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Chronic obstructive pulmonary disease (COPD) is an inflammatory respiratory disease usually caused by exposure to tobacco smoke. It is characterized by the presence of airflow limitation that is not fully reversible The pathophysiology of COPD is related to chronic airway irritation, mucus production, and pulmonary scarring Traditionally, COPD was described as encompassing emphysema, characterized by loss of lung elasticity and destruction of lung parenchyma with enlargement of air spaces, andchronic bronchitis, characterized by obstruction of small airways and productive cough >3 mo for more than 2 successive yr. These terms are no longer included in the formal definition of COPD, although they are still used clinically Between 10% and 20% of COPD in the U.S. is due to occupational or other exposure to chemical vapors, irritants, and fumes; 80% to 90% is due to cigarette smoking


Blue bloaters Are patients with chronic bronchitis; The name is derived from the bluish tinge of the skin (as a result of chronic hypoxemia and hypercapnia) and from the frequent presence of peripheral edema (from cor pulmonale); Chronic cough with production of large amounts of sputum is characteristic. Pink puffers Are patients with emphysema; They have a cachectic appearance but pink skin color (adequate oxygen saturation); Shortness of breath is manifested by pursed-lip breathing and use of accessory muscles of respiration.


COPD may present with combinations of the following manifestations: 1. 2. 3. 4. 5. Cyanosis, chronic cough (usually productive but may be intermittent and may be unproductive), tachypnea, tachycardia. Dyspnea (persistent, progressive), pursed-lip breathing with use of accessory muscles for respiration, decreased breath sounds, wheezing. Chronic sputum production. Chest wall abnormalities (hyperinflation, barrel chest, protruding abdomen). Flattening of diaphragm.

Acute exacerbation of COPD is mainly a clinical diagnosis and generally manifests with worsening dyspnea, increase in sputum purulence, and increase in sputum volume. However, respiratory symptom status is not a reliable indicator of the presence of airflow obstruction. Individuals with normal spirometric values may report respiratory symptoms, whereas individuals who have severe to very severe airflow obstruction by spirometry may report no symptoms.

Differential Diagnosis
Congestive heart failure Asthma Tuberculosis, other respiratory infections Bronchiectasis Cystic fibrosis Neoplasm Pulmonary embolism Obliterative bronchiolitis Diffuse panbronchiolitis Sleep apnea, obstructive Hypothyroidism <50% predicted

Examenes complementarios
Chest x-ray (seldom diagnostic but useful to exclude alternative diagnosis [CHF, TB]), pulmonary function testing (spirometry), o Hyperinflation with flattened diaphragm, tenting of the diaphragm at the rib, and increased retrosternal chest space o Decreased vascular markings and bullae in patients with emphysema o Thickened bronchial markings and enlarged right side of the heart in patients with chronic bronchitis Oxygen saturation, Blood gases (in selected patients with FEV1 < 50% predicted or with acute exacerbation). Alpha-1-antitrypsin deficiency screening may be useful in Caucasians with suspected COPD and no clear risk factors.

Laboratory Tests
Spirometry pulmonary function testing (PFT) with measurement of forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1).
o o o o o
Spirometry should be obtained to diagnose airflow obstruction in patients with respiratory symptoms. It should not be used to screen for airflow obstruction in individuals without respiratory symptoms. PFT results in COPD reveal abnormal diffusing capacity, increased total lung capacity and/or residual volume, and fixed reduction in FEV1 in patients with emphysema; Normal diffusing capacity and reduced FEV1 are found in patients with chronic bronchitis. It is important to note that FEV1 does not correlate well with individual patients' severity of dyspnea, exercise limitations, or health status.

Patients with COPD can generally be distinguished from asthmatics: o By their incomplete response to albuterol (change in FEV 1 <200 ml and 12%) o And absence of an abnormal bronchoconstrictor response to methacholine or other stimuli. However, nearly 40% of patients with COPD respond to bronchodilators.

Appoximately 50% of COPD exacerbations are caused by bacterial infection. Antibiotics are indicated in suspected respiratory infection (e.g., increased purulence and volume of phlegm). Haemophilus influenzae and Streptococcus pneumoniae are frequent causes of acute bronchitis. Oral antibiotics of choice are azithromycin, levofloxacin, amoxicillin-clavulanate, trimethoprimsulfamethoxazole, doxycycline, and cefuroxime. The use of antibiotics is beneficial in exacerbations of COPD presenting with increased dyspnea and sputum purulence (especially if the patient is febrile).

All patients with COPD should receive pneumococcal vaccine and yearly influenza vaccine. Early antibiotic administration is associated with improved outcomes among patients hospitalized for acute exacerbations of COPD regardless of the risk of treatment failure. In assessing the severity of COPD, the FEV1 is limited by the fact that it does not take into account the systemic manifestations of COPD. The BODE index (body mass index, degree of obstruction, dyspnea, and exercise capacity) has been proposed as a multidimensional scale to better assess the morbidity and mortality associated with COPD. It is better than the FEV1 alone at predicting the risk of death from any cause and from respiratory causes among patients with COPD. In the BODE index, obstruction is measured by FEV1 and dyspnea is measured by the modified Medical Research Council (MMRC) dyspnea questionnaire in a 6-minute walk test. A score of 0 on the MMRC indicates that the individual is not troubled with breathlessness except with strenuous exercise, 1 indicates shortness of breath when hurrying or walking up a slight hill, and 2 means the

individual walks slower than people of the same age due to breathlessness or has to stop for breath when walking at own pace on level ground. A score of 3 means severe dyspnea because the person has to stop for breath after walking approximately 100 meters or after a few minutes on level ground, and a score of 4 indicates very severe dyspnea and is given when the individual is too breathless to leave the house or is breathless when dressing or undressing. Pulmonary artery enlargement as determined by a ratio of the diameter of the pulmonary artery to the diameter of the aorta [PA:A ratio] of >1 detected by CT is associated with severe exacerbations of COPD. The average person with COPD has one or two acute exacerbations each year. Prophylactic use of macrolide antibiotics (azithromycin 250 mg/day) has been shown to decrease the frequency of exacerbations and improve quality of life among selected patients with COPD; however, it leads to hearing decrements in a small percentage of patients and increased prevalence of macrolide-resistant bacteria colonizing the airway and is therefore not recommended.

Nonpharmacologic Therapy
Avoidance of tobacco and elimination of air pollutants. Supplemental oxygen, usually through a face mask, to ensure oxygen saturation >90% as measured by pulse oximetry. Continuous oxygen therapy o should be prescribed for patients with COPD who have arterial partial pressure of oxygen 55 mm Hg or less, o Or oxygen saturation 88% or less as measured by pulse oximetry. Pulmonary clearing: careful nasotracheal suction is indicated only in patients with excessive secretions and an inability to expectorate. Mechanical percussion of the chest as applied by a physical or respiratory therapist is ineffective with acute exacerbations of COPD. Pulmonary rehabilitation should be considered in COPD patients who remain symptomatic despite optimal medical management. Medicare will cover up to 36 sessions of pulmonary rehabilitation in COPD patients. Weight loss in obese patients.

General Rx
Pharmacologic treatment should be administered in a stepwise approach according to the severity of disease and patient's tolerance for specific drugs. Fig. E1-224 describes general management

approaches for COPD. Bronchodilators improve symptoms, quality of life, and exercise tolerance, and decrease incidence of exacerbations. Inhaled bronchodilators may be used for stable COPD patients with respiratory symptoms and FEV1 between 60% and 80% of predicted. They are recommended for stable COPD patients with respiratory symptoms and FEV1 <60% of predicted. Recent guidelines from ACP, ACCP, ATS, and ERS recommend that clinicians prescribe monotherapy using either long-acting inhaled anticholinergics or long-acting inhaled beta-agonists for symptomatic patients with COPD and FEV1 <60% of predicted. Clinicians should base the choice of specific monotherapy on patient preference, cost, and adverse effect profile. Short-acting beta-2 agonists (e.g., albuterol metered-dose inhaler 1 to 2 puffs q4 to 6h prn) or short-acting anticholinergic agents (e.g., ipratropium inhaler 2 puffs qid) are acceptable in patients with mild, variable symptoms. Anticholinergics are also effective and are available in combination with albuterol (Combivent). Long-acting inhaled agents are preferred in patients with mild to moderate or continuous symptoms. Tiotropium is an excellent long-acting bronchodilator. It is very effective for long-term, once-a-day use. It has been shown to be superior to salmeterol, an inhaled long-acting beta-agonist (LABA) in patients with moderate to severe COPD; however, recent trials have shown higher hospitalization rates and mortality with tiotropium compared to LABAs. Aclidinium is another orally inhaled long-acting anticholinergic for long-term maintenance treatment of bronchospasm associated with COPD. Unlike tiotropium, which is predominantly renally excreted, it can be used safely in renal impairment. Addition of inhaled steroids (fluticasone, budesonide, triamcinolone) is used to reduce exacerbations in patients with moderate to severe COPD. Inhaled steroids are reserved for patients with either 2 exacerbations annually or FEV1 <50% of predicted. The role of inhaled corticosteroids (ICS) in COPD is controversial. Although some trials have demonstrated mild improvement in patients symptoms and decreased frequency of exacerbations, most pulmonologists believe that these drugs are ineffective in most patients with COPD but should be considered for patients with moderate to severe airflow limitation who have persistent symptoms despite optimal bronchodilator therapy. ICS therapy does not affect 1-yr all-cause mortality among patients with COPD and is associated with a higher risk of pneumonia. Roflumilast is a selective oral PDE4 inhibitor useful to reduce the risk of COPD exacerbations in patients with severe COPD associated with chronic bronchitis and a history of exacerbations. It is not a bronchodilator and is not indicated for the relief of acute bronchospasm.

Recent guidelines from ACP (American College of Physicians), ACCP (American College of Chest Physicians), ATS (American Thoracic Society), and ERS (European Respiratory Society) suggest that clinicians may administer combination inhaled therapies for symptomatic patients with stable COPD and FEV1<60% predicted.

They also recommend that clinicians should prescribe pulmonary rehabilitation for symptomatic patients with an FEV1 <50% predicted and continuous oxygen therapy in patients with COPD who have resting hypoxemia (PaO2 <55 mm Hg or SpO2 <88%).

Acute exacerbation of COPD (increase in sputum volume and purulence, worsening dyspnea) can be treated with: Aerosolized beta-2 agonists (e.g., metaproterenol nebulizer solution 5% 0.3 ml or albuterol nebulized 5% solution 2.5 to 5 mg).

Anticholinergic agents, which have equivalent efficacy to inhaled beta-adrenergic agonists. Inhalant solution of ipratropium bromide 0.5 mg can be administered every 4 to 8 hr.

Short courses of systemic corticosteroids have been shown to improve spirometric and clinical outcomes. Treatment failure occurs less often in patients who receive low-dose steroids than in those receiving high-dose parenteral steroids. Oral prednisone 40 mg/day for 10 to 14 days is generally effective. Courses of treatment that are extended for >14 days confer no added benefit and increase the risk of adverse events. Use of noninvasive positive pressure ventilation (NIPPV) decreases the risk of endotracheal intubation and decreases intensive care unit admission rates. Contraindications to its use are uncooperative patient, decreased level of consciousness, hemodynamic instability, inadequate mask fit, and severe respiratory acidosis. Increased airway pressure can be delivered by using inspiratory positive airway pressure, continuous positive airway pressure, or bilevel positive airway pressure, which combines the other modalities. When using NIPPV, the nasal mask is usually tolerated the best; however, patients must be instructed to keep their mouths closed while breathing with the nasal apparatus. Oxygen can be delivered at 10 to 15 L/min and started in spontaneous ventilation mode with an initial expiratory positive airway pressure setting of 3 to 5 cm H2O and an inspiratory positive airway pressure setting of up to 10 cm H 2O. Adjustments in these settings should be made in 2-cm H2O increments. It is important to monitor patients with frequent vital signs measurements, arterial blood gases, or pulse oximetry. Intubation and mechanical ventilation may be necessary if previous measures fail to provide improvement. IV aminophylline administration is controversial and generally not recommended. When used in patients with refractory symptoms, serum levels should be closely monitored (keep level 8 to 12 mcg/ml) to minimize risks of tachyarrhythmias.