COPD - Cor Pulmonale

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COPD Cor Pulmonale:

COPD Cor Pulmonale


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


COPD Emphysema Chronic Bronchitis Chronic Bronchiolitis / Small Airway Disease


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


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


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.

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


Management Smoking Cessation Oxygen Therapy Lung Volume reduction surgery


Management Smoking Cessation Bronchodilators  2 agonist Anticholinergic Theophylline preparations


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 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

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


Pathophysiology Pulmonary Hypertension Hypoxic Vasoconstriction Acidemia Hypercapnia Lung destruction and fibrosis


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


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


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


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


Treatment Treat underlying condition Bronchodilators Steroids NIV Oxygen Therapy


Treatment RV Failure Diuretics Digoxin


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

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