Lecture Notes. Chapter 4: Chronic Obstructive Pulmonary Disease (COPD)

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1 Lecture Notes Chapter 4: Chronic Obstructive Pulmonary Disease (COPD)

2 Objectives Define COPD Estimate incidence of COPD in the US Define factors associated with onset of COPD Describe the clinical features of patients with COPD List the criteria for mild, moderate, and severe COPD Describe the management of patients with COPD Define the treatment during acute exacerbation of COPD

3 Introduction Progressive airflow limitation that is not completely reversible Emphysema and chronic bronchitis CB is characterized by excessive sputum production for at least three months of the year for at least two consecutive years. Emphysema is defined in pathological terms and refers to the destruction of gas exchange surfaces of the lung (alveoli)

4 Introduction In the year million people had COPD 730,000 patients were hospitalized 8 million outpatient visits Fourth leading cause of death in the US Most patients with COPD have elements of CB, emphysema and asthma.

5 Etiology: Risk Factors Combination of exposure to noxious particles and fumes and host factors Cigarette smoke Smog Occupational dusts Indoor pollutants Genetic predisposition

6 Etiology: Cigarette Smoking Associated with higher incidence of COPD Larger decline in lung function over time Greater COPD mortality rate Number 1 cause of COPD Cigarette smoke and exposure to occupational dusts and fumes act additively in increasing a person s risk of COPD.

7 Etiology: api Deficiency Previously called alpha1-antitrypsin deficiency Liver produces mg/dl of api api inactivates neutrophil elastase Responsible for breaking down elastin during inflammatory response api deficiency results in elastase-induced destruction of lung tissue 1% of emphysema patients liver disease

8 Clinical Features: History Symptoms often start in fourth decade of life Cough and sputum production due to the hypertrophy and hyperactivity of the mucous glands lining the airways. Increase with onset of acute infection Exertional dyspnea Progresses over time COPD who has no smoking history, api deficiency must be considered.

9 Clinical Features: Physical Examination (Moderate to Severe) Prolonged expiratory phase Severe hyperinflation Hoover s sign (Severe hyperinflation)

10 During exacerbation Tachypnea, tachycardia Tripoding Abnormal sensorium if severe hypoxia Digital clubbing

11 Clinical Features: Physical Examination (Moderate to Severe) Auscultation Diminished breath sounds Early-inspiratory crackles (sudden opening of more proximal airways) Expiratory wheezing (during acute exacerbations) Distant heart sounds Point of maximal impulse (PMI) may shift to the epigastrium Loud P2 if pulmonary hypertension present (loud closure of the pulmonic valve)

12 Clinical Features: Physical Examination (Cor pulmonale) Jugular venous distension (JVD) Hepatomegaly Pedal edema Hepatojugular reflex

13 Clinical Features: Laboratory Studies Polycythemia Lekocytosis if infection present Hypochloremia Elevated bicarbonate

14 Clinical Features: Arterial Blood Gases To determine severity and guide treatment Initially mild to moderate hypoxemia with normal PaCO2 levels Gradual hypercarbia Exacerbations Acute hypercarbia Acute acidosis

15 Clinical Features: Chest Radiograph Mild to moderate Minimal hyperinflation Flat diaphragm Severe Severe hyperinflation Small narrow heart Tram tracks thickening of the airways when chronic bronchitis is severe.

16 Clinical Features: Pulmonary Function Studies Acute exacerbation Peak flow < 100 L/min FEV1 < 1.0 L Severe hyperinflation Increased RV, FRC, and TLC Reduced DLCO (emphysema)

17 Clinical Features: Pulmonary Function Studies ATS Classification Stage 1. FEV1 > 50% of predicted Stage 2. FEV1 35% 49% of predicted Stage 3. FEV1 < 35% of predicted GOLD Classification Stage 1. FEV1 > 80% of predicted Stage 2. FEV1 50% < 80% of predicted Stage 3. FEV1 30% 49% of predicted Stage 4. FEV1 < 30% of predicted

18 Clinical Features: Electrocardiography Tachycardia Right axis deviation if RV hypertrophy is present Low voltage in limb leads if hyperinflation is present

19 Treatment: Management of Stable COPD (Stage 1) Removal of noxious agent from patient s environment Smoking cessation Change in employment Change of geographical location Bronchodilators as needed

20 Treatment: Management of Stable COPD (Stages 2 3) Pharmacological Agents Beta-2 agonists Short-acting (albuterol) Anticholinergic agents Short-acting (Ipratropium) Long-acting (tiotropium) Beta-2 agonist + anticholinergic

21 Treatment: Management of Stable COPD (Stages 2 3) Pharmacological Agents Use of methylxanthines is controversial (Improve breathing by increasing the strength of the diaphragm and by stimulating the breathing control centers in the brain). Corticosteroids If lack of response to bronchodilators (MDI is best) Long-term oxygen therapy PaO 2 < 55 mm Hg SaO 2 < 88% Improves survival, exercise tolerance, and hemodynamics in COPD

22 Treatment: Management of Stable COPD (Stages 2 3) Pulmonary Rehabilitation Program Improves exercise tolerance Educates patients about their disease Overall quality of life improves

23 Treatment: Management of Stable COPD (Stages 2 3) Surgery Remove those the most diseased parts Lung volume reduction In cases of severe upper lobe emphysema Patient must meet certain criteria

24 Treatment: Management of Acute Exacerbation Pharmacologic Agents Oxygen therapy Keep PaO mm Hg Bronchodilators Beta agonists Anticholinergics MDI or Oral or IV corticosteroids

25 Treatment: Management of Acute Exacerbation Mechanical Ventilation Noninvasive positive pressure ventilation (NPPV) Avoids complications of intubation Improves acid base balance Reduces hospital length of stay Endotracheal intubation if lack of response to NPPV Small tidal volumes Long expiratory times

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