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Chronic Obstructive Pulmonary Disease: COPD

dr. Tjatur Winarsanto SpPD

Chronic Obstructive Pulmonary Disease: COPD


Disease of airflow obstruction that is not totally reversible
Chronic

Bronchitis Emphysema

COPD: Etiology
Cigarette smoking #1 Recurrent respiratory infection Alpha 1-antitrypsin deficiency Aging

Def: Chronic Bronchitis

1. 2. 3. 4.

Excessive tracheobronchial mucus production sufficient to cause cough with expectoration for most days of at least 3 months of the year for 2 consecutive years. Classification: Simple chronic bronchitis Chronic mucopurulent bronchitis Chronic bronchitis with obstruction Chronic bronchitis with obstruction and airway hyperreactivity.

Chronic Bronchitis
Recurrent or chronic productive cough for a minimum of 3 months for 2 consecutive years. Risk factors

Cigarette smoke Air pollution

Chronic Bronchitis Pathophysiology


Chronic inflammation Hypertrophy & hyperplasia of bronchial glands that secrete mucus Increase number of goblet cells Cilia are destroyed

Chronic Bronchitis Pathophysiology

Narrowing of airway
Starting w/ bronchi smaller airways airflow resistance work of breathing Hypoventilation & CO2 retention hypoxemia & hypercapnea

Chronic Bronchitis Pathophysiology


Bronchospasm often occurs End result

Hypoxemia Hypercapnea Polycythemia (increase RBCs) Cyanosis Cor pulmonale (enlargement of right side of heart)

Chronic Bronchitis: Clinical Manifestations

In early stages

Clients may not recognize early symptoms Symptoms progress slowly May not be diagnosed until severe episode with a cold or flu Productive cough
Especially in the morning Typically referred to as cigarette cough

Bronchospasm Frequent respiratory infections

Chronic Bronchitis: Clinical Manifestations

Advanced stages
Dyspnea on exertion Dyspnea at rest Hypoxemia & hypercapnea Polycythemia Cyanosis Bluish-red skin color Pulmonary hypertension Cor pulmonale

Chronic Bronchitis: Diagnostic Tests

PFTs

FVC: Forced vital capacity FEV1: Forcible exhale in 1 second FEV1/FVC = <70% PaCO2 PaO2 Hct

ABGs

RBC

Emphysema

Abnormal distension of air spaces Actual cause is unknown

Def: Emphysema

1. 2. 3. 4.

Permanent abnormal distention of air spaces distal to the terminal bronchiole with destruction of alveolar septa (containing alveolar capillaries) and attachments to the bronchial walls. Classification: Centriacinar ( centrilobular) emphysema Panacinar emphysema Paraseptal emphysema Senile emphysema

Emphysema: Pathophysiology

Structural changes

Hyperinflation of alveoli Destruction of alveolar & alveolar-capillary walls Small airways narrow Lung elasticity decreases

Emphysema: Pathophysiology

Mechanisms of structural change


Obstruction of small bronchioles Proteolytic enzymes destroy alveolar tissue Elastin & collagen are destroyed

Support structure is destroyed paper bag lungs

Emphysema: Pathophysiology

The end result: Alveoli lose elastic recoil, then distend, & eventually blow out. Small airways collapse or narrow Air trapping Hyperinflation Decreased surface area for ventilation

Emphysema: Clinical Manifestations

Early stages

Dyspnea Non productive cough Diaphragm flattens A-P diameter increases


Barrel chest

Hypoxemia may occur


Increased respiratory rate Respiratory alkalosis

Prolonged expiratory phase

Emphysema: Clinical Manifestations

Later stages
Hypercapnea Purse-lip breathing Use of accessory muscles to breathe Underweight

No appetite & increase breathing workload

Lung sounds diminished

Emphysema: Clinical Manifestations

Emphysema: Clinical Manifestations

Pulmonary function
residual volume, lung capacity, DECREASED FEV1, vital capacity maybe normal

Arterial blood gases

Normal in moderate disease May develop respiratory alkalosis Later: hypercapnia and respiratory acidosis
Flattened diaphragm hyperinflation

Chest x-ray

Assess for COPD: A Common Story

Cough intermittent or daily present throughout day- seldom only nocturnal Sputum Any pattern of chronic sputum production Dyspnea Progressive and Persistent "increased effort to breathe" "heaviness" "air hunger" or "gasping" Worse on exercise Worse during respiratory infections Exposure to risk factors Tobacco smoke Occupational dusts and chemicals Smoke from home cooking and heating fuels

Assess and Monitor Disease Classification of COPD Stage 0 At Risk Stage I Mild COPD Stage II Moderate COPD Stage III Severe COPD Stage IV Very Severe COPD

Stage 0

At Risk

Normal spirometry +/- Chronic symptoms (cough, sputum, production)

Stage I

Mild COPD

FEV1/FVC <70% FEV1 >80% predicted With or without chronic symptoms (cough, sputum production)

Stage II

Moderate COPD

FEV1/FVC <70% 50% <FEV1 <80% predicted With or without chronic symptoms (cough, sputum production)

Stage III

Severe COPD

FEV1/FVC <70% 30% <FEV1 <50% predicted With or without chronic symptoms (cough, sputum production)

Stage IV

Very Severe COPD

FEV1/FVC <70% FEV1 <30% predicted or FEV1 <50% predicted plus chronic respiratory failure

Goals of Treatment: Emphysema


& Chronic Bronchitis
Improved ventilation Remove secretions Prevent complications Slow progression of signs & symptoms Promote patient comfort and participation in treatment

Collaborative Care: Emphysema &


Chronic Bronchitis
Treat respiratory infection Monitor spirometry and PEFR Nutritional support Fluid intake 3 lit/day O2 as indicated

Collaborative Care: Medications


Anti-inflammatory

Corticosteroids Beta-adrenergic agonist: Proventil Methylxanthines: Theophylline Anticholinergics: Atrovent

Bronchodilators

Mucolytics: Expectorants: Antihistamines:

Collaborative Care: Emphysema &


Chronic Bronchitis

Client teaching

Support to stop smoking Conservation of energy Breathing exercises


Pursed lip breathing Diaphragm breathing

Chest physiotherapy
Percussion, vibration Postural drainage

Self-manage medications
Inhaler & oxygen equipment

Therapy by Stage- Pretty Simple

Bronchodilators Beta2-agonists

Short-acting
Fenoterol Salbutamol (albuterol) Terbutaline

Long-acting
Formoterol Salmeterol

Bronchodilators Anticholinergics

Mode of Action

Cholinergic tone is only reversible component of COPD Normal airway have small degree of vagal cholinergic tone Ipratropium bromide Oxitropium bromide Tiotropium

Short-acting

Long-acting

BronchodilatorsCombos and Methylxanthines

Combination beta2-agonists plus anticholinergic in one inhaler


Fenoterol/Ipratropium Salbutamol/Ipratropium

Methylxanthines
Aminophylline (slow release preparations) Theophylline (slow release preparations) RARELY OF SIGNIFICNAT BENEFIT LEVEL 8-12 mcg/ml

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