||||
| Beclomethasone | 50–400 (MDI & DPI) | 0.2–0.4 | — | — | — |
| Budesonide | 100, 200, 400 (DPI) | 0.2, 0.25, 0.5 | — | — | — |
| Fluticasone | 50–500 (MDI & DPI) | — | — | — | — |
| Combination long-acting beta2-agonist plus corticosteroid in one inhaler | |||||
| Formoterol/beclometasone | 6/100 (MDI & DPI) | — | — | — | — |
| Formoterol/budesonide | 4.5/160 (MDI), 9/320 (DPI) | — | — | — | — |
| Formoterol/mometasone | 10/200, 10/400 (MDI) | — | — | — | — |
| Salmeterol/fluticasone | 50/100, 250, 500 (DPI) | — | — | — | — |
| Vilanterol/fluticasone furoate | 25/100 (DPI) | — | — | — | — |
| Systemic corticosteroids | |||||
| Prednisone | — | — | 5–60 mg (pill) | — | — |
| Methylprednisolone | — | — | 4, 8, 16 mg (pill) | — | — |
| Phosphodiesterase-4 inhibitors | |||||
| Roflumilast | — | — | 500 mcg (pill) | — | 24 |
| MDI = metered-dose inhaler, DPI = dry-powder inhaler, SMI = soft-mist inhaler, SR = sustained release. | |||||
| A) | 4 to 6 hours. | ||
| B) | 6 to 8 hours. | ||
| C) | 12 hours. | ||
| D) | up to 24 hours. |
MEDICATIONS COMMONLY USED IN THE MANAGEMENT OF COPD
| Drug | Inhaler (mcg) | Solution for Nebulizer (mg/mL) | Oral | Vials for Injection (mg) | Duration of Action (hours) |
|---|---|---|---|---|---|
| Short-acting beta2-agonists | |||||
| Fenoterol | 100–200 (MDI) | 1 | 0.05% (syrup) | — | 4–6 |
| Levalbuterol | 45–90 (MDI) | 0.21, 0.42 | — | — | 6–8 |
| Salbutamol (albuterol) | 100, 200 (MDI & DPI) | 5 | 5 mg (pill), 0.024% (syrup) | 0.1, 0.5 | 4–6 |
| Terbutaline | 400, 500 (DPI) | — | 2.5 mg, 5 mg (pill) | — | 4–6 |
| Long-acting beta2-agonists | |||||
| Arformoterol | — | 0.0075 | — | — | 12 |
| Formoterol | 4.5–12 (MDI & DPI) | 0.01 | — | — | 12 |
| Indacaterol | 75–300 (DPI) | — | — | — | 24 |
| Olodaterol | 5 (SMI) | — | — | — | 24 |
| Salmeterol | 25–50 (MDI & DPI) | — | — | — | 12 |
| Tulobuterol | — | — | 2 mg (transdermal) | — | 24 |
| Short-acting muscarinic antagonists | |||||
| Ipratropium bromide | 20, 40 (MDI) | 0.25–0.5 | — | — | 6–8 |
| Oxitropium bromide | 100 (MDI) | 1.5 | — | — | 7–9 |
| Long-acting muscarinic antagonists | |||||
| Aclidinium bromide | 322 (DPI) | — | — | — | 12 |
| Glycopyrronium bromide | 44 (DPI) | — | — | — | 24 |
| Tiotropium | 18 (DPI), 5 (SMI) | — | — | — | 24 |
| Umeclidinium | 62.5 (DPI) | — | — | — | 24 |
| Combination short-acting beta2-agonist plus muscarinic antagonist in one inhaler | |||||
| Fenoterol/ipratropium | 200/80 (MDI) | 1.25/0.5 | — | — | 6–8 |
| Salbutamol/ipratropium | 100/20 (SMI) | — | — | — | 6–8 |
| Combination long-acting beta2-agonist plus muscarinic antagonist in one inhaler | |||||
| Formoterol/aclidinium | 12/340 (DPI) | — | — | — | 12 |
| Indacaterol/glycopyrronium | 85/43 (DPI) | — | — | — | 24 |
| Olodaterol/tiotropium | 5/5 (SMI) | — | — | — | 24 |
| Vilanterol/umeclidinium | 25/62.5 (DPI) | — | — | — | 24 |
| Methylxanthines | |||||
| Aminophylline | — | — | 200–600 mg (pill) | 240 | Variable, up to 24 |
| Theophylline (SR) | — | — | 100–600 mg (pill) | — | Variable, up to 24 |
| Inhaled corticosteroids | |||||
| Beclomethasone | 50–400 (MDI & DPI) | 0.2–0.4 | — | — | — |
| Budesonide | 100, 200, 400 (DPI) | 0.2, 0.25, 0.5 | — | — | — |
| Fluticasone | 50–500 (MDI & DPI) | — | — | — | — |
| Combination long-acting beta2-agonist plus corticosteroid in one inhaler | |||||
| Formoterol/beclometasone | 6/100 (MDI & DPI) | — | — | — | — |
| Formoterol/budesonide | 4.5/160 (MDI), 9/320 (DPI) | — | — | — | — |
| Formoterol/mometasone | 10/200, 10/400 (MDI) | — | — | — | — |
| Salmeterol/fluticasone | 50/100, 250, 500 (DPI) | — | — | — | — |
| Vilanterol/fluticasone furoate | 25/100 (DPI) | — | — | — | — |
| Systemic corticosteroids | |||||
| Prednisone | — | — | 5–60 mg (pill) | — | — |
| Methylprednisolone | — | — | 4, 8, 16 mg (pill) | — | — |
| Phosphodiesterase-4 inhibitors | |||||
| Roflumilast | — | — | 500 mcg (pill) | — | 24 |
| MDI = metered-dose inhaler, DPI = dry-powder inhaler, SMI = soft-mist inhaler, SR = sustained release. | |||||
| A) | are a first-line option for stable COPD. | ||
| B) | tend to be less predictable and more toxic. | ||
| C) | are preferred over inhaled bronchodilators. | ||
| D) | have strong bronchodilator and respiratory stimulant properties. |
Methylxanthines have weak bronchodilator and respiratory stimulant properties. Both of the available methylxanthines (aminophylline and theophylline) are administered orally and have variable durations of action (up to 24 hours). The inhaled bronchodilators are preferred over these oral agents, as the latter tends to be less predictable and more toxic. Although useful for some patients, the methylxanthines are a third-line option in the treatment of stable COPD [199].
| A) | Depression | ||
| B) | Airflow obstruction | ||
| C) | Exercise deconditioning | ||
| D) | Muscle weakness and wasting |
Pulmonary rehabilitation can address nonpulmonary conditions that are not addressed by the medical management of COPD, including:
Muscle weakness and wasting
Exercise deconditioning
Depression
Relative social isolation
Weight loss
| A) | oxygen saturation (SaO2) greater than or equal to 90%. | ||
| B) | partial pressure of oxygen (PaO2) greater than or equal to 8 kPa (60 mm Hg). | ||
| C) | PaO2 of 7.5 kPa with evidence of pulmonary hypertension. | ||
| D) | All of the above |
Long-term oxygen therapy is usually indicated in stage 4 COPD for patients who have [199]:
PaO2≤7.3 kPa (55 mm Hg) or SaO2≤88%, with or without hypercapnia confirmed twice over a three-week period
PaO2 between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg) or SaO2 of 88%, if there is evidence of pulmonary hypertension, peripheral edema suggesting congestive cardiac failure, or polycythemia (hematocrit >55%)
| A) | improves expiratory flow rates. | ||
| B) | decreases the elastic recoil pressure of the lung. | ||
| C) | involves removal of a damaged lung and replacement with donor lung. | ||
| D) | is considered for patients with unilateral emphysema and mild obstruction. |
Lung volume reduction surgery (LVRS) is a surgical procedure in which damaged parts of the lung are resected to reduce hyperinflation, thus improving efficacy of respiratory muscles. LVRS also improves expiratory flow rates by increasing the elastic recoil pressure of the lung. LVRS is considered for patients with bilateral emphysema on HRCT and severe obstruction with hyperinflation and air trapping [194]. As with bullectomy, certain characteristics may indicate the likelihood of a favorable or unfavorable outcome with LVRS (Table 16) [73].
| A) | Acute confusion | ||
| B) | Mild breathlessness | ||
| C) | Arterial PaO2 8 kPa | ||
| D) | Insidious or gradual onset of symptoms |
FACTORS TO CONSIDER WHEN DECIDING WHERE TO TREAT THE PATIENT WITH COPD EXACERBATION
| Factor | Treat at Home | Treat in Hospital |
|---|---|---|
| Able to cope at home | Yes | No |
| Breathlessness | Mild | Severe |
| General condition | Good | Poor/deteriorating |
| Level of activity | Good | Poor/confined to bed |
| Cyanosis | No | Yes |
| Worsening peripheral edema | No | Yes |
| Level of consciousness | Normal | Impaired |
| Already receiving long-term oxygen therapy | No | Yes |
| Social circumstances | Good | Living alone/not coping |
| Acute confusion | No | Yes |
| Rate of onset | Insidious or gradual | Rapid |
| Significant comorbidity (particularly cardiac disease and insulin-dependent diabetes) | No | Yes |
| SaO2 <90% | No | Yes |
| Changes on chest radiograph | No | Present |
| Arterial pH level | ≥7.35 | <7.35 |
| Arterial PaO2 | ≥7 kPa | <7 kPa |
| PaO2 = partial pressure of oxygen, SaO2 = oxygen saturation. | ||
| A) | respiratory arrest. | ||
| B) | life-threatening hypoxemia. | ||
| C) | altered mental status or inability to cooperate. | ||
| D) | moderate-to-severe dyspnea with signs of increased breathing load and tachypnea. |
The selection criteria for NIV are based on clinical observations and gas exchange measurements. Patients with moderate-to-severe dyspnea with signs of increased breathing load (i.e., use of accessory muscles and paradoxical abdominal motion) and tachypnea (>25 breaths per minute) as well as moderate-to-severe acidosis (pH ≤7.35) and/or hypercapnia (PaCO2 >6.0 kPa OR 45 mm Hg) are considered candidates for NIV [199]. Relative contraindications include [199]:
Respiratory arrest
Life-threatening hypoxemia
Unstable cardiovascular status (e.g., cardiac arrhythmias, myocardial infarction, hypotension)
Altered mental status or inability to cooperate (e.g., low Glasgow coma score)
High aspiration risk, vomiting
Viscous or copious secretions
Recent history of facial or gastroesophageal surgery
Craniofacial trauma
Bowel obstruction
Fixed nasopharyngeal abnormalities
Severe burns
Morbid obesity
| A) | stage 1 COPD. | ||
| B) | respiratory failure. | ||
| C) | a history of exacerbations. | ||
| D) | alpha-1 antitrypsin deficiency. |
Only patients with respiratory failure require assessment of pulmonary artery pressure; otherwise, its measurement is not recommended. The development of respiratory failure is indicated by a PaO2 less than 8.0 kPa (60 mm Hg) with or without PaCO2 greater than 6.7 kPa (50 mm Hg) in arterial blood gas measurements while breathing air at sea level. Patients may be screened with pulse oximetry and arterial blood gases if SaO2 is less than 92%.
| A) | Pneumonia | ||
| B) | Lung cancer | ||
| C) | Pulmonary embolism | ||
| D) | Musculoskeletal dysfunction |
Pneumonia is the most common comorbid condition in patients with COPD. Pneumonia can present as a part or a trigger of COPD exacerbations; however, there are important clinical differences between pneumonia and acute COPD exacerbations without pneumonia. COPD exacerbation with pneumonia has a more rapid onset of symptoms, more severe illness, longer length of hospital stay, and higher rate of ICU admission and mortality compared to an exacerbation without pneumonia [144].