1. COPD Slides by Harleen Johal and Anna Longshaw Presented by Anna Longshow Notes available online

2. What do you already know? TRUE OR FALSE?

3. COPD is largely reversible. COPD is in fact largely irreversible.

4. Asthma is classified as a chronic obstructive pulmonary disease. Obstruction to airways in asthma is largely reversible.

5. Smoking is the main aetiology. Inhaled carbon is ingested by macrophages and lingers in lung tissue.

6. The FEV in COPD is reduced.

7. Definition 0 COPD: 0 Common, progressive disorder characterised by airway obstruction which is not fully reversible. 0 Umbrella term for emphysema and chronic bronchitis Emphysema Abnormal, permanent enlargement of distal airspaces Chronic Bronchitis Productive cough on most days for 3 consecutive months in at least 2 consecutive years

8. Epidemiology 0 Major public health problem 0 Prevalence of 1.5 million 0 30,000 deaths/year in UK 0 Rates highest in: inner city areas and lower SE groups 0 By 2020, predicted to become 3 rd leading cause of death worldwide 0 Related to 1 in 8 hospital admissions

9. Aetiology 0 90%  cigarette smoking: 0 inhaled carbon ingested by macrophages and persists in lung tissue. 0 may also cause mucous gland. 0 (but only 20% of smokers develop COPD so strong individual susceptibility) 0 Atmospheric pollutants 0 α 1 -antritrypsin deficiency: 0 early onset of emphysema. 0 α 1 -antritrypsin is a protease. 0 deficiency means proteolytic enzymes (neutrophil elastase) cannot be inactivated (protease/antiprotease imbalance).

10. Pathophysiology 3 parts to the mechanism: 1. Increased mucus secretion 2. Loss of elastic recoil and airway collapse in expiration 3. Inflammation and fibrosis  airway narrowing

11. Chronic Bronchitis: Pathophysiology 0 Aetiology: 0 ***smoking 0 Other pollutants 0 Pathogenesis: Irritants | Mucus gland hypertrophy in trachea and bronchus | Increased goblet cells in bronchioles | Mucus hypersecretion | Mucus plugging

12. Chronic Bronchitis: Signs 0 Blue bloater! 0 Low PaO2 0 High PaCO2 0 Chronic productive cough 0 Not breathless at rest 0 Exercise intolerance 0 Hypoxia, cyanosis 0 Crackles and wheezes 0 Bloated due to renal hypoxia causing fluid retention Ineffective exacerbation = predisposition to infections (bronchopneumonia). Chronic rise in CO2 desensitises this as a drive for respiration | Dependant on hypoxaemia to drive ventilation

13. Can you explain each symptom’s pathology?

14. Chronic Bronchitis SymptomsPathology 0 Blue bloater! 1. Chronic productive cough. 2. Exercise intolerance. 3. Breathlessness, hypoxia, cyanosis. 4. Crackles and wheezes. 5. Ineffective exacerbation = predisposition to chest infections (bronchopneumonia). 1. Hypersecretion of mucus. 2. Failure in gas exchange. 3. Insufficient respiratory drive, increased deoxyhaemoglobin (blue!). 4. Air passes through narrowed airways. 5. Excess mucus stagnating airways.

15. Emphysema: Pathology 0 Aetiology: 0 Smoking 0 α 1 anti-trypsin deficiency 0 Pathogenesis: 0 2 critical imbalances 1.Protease – Antiprotease Proteases released by neutrophils (released during inflammation, smoking aggravates) Antiprotease action > 2. Oxidant – Antioxidant Build up of free radicals (smoking aggravates a number of free radicals) Antioxidants >

16. Emphysema: Pathology 0 Progresses from centriacinar emphysema  panacinar emphysema

17. Emphysema: Pathology 0 NB bullous emphysema – pneumothorax!!

18. Emphysema: Clinical Signs 0 Pink puffer! 0 Normal PaO2 0 Normal PaCO2 0 Breathless at rest. 0 Not cynanosed. 0 Pursed lips on expiration. 0 Non-productive cough. 0 Barrel chest. 0 Low BMI. May develop type 1 respiratory failure (more on this later)

19. Can you explain each symptom’s pathology?

20. Emphysema SymptomsPathology 0 Pink puffer! 1. Pursed lips on expiration. 2. Non-productive cough. 3. Barrel chest. 4. Low BMI. 1. Maintains small positive pressure within lungs, keeping small alveoli open. 2. No excess of sputum. 3. Caused by chronic hyperventilation associated with outflow obstruction. 4. Continual respiratory effort.

21. Other general clinical features 0 Hypercapnia: 0 Peripheral vasodilation 0 Asterixis 0 Bounding pulse 0 Right heart failure: 0 Oedema 0 Raised JVP 0 Depression

22. Investigations: Forced Expiratory Volume 0 Spirometry - measurement of airways obstruction using spirometer. 0 Instrument records volume of air exhaled within given time (FEV) 0 FEV demonstrates COPD - air expelled more slowly.

23. Investigations: cont. lung function tests StageDescriptionFEV1/FVCFEV1Symptoms 1Mild<70%>80%No/mild breathlessness 2Moderate<70%<80%SOB on exertion 3Severe<70%<50%SOB on minimal exertion 4Very Severe <70%<30%SOB at rest

24. Investigations continued 0 ABG 0 Respiratory failure 0 CXR 0 Often normal 0 May show hyperinflation (>7 anterior ribs): low flattened diaphragm and presence of large bullae. 0 If very severe RHF can be seen 0 High resolution CT 0 May show emphysematous bullae. 0 Raised Hb and MCV 0 Due to persistent hypoxaemia and development of secondary polycythaemia. 0 ECG 0 May show cor pulmonale (tall P waves, RV hypertrophy) 0 Genotype 0 identifies α1-antritrypsin deficiency in premature disease/non-smokers.

26. Complications 0 Respiratory failure. 0 Cor pulmonale. 0 Secondary polycythaemia. 0 Nocturnal hypoxaemia. 0 Bullous emphysema. 0 Pneumothorax. 0 Infective exacerbations of chronic bronchitis.

28. Management 0 Conservative: 0 smoking cessation. 0 pulmonary rehabilitation. 0 Pneumococcal vaccine 0 Influenza vaccine

29. Management: cont. 0 Medical:

30. Management continued 0 Relievers: inhaled therapy, helpful to treat sudden episodes of dyspnoea and improve exercise tolerance. 0 short-acting ß-agonists - salbutamol. 0 short-acting antimuscarinics - ipratropium bromide. 0 Maintenance: 0 long-acting ß-agonists – salmeterol. 0 long-acting antimuscarinics - tiatropium. 0 inhaled corticosteroids - beclometasone dipropionate 0 combination inhalers - LABA + ICS. 0 antimucolytics - carbocisteine. 0 diuretics - furesomide.

31. Management continued 0 O 2 therapy: 0 maintain SpO 2 between 88-92% (patients dependent on hypoxic drive). 0 long-term domiciliary, 2 L/min via nasal prongs - continuous administration prolongs life. 0 nocturnal hypoxia - alveolar hypoventilation during REM sleep, treated with BIPAP. 0 Surgery: 0 lung volume reduction surgery.

32. Prognosis 0 Cannot be cured 0 Poor prognostic factors: 0 Continued smoker 0 Frequent exacerbations 0 Severe airflow obstruction 0 Development of complications

33. 33 Obstructive vs. Restrictive Lung Disease 0 Obstructive = inability to get air out 0 Restrictive = inability to get air in Obstructive lung disease: COPD, Asthma, Bronchiectasis, CF Decreased PEFR, FVC, FEV 1 : FVC Restrictive Lung Disease: Fibrosis (2º to radiation, medication, asbestos exposure) Decreased FEV 1, FVC, but normal FEV 1 : FVC ratio

34. 34 Respiratory Failure Organ failure represents that systems inability to perform its primary function Type II : Hypercapnic respiratory failure PaCO 2 is > 6.5 kPa Hypoxaemia is also common Type I: Hypoxaemic respiratory failure PaO 2 is < 8 kPa CO 2 is low to normal Caused by V/Q mismatching