COPD - Cor Pulmonale

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COPD Cor Pulmonale:

COPD Cor Pulmonale

COPD:

COPD Disease state characterised by airflow limitation that is not fully reversible

COPD:

COPD Emphysema Chronic Bronchitis Chronic Bronchiolitis / Small Airway Disease

EMPHYSEMA:

EMPHYSEMA Permanent and destructive enlargement of air spaces distal to terminal bronchioles with loss of architecture. Congenital or Acquired

CHRONIC BRONCHITIS:

CHRONIC BRONCHITIS Productive cough on most of the days for at least three months over two consecutive years.

Risk Factors:

Risk Factors Tobacco smoke – 10 pack years Biomass solid fuel fire Occupation–Coal Miners / Cadmium Air Pollution Infections Lung Growth – Infection / Maternal / Inutero

Slide 7:

7 Risk Factors for COPD Nutrition Infections Socio-economic status Aging Populations

Host / Genetic factors:

Host / Genetic factors  1 Antitrypsin deficiency Airway hyper-reactivity

Pathophysiology:

Pathophysiology Enlargement of mucus secreting glands  number of goblet cells Loss of elastic tissue / inflammation and fibrosis in airway wall / mucus accumulation / enhanced cholinergic tone  airflow limitation Decreased pulmonary and chest wall compliance

Pathophysiology:

Pathophysiology Ventilation perfusion mismatch Flattening of diaphragmatic muscles and horizontal alignment of intercostal muscles  work of breathing Unopposed action of proteases & antioxidants  Alveoli destruction

Emphysema Types:

Emphysema Types Centriacinar Panacinar

Clinical Features:

Clinical Features Symptoms Cough / Sputum production Dyspnoea Hemoptysis Morning Headache Oedema

Clinical Features:

Clinical Features General Examination Odour of smoke Nicotine staining of finger nails Accessory muscle of respiration Pursed Lip breathing Cyanosis

Clinical Features:

Clinical Features General Examination Systemic wasting Signs of RVF Clubbing Body built asthenic

Clinical Features:

Clinical Features “Pink Puffers” – thin, breathless “Blue Blotters” – Oedema, Cyanosis

Clinical Features:

Clinical Features Inspection Shape - Barrel shaped Symmetry - Bilaterally Symmetrical Trachea - Central Apex Beat - Not visualized Movements - Decreased Bilaterally

Clinical Features:

Clinical Features Palpation Trachea - Central Apex - Not Palpable Movements - Decreased bilaterally Measurement - AP / TD Chest Expansion

Clinical Features:

Clinical Features Percussion Hyper resonant Cardiac dullness obliterated Liver dullness – pushed down

Clinical Features:

Clinical Features Auscultation Intensity of breath sounds decreased bilaterally NVBS with prolonged expiration Rhonchi / Crepitations

Investigations:

Investigations Chest X-Ray PA View Hyperlucent lung fields Wide intercostal spaces Horizontally placed ribs Low set diaphragm Tubular Heart Bullae

Investigations:

Investigations Polycythemia PFT FEV 1 < 80% FEV 1 / FVC < 70% Exercise tests ABG CT Scan

Slide 26:

26 A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. Confirmed by spirometry. A post-bronchodilator FEV 1 /FVC < 0.70 confirms Airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.

Slide 27:

SYMPTOMS Cough Sputum Shortness of breath EXPOSURE TO RISK FACTORS Tobacco Occupation Indoor / outdoor pollution SPIROMETRY Diagnosis of COPD è

Management:

Management Smoking Cessation Oxygen Therapy Lung Volume reduction surgery

Management:

Management Smoking Cessation Bronchodilators  2 agonist Anticholinergic Theophylline preparations

Management:

Management Corticosteroids Inhaled Oral Parentral Oxygen Therapy

Oxygen Therapy:

Oxygen Therapy

Surgical Intervention:

Surgical Intervention Giant Bullous Disease Consider bullectomy if bullae compress smoking normal lung tissue Lung Volume Reduction Surgery Lung Transplantation

Management:

Management Vaccination Influenzae Pneumococcal Mucolytic therapy Acetylcysteine

Slide 34:

COPD Exacerbation Bacterial Infection 50% Viral Infection 25% Air Pollution 5% Unknown 20% Exacerbation Acute Inflammation Pathophysiology - Current Hypothesis Chronic Inflammation

Acute Exacerbation of COPD:

Acute Exacerbation of COPD Oxygen therapy Bronchodilators  2 agonists / Ipratropium Bromide Corticosteroids Parentral / oral Antibiotics NIV

Slide 36:

It is not enough for the physician to do what is necessary, but the patient and the attendants must do their part as well and circumstances must be favorable. Hippocrates

Cor Pulmonale:

Cor Pulmonale Dilation and Hypertrophy of RV in response to disease of pulmonary vasculature and or lung parenchyma

Cor Pulmonale:

Cor Pulmonale Acute Chronic

Etiology:

Etiology Chronic Bronchitis COPD ILD Pneumoconiosis Sarcoidosis Bronchiectasis Hypoventilation Syndromes / Cystic Fibrosis

Pathophysiology:

Pathophysiology Pulmonary Hypertension Hypoxic Vasoconstriction Acidemia Hypercapnia Lung destruction and fibrosis

Symptoms:

Symptoms Underlying lung disorder Dyspnoea, Fatigue,. Angina Tussive / effort related syncope RVF

Signs:

Signs Pulmonary Hypertension Visible & palpable pulmonary artery pulsations Left 2 nd ICS – dull on percussion Loud P 2 Systolic pulmonary ejection click Pulmonary ESM Graham Steel Murmur Prominent a-waves in JVP

Signs:

Signs RVH Parasternal heave RV pulsation in epigastrium TR (Carvallo’s sign) Cyanosis - Late finding

Investigations:

Investigations ECG P Pulmonale RAD RVH ECHO – RV / Pulmonary / Tricuspid valve / Pulmonary Artery

Investigations:

Investigations X-Ray Enlargement of main pulmonary artery CT scan (VP Scan)

Treatment:

Treatment Treat underlying condition Bronchodilators Steroids NIV Oxygen Therapy

Treatment:

Treatment RV Failure Diuretics Digoxin

Treatment:

Treatment PAH Avoid Physical stress Calcium Channel Blockers Endothelial receptor antagonists – Bosentan Phosphodiesterase – 5 inhibitors – Sildenafil Prostacyclins

Slide 49:

WORLD COPD DAY November 14 Raising COPD Awareness Worldwide