Snapshot A 46-year-old female presents to her primary care physician for follow up for a severe, unrelenting, productive cough that she has had on and off for more than 2 years. She also complains of worsening dyspnea on exertion. She has smoked 1 pack per day since she was 18. A chest radiograph is obtained. Introduction Clinical definition chronic obstructive pulmonary disease (COPD) is defined as persistent airflow limitation due to mixture of small airway disease and parenchymal destruction early classifications distinguished chronic bronchitis and emphysema no longer distinguished but helpful to separate for pathophysiologic understanding and clinical management chronic bronchitis is defined as a productive cough for > 3 months of the year for 2 consecutive years Epidemiology Demographics males > females 4th most common cause of death globally Risk factors tobacco use (most common) air pollution occupational exposure cystic fibrosis ETIOLOGY Pathogenesis chronic irritation promotes hyperplasia of mucus gland cells, mucus hypersecretion, cilia damage, and infiltration of neutrophils and CD8+ T cells Presentation Symptoms dyspnea, especially on exertion productive cough worse in the morning hemoptysis Physical exam "blue bloaters" cyanosis peripheral edema hypoxia coarse rhonchi end-expiratory wheezing and/or prolonged expiration pursed-lip breathing decreased breath sounds, if advanced signs of pulmonary hypertension right ventricular hypertrophy with signs of right heart failure jugular venous distension (JVD) hepatomegaly edema imaging Chest radiograph not required for routine diagnosis increased bronchial markings (due to mucus) hyperinflation/flattened diaphragm cardiomegaly studies Pulmonary function tests (PFTs) best initial test decreased FEV1 / FVC (< 0.7) that is incompletely reversible obstructive pattern diagnostic FEV1 = forced expiratory volume FVC = forced vital capacity decreased % FEV1 used to categorize severity based on Global initiative for chronic Obstructive Lung Disease (GOLD) mild: > 80% moderate: 50-79% severe: 30-49% very severe: < 30% normal or decreased FVC normal or increased total lung capacity (TLC) less than with emphysema roughly normal DLCO (vs. decreased DLCO in emphysema) DLCO = diffusing capacity of the lungs for carbon monoxide Arterial blood gas (ABG) indicated for O2 saturation < 92%, altered mental status, or acute exacerbation hypoxemia decreased PO2 may cause increased hemoglobin/polycythemia acute or chronic respiratory acidosis increased PCO2 (hypercapnia) due to retention Differential Asthma distinguishing factor obstructive pattern on PFTs are reversible after administration of inhaled bronchodilator Bronchiectasis distinguishing factor computed tomography (CT) is gold standard for diagnosis large internal bronchial diameter, thickened bronchial wall, and altered airway geometry "tram-track" and "signet-ring" signs Treatment First-line conservative smoking cessation greatest impact on mortality home O2 indicated if resting PaO2 < 55 mmHg or SaO2 < 89% flu and pneumococcal vaccines pharmacological step-wise depending on GOLD classification of disease severity mild short-acting inhaled bronchodilators short-acting inhaled beta-agonist (e.g., albuterol) as needed short-acting inhaled anticholinergic (e.g., ipratropium) as needed most patients will present in more advanced stages moderate long-acting inhaled bronchodilator long-acting beta-agonist (e.g., salmeterol or formoterol) long-acting anticholinergic (e.g., tiotropium) can be used in combination severe inhaled corticosteroid (e.g., budesonide or fluticasone) + long-acting bronchodilator very severe triple therapy inhaled corticosteroid + long-acting anticholinergic + long-acting beta-agonist may require roflumilast phosphodiesterase (PDE)-4 inhibitor theophylline PDE inhibitor and adenosine receptor blocker indicated for severe and refractory disease low therapeutic index Second-line lung resection or transplantation may be beneficial in severe cases refractory to medical management Other treatments mucolytics (e.g., N-acetylcysteine) Complications Acute exacerbation Cor pulmonale pathogenesis alveolar hypoventilation and hypoxia cause pulmonary vasoconstriction leads to pulmonary hypertension if severe can cause eventual right heart failure