ASTHMA AND COPD

1. ASTHMA AND COPD Dr sanjenaMithra, fy1

2. Objectives Differentiate severity of acute asthma exacerbations Pathophysiology of Asthma and COPD Discuss CXR and ABG Type 1 vs Type 2 respiratory failure

3. 5 mins – pretest 10 mins – case 1 10 mins – case 2 5 mins – end of session test feedback

4. Pretest Define asthma What constitutes COPD? Briefly outline the pathophysiology of asthma Describe 4 differences in the airways of acute and chronic asthmatics. How can you categorise severity of acute asthma attacks? List 4 classes of drug used to treat Asthma/COPD What are their mechanisms of action and side effects? How can you determine severity of COPD? Compare type 1 and type 2 respiratory failure

5. Take a history from this patient who is short of breath… Cough +/- sputum Chest pain (pleuritic) Wheeze SMOKING Allergies, Pets Foreign travel History of DVT, PE *Compliance with meds* Weight loss Haemoptysis • Atopy • Family history • Exercise tolerance • Diurnal variation • Complications: • Oedema • SOBOE • Recurrent infections • Fever

6. CASE 1- Summary • 28 year old lady presents to A&E after becoming short of breath whilst visiting friends. She was feeling well during the day and had been to work. Non-smoker • PMH: Asthma since childhood – Salbutamol PRN • Inhaler currently not relieving symptoms; SOB worse over last 2 hours. Chest starting to feel tight, she is getting lightheaded. • On examination: • T 36.2 BP 124/71 HR 90 RR26 96% sats on air • Alert, talking in full sentences but distressed. • CVS and Abdo – NAD • Resp – widespread wheeze, no crackles, no friction rub

7. What are your differentials for this patient and why? • Acute asthma exacerbation (non-life threatening) • PE • Inhaled foreign body • Allergic reaction • Anxiety • Pathophysiology • Define asthma • 4 characteristics of acute and chronic asthma

8. Asthma • ASTHMA – chronic, inflammatory disease of the airways resulting in variable, often reversible airflow obstruction and airway hyperresponsiveness. • Acute asthma airway changes- • Airway constriction, microvascular leakage / oedema, vasodilation, mucus hypersecretion • IgE mediated inflammatory response. Cross-linking of IgE results in degranulation of mast cells, histamine release and inflammatory cell infiltration • Chronic asthmaairway changes– airway remodelling • Subepithelial fibrosis, smooth muscle hyperplasia / hypertrophy, goblet cell hyperplasia, new vessel formation

9. Investigations • What investigations would you like to do? • Bedside: Peak flow – 45% of best • Bloods: ABG, FBC, U&E, CRP • Imaging: CXR • ABG: • pH 7.46 • pCO2 4.1 • pO2 10.3 • HCO3 26

10. Reading Chest X-RaysRIP...ABCDE • Adequacy: • Rotation (symmetry of clavicles) • Inspiration (ribs) • Penetration (vertebral bodies) • Mention central lines, NG tubes, pacemakers etc • Airway: is the trachea central? • Boundaries and Both lungs: lung borders, consolidation, hazy etc • Cardiac: Heart size • Diaphragm • Everything else: soft tissue mass, fractures

11. What investigations would you like to do? • Bedside: Peak flow – 45% of best • Bloods: ABG, FBC, U&E, CRP • Imaging: CXR Allergic bronchopulmonaryaspergillosis: refractory asthma with fever, cough and sputum. Eosinophilia and raised IgE

12. Acute severe asthma • How would you like to manage this patient? • Immediate • A to E • Salbutamol 5mg via oxygen driven nebuliser • Repeat obs (SpO2, HR, RR) and PEF to assess for progression of severity and risk to life • If clinically stable and PEF >75%, can repeat Salbutamol nebs and consider oral prednisolone 40-50mg

13. Moderate PEF >50-75% SpO2 >92% No features of severe Acute Severe PEF 33-50% RR >25 SpO2 >92% HR >110 Cannot complete sentences Life threatening 33-92-CHEST PEF <33% SpO2 <92% Cyanosis/Confusion, Hypotension, Exhaustion, Silent chest, Tachycardia Salbutamol 4 puffs, then 2 puffs every 2 mins Salbutamol 5mg via O2 driven nebuliser Senior help (ITU, anaesthetics) ABG, CXR If life threatening features present • O SHIT! • O2 to maintain sats 94-98% • Salbutamol 5mg via O2 driven nebs • Hydrocortisone IV/oral prednisolone • Ipratropium via O2 driven nebs • Consider Magnesium Sulphate IV Repeat salbutamol nebs, give oral prednisolone 40-50mg

14. Long term management • Long term • Conservative: Follow up by GP, check inhaler technique, refer to chest clinic/asthma liaison nurse • Medical: If PEF <50% on admission, can consider prednisolone, adequate inhaler supply • Stepwise treatment of asthma

15. Communication • Please explain to Mr X how to correctly use his inhaler • Check understanding • If you haven’t used it for a while, spray in the air to check it works • Shake it • As you breathe in, simultaneously press down on the inhaler • Continue to breathe deeply • Hold your breath for 10 seconds or as long as you comfortably can, before breathing out slowly. • If you need to take another puff, wait for 30 seconds, shake your inhaler again then repeat • Advise on using a spacer

16. Chronic Management of Asthma

17. Case 2 – Summary • A 64 year old gentleman presents to A&E with increasing SOB over the last 3 days. This is associated with a cough productive of thick, green sputum. • Gets SOB normally after about 5-10 mins walking on the flat • PMH: “asthma” • SH: 50 cigarettes a day for the past 40 years. • On examination he is alert but visibly SOB • T 37.7 RR 25 HR 110 O2 sats 89% on air, you notice he is using his accessory muscles to breathe. • Resp: hyperinflated chest, diffuse coarse crepitations, widespread wheeze, reduced air entry bilaterally • CVS: JVP raised, ankle oedema (non-pitting) • Abdo SNT

18. Case 2

19. What are your differentials for this patient and why? • Acute infective exacerbation of COPD • Pneumonia • Corpulmonale • Bronchiectasis • Pathophysiology • Define COPD clinically • Histopathology? • Pathophysiology?

20. Definitions COPD: Umbrella term encompassing chronic bronchitis (chronic cough and sputum production on most days for at least 3 months per year for 2 years) and emphysema (pathological diagnosis of permanent destructive enlargement of distal air spaces) Chronic bronchitis: airway narrowing due to bronchiole inflammation, mucosal oedema and mucus hypersecretion Emphysema: Destruction and enlargement of alveoli that reduces elastic recoil and results in bullae.

21. Investigations • What investigations would you like to do? • Bedside: ECG, sputum culture • Bloods: ABG, FBC, U&E, CRP, blood cultures • Imaging: CXR • Special tests: ECHO, α1-antitrypsin levels • ABG: assess the oxygenation • Checking for respiratory failure- failure to fully oxygenate the blood passing through the lungs giving rise to hypoxia +/- hypercapnea.

22. ABG • pH 7.29 • pCO2 6.8 • pO2 7.9 • HCO3 25

23. Respiratory failure • Type 1- hypoxia with low or normal pCO2 – anything that impairs gas exchange • Atelectasis, pulmonary oedema, pneumonia, pneumothorax • Type 2 – hypoxia with hypercapnea – alveolar hypoventilation • Same causes for a respiratory acidosis • COPD, neuromuscular disorders (GBS, MND), CNS depression (drugs, brainstem injuries)

24. Initial management – infective exacerbation of COPD • How would you like to manage this patient? • Immediate • A to E • Maintain sats 88-92% (titrate to ABG) • Corticosteroids (oral/IV) • Empirical antibiotics • Salbutamol 5mg and Ipratropium via O2 driven nebulisers • Consider need for NIV – if desaturating/decompensating • Admit, chest physiotherapy

25. Flow volume loops - Spirometry

26. FEV1/FVC • Determines the severity of COPD • Describes the proportion of a person’s vital capacity (maximum air expelled after maximum inhalation) that can be expired in the first second. • Normal ~ 70% • Mild 50-70% • Moderate 30-50% • Severe <30%

27. Management • Long term • Conservative – smoking cessation, pulmonary rehabilitation, flu vaccination, Spirometry • Medical – LTOT (only if not smoking), bronchodilators, steroids (can consider if more than 2 infective exacerbations/year), prophylactic antibiotics • Surgical – Transplant, lobectomy, bullectomy • LTOT criteria • PaO2 <7.3 kPa on air during period of clinical stability • PaO2 7.3-8.0 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension

28. Drugs 1 • Bronchodilators: • Beta-2 agonists – Short acting/Long acting (Salbutamol/Salmeterol) • MOA: increases cAMP production in the lung which decreases calcium concentration • Effect: Smooth muscle relaxation, bronchial dilatation • S/e: tachycardia, sweating, tremor • Anticholinergics: • Ipratropium (Atrovent), Tiotropium (Spiriva) • MOA: Anti-muscarinic. Ipratropium is non-selective, Tiotropium is selective (M3) • s/e: dry mouth, sedation, skin flushing, tachycardia

29. Drugs 2 • Methyxanthines • Theophylline, Aminophylline • MOA: Phosphodiesterase antagonists – raise intracellular cAMP levels. Works well with beta-2 agonists • s/e: narrow therapeutic window • Leukotriene receptor antagonists • Montelukast, Zafirlukast • s/e: GI upset, drowsiness • Corticosteroids • Prednisolone, Beclamethosone • MOA: upregulates intracellular proteins after binding with receptor and causes expression of anti-inflammatory agents • s/e: weight gain, immunosuppression, skin thinning, bruising, osteoporosis, cataracts

30. Pretest Define asthma What constitutes COPD? Briefly outline the pathophysiology of asthma Describe 4 differences in the airways of acute and chronic asthmatics. How can you categorise severity of acute asthma attacks? List 4 classes of drug used to treat Asthma/COPD What are their mechanisms of action? How can you determine severity of COPD? Compare type 1 and type 2 respiratory failure

31. Take home message 33-92 CHEST Focussed history taking: Symptoms, red flags, complications Structure your answers Questions?