1. DR SANJENA MITHRA, FY1 ASTHMA AND COPD

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 36.2BP 124/71HR 90RR26 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 asthma airway 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 Respiratory Acidosis Respirator y Alkalosis Metabolic Acidosis Metabolic Alkalosis pH ↓ pH ↑ pH ↓ pH ↑ Primary problem: pCO2 ↑ Primary problem: pCO2 ↑ Primary problem: HCO3 ↓ Primary problem: HCO3 ↑ Compensatio n: HCO3 ↑ Compensatio n HCO3 ↓ Compensati on: pCO2 ↓ Compensation: pCO2 ↑

10. Reading Chest X-Rays RIP...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 bronchopulmonary aspergillosis: 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 Senior help (ITU, anaesthetics) 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 ABG, CXR Salbutamol 4 puffs, then 2 puffs every 2 mins Salbutamol 5mg via O2 driven nebuliser If life threatening features present 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 37.7RR 25HR 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  Cor pulmonale  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?