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Respiratory Final Year Lecture DR NEELAN SURENDRARAJ (RESPIRATORY SENIOR CLINICAL FELLOW)Case 1: History Examination u 70-year-old patient u No finger clubbing u Increased breathlessness u Chest clear u No chest pain u No peripheral oedema PMHx: 1. Non Hodgkins LymphomaCXRABG on 40% FIO2 pH: 7.52 PO2: 8.5 PCO2 3.9 HCO3 26Most likely diagnosis: 1. Exacerbation of asthma 2. Exacerbation of COPD 3. Pulmonary embolism 4. Pulmonary fibrosisHypoxaemia Definition: PAO2 <8 Causes: 1. Hypoventilation 2. V/Q mismatch (Shunting vs Deadspace) 3. Diffusion impairment 4. High altitudeApproach to Hypoxaemia Ventilation Vs Perfusion Insufficient movement Impaired blood supply of air into alveoli to ventilated alveoliHypoventilation V/Q mismatch u Reduction in alveolar ventilationentilation and perfusion u Causes an increase in PCO2 mismatched u Shunt vs Deadspace Diffusion impairment u Impairment of blood-gas barrierPulmonary Embolism History: Examination 1. SOB 1. Sinus tachycardia 2. Chest pain 3. Haemoptysis 2. Tachypnea 4. Calf pain 3. Hypoxaemia 5. Cough 4. Loud S2 6. PMHx: i.e. malignancy 7. Medication: HRT 5. Elevated JVP 6. Calf swelling/tenderness 8. Family history: VTE and thrombophilia 9. Other Risk factors: Long haul flight etcP.E risk factors Investigations: Genetic 1. FBC, U&Es, Clotting screen 1. Protein C & S deficiency 2. D-dimer and troponin 2. Factor V Leiden 3. CXR 3. Family history 4. ABG 5. ECG 6. CTPA Acquired 7. V/Q Scan (if cannot have 1. Recent surgery CTPA) 8. CT CAP (if confirmed 2. Immobility 3. Cancer unprovoked P.E) 9. Thrombophilia screen (if 4. Inflammatory disease confirmed unprovoked P.E) 5. Recent flight 6. PregnancyCTPA V/Q scanQ2: u 75 year old gentleman admitted with central chest pain and increased shortness of breath over 1 day. u Blood pressure: 85/40, HR 120, Sats 90% on Fi02 60%, RR 28 Next step in management: 1. Treatment dose low molecular weight heparin 2. Thrombolysis 3. Iv fluids 4. Warfarin 5. NOACTreatment 1. Anticoagulation (warfarin, DOACs, LMWH) 2. Thrombolysis 3. ThrombectomyPulmonary Hypertension Definition: Pulmonary artery systolic pressure >25mmHgPulmonary Hypertension Group 1 u Pulmonary Arterial Hypertension (idiopathic, hereditary, drug/toxin, CTD) Group 2 u PH secondary to left sided heart failure (Raised capillary wedge pressure) Group 3 u PH secondary to underlying lung disease and hypoxia Group 4 u Chronic thromboembolic pulmonary hypertension Group 5 u Secondary to conditions with multifactorial mechanisms causing PHSymptoms Diagnosis: u ECG u Breathlessness on exertion u ABG (any hypoxaemia) u Lower leg swelling u Echocardiogram (bubble contrast) u PFTs (particularly transfer factor) Examination u CTPA (any P.E) u Pansystolic murmur (tricuspid u V/Q scan (more sensitive for CTPE regurgitation) u HRCT (ILD) u Central cyanosis (congenital heart disease) u Cardiac catheterisation u Autoimmune screen (scleroderma etc) u Signs of connective tissue diseases u BNP (heart failure) Features of right heart failure: u 6 minute walk test u Sleep studies (OSA/OHS) u Peripheral oedema u Ascites u Raised JVPManagement: General: LTOT if hypoxaemic, diuretics Group 1: IPAH (vasoreactivity studies) if positive then can be treated with calcium channel blockers Group 2: Optimise treatment for heart failure Group 3: Treat underlying lung disease, I.E CPAP for OSA LTOT for hypoxaemia Group 4: CTEPH – anticoagulation, pulmonary endarterectomy, vasodilator therapy (if not surgical candidate)History Shortness of Breath Haemoptysis: 1. Onset and duration 1. Onset, timing and amount of blood 2. Severity i.e only on exertion/at rest Chest pain: Cough 1. Usually pleuritic pain (worse on deep inhalation/coughing) 1. Acute vs Chronic 2. Productive vs non productive 3. Timing of cough 4. Colour of sputumMedical History: Family History: 1. Childhood asthma 1. Asthma, lung Ca, cystic fibrosis, alpha 1 antitrypsin deficiency 2. CTD 3. Hx of recurrent infections 4. Cardiac history Social History: 1. Smoking Drug History: 2. Occupational history 1. ACE inhibitors 3. Home environment 4. Pets 2. Medication associated with ILD 3. Beta Blockers Q3. u 19-year-old gentleman admitted with increased SOB over 1 day. Non- productive cough with no fever. u On examination unable to complete a sentence in a single breathe. u RR 32, Sats 90% on air, bilateral expiratory wheezeQ3. Most likely diagnosis 1. Exacerbation of COPD 2. Exacerbation of Asthma 3. Pulmonary embolism 4. Exacerbation of pulmonary fibrosisAsthma Aetiology: Diagnosis: Acute Treatment: • Reversible airway obstruction § Diurnal variation of peak flow 1. Oxygen therapy • Airway hypersensitivity driving increased mucus production, § History of Atopy 2. Nebulised Salbutamol inflammation and bronchoconstriction § Obstructive Spirometry 3. Nebulised Ipratropium § Reversibility with 4. I.V Hydrocortisone (or Episodic symptoms: bronchodilator (FEV1 prednisolone) 1. Breathlessness increase of 12% or 200mls) 5. Antibiotics (if bacterial 2. Wheeze § Raised FeNO (>40ppb) infection suspected) 3. Chest tightness § Raised eosinophils 6. I.V Magnesium sulphate 4. Cough § Raised total IgE 7. I.V Aminophylline Signs: § Positive provocation testing 1. Bilateral wheeze 2. Tachypnoea 3. Use of accessory musclesAssessing severity Moderate acute asthma u Increasing symptoms u Peak flow > 50-75% best or predicted u No features of acute severe asthma u Severe acute asthma u Any one of the following: u Peak flow 33-50% best or predicted u Respiratory rate ≥ 25/min u Heart rate ≥ 110/min u Inability to complete sentences in one breathLife-threatening acute asthma u Any one of the following, in a patient with severe asthma: u Peak flow < 33% best or predicted u Arterial oxygen saturation (Sp2 ) < 92% u Partial arterial pressure of oxygen (2aO ) < 8 kPa u Normal partial arterial pressure of carbon dioxide (Pa2O ) (4.6–6.0 kPa) u Silent chest u Cyanosis u Poor respiratory effort u Arrhythmia u Exhaustion u Altered conscious level u Hypotension Near-fatal acute asthma u Raised PaCO 2 requiring mechanical ventilation with raised inflation pressures, or bothQ4 u You have reviewed a 24 year old patient with an exacerbation of asthma in resus. His initial ABG is overleaf. ABG on air pH 7.37 pO2 7.3 pCO2 3.3 HCO3 26 Base Excess -1.5u Following this ABG you have given: u Salbutamol and ipratropium nebulisers u Hydrocortisone 200mg iv stat u Iv magnesium sulphate 2g u Oxygen via venturi mask ABG on 28% Fio2 pH 7.35 A repeat ABG is taken after 20minutes pO2 7.8 pCO2 5.0 HCO3 26 Base Excess -1.5Q4. What would your next step in management be? 1. Iv aminophylline 2. ITU review for consideration of intubation 3. Start NIV 4. Repeat nebuliser therapyChronic Asthma Management: u Intermittent: SABA u Mild: SABA + ICS u Moderate: LABA/ICS combination u Severe: LABA/ICS (medium/high dose) + leukotriene receptor antagonist + theophylline + (immunotherapy)COPD Aetiology: Signs: Diagnosis: • Incompletely reversible airway 1. Bilateral wheeze obstruction § Spirometry (FEV1: FVC ratio 2. Tachypnoea <0.7) • Emphysema: Enlargement of air 3. Use of accessory muscles spaces distal to the terminal 4. Barrell Shaped chest § Increased TLC and RV bronchiole with destruction of walls (hyperinflation) § Increased RV/TLC ratio • Cigarette smoking 5. Prolonged expiratory • Alpha 1 antitrypsin deficiency § Reduced diffusion capacity phase • Premature airway collapse on 6. Pursed lip breathing § CXR/CT chest expiration 7. Tar staining on finger nails § ABG 8. Loud P2 heart sound § Alpha-1 antitrypsin level Symptoms: • Breathlessness 9. Peripheral oedema • Productive cough Q5 u 78 year old patient with a background of COPD attends with breathlessness and cough for 4 days. On examination patient has RR 36, temp 39 and bilateral wheeze. CXR shows right basal consolidation. Nebulisers, antibiotics and steroids were given. ABG post treatment shown below. 40% FIO2 pH 7.25 pO2 7.5 pCO2 9.2 HCO3 34 Base Excess +8.0What’s the next best step in management? 1. Iv aminophylline 2. Start NIV (BIPAP) 3. ITU review for consideration of intubation 4. Aim target saturations 88-92% 5. Increase FI02Acute Treatment: 1. Targeted oxygen therapy 2. Nebulised Salbutamol 3. Nebulised Ipratropium 4. I.V Hydrocortisone (or prednisolone) 5. Antibiotics 6. I.V Magnesium sulphate 7. NIV (BIPAP)Bacterial Chest Infection Epidemiology: u Most common cause of community acquired pneumonia in immune competent patients is streptococcus pneumonia u Other organisms: Moraxella catarrhalis, Haemophilus influenza, legionella pneumophila u Atypical pathogens: Chlamydia pneumoniae and mycoplasma pneumoniaePresentation: 1. Cough, fever productive sputum 2. Extrapulmonary symptoms/signs: rash, athralgia Investigations: 1. CXR 2. Bloods: WCC, CRP 3. ABG 4. Sputum culture 5. Atypical pneumonia screenCURB-65 score: C: Confusion U: Urea >7 R: Respiratory rate >20 B: Blood pressure <90 systolic or <60 diastolic 65: Age > 65Treatment: u CURB Score 1: amoxicillin or tetracycline/macrolide if allergic u CURB Score 2: amoxicillin + macrolide u CURB Score >3: Beta lactamase (co-amoxiclav) + macrolide Hospital acquired pneumonia: Antibiotic covering pseudomonas i.e Tazocin Bronchiectasis Investigations: Aetiology: History: • Recurrent childhood infection i.e. § Productive cough with high 1. Bloods: FBC, immunoglobulins, pertussis, measles HIV, Alpha-1 antitrypsin, ANA, • Previous TB, lung carcinoma sputum burden ANCA, RF 2. Sputum MC&S, AFB and Fungal • ABPA § Fever culture • Hypogammaglobinaemia § Breathlessness 3. ABPA screening (total IgE, IgE to • Primary Ciliary Dyskinesia aspergillus and IgG to aspergillus § History of recurrent symptoms (Kartagener’s syndrome) 4. CXR • Cystic fibrosis § ENT symptoms 5. HRCT • IBD, RA § Previous TB 6. Bronchoscopy • Idiopathic 7. Pulmonary function testing § Smoking 8. Nasal nitric oxide Mechanism: Examination: 9. Genetic testing for CF • Cole’s Vicious cycle theory • Bacterial infection causes airway § Purulent sputum (check sputum pot) inflammation and impaired mucociliary escalator § Finger clubbing • Causes bronchial obstruction (airway § Coarse late inspiratory dilation) with mucus stasis and crackles bacterial colonisation Allergic bronchopulmonary aspergillosis (ABPA) u Hypersensitivity reaction u When bronchi become colonised with aspergillus u Causes repeated inflammation and mucus stasis causing obstruction of the bronchiCystic fibrosis u Mutation in the CF transmembrane conductance regulator gene u Causes abnormal sweat chloride test, recurrent respiratory infections and pancreatic insufficiency u Diffuse bronchiectasis u Sweat chloride concentration >60Management 1. Common organisms: Haemophilus influenza, streptococcus pneumonia and pseudomonas aeruginosa 2. Antibiotics (covering pseudomonas i.e quinolones) 3. Looking at previous sputum cultures 4. Mucolytics (carbocisteine, saline nebulisers) 5. Prophylactic antibiotics (azithromycin) 6. Nebulised antibioticsQ6 u 70 year old gentleman who is a never smoker describes increased breathlessness on exertion over 2 years and non productive cough. He has previously worked in the dockyard for many years. On examination he has fine end inspiratory crepitations bilaterally from midzones to base. What findings would you expect on the lung function tests?Interstitial lung diseaseInterstitial Lung Disease u Combination of chronic inflammation and various degrees of lung fibrosis u Some ILD’s present as more inflammatory disease and respond better to anti- inflammatories and immunosuppressive therapy u However in idiopathic pulmonary fibrosis there is predominately a fibrotic process which responds poorly to anti-inflammatory/immunosuppressive therapyIdiopathic Pulmonary Fibrosis Aetiology: Examination: Investigations: • Thickening of interstitium (between alveolar epithelium and capillary § Mild cyanosis 1. Bloods: including auto- § Fine late inspiratory immune screen endothelium) • Process of fibrosis and collagen crepitations 2. HRCT (UIP pattern) deposited in interstitium § Tachypnea 3. Spirometry • Usually affects between 50-70 years old patients Management: History: • Pirfenidone (anti-fibrotic) • Nintedanib (tyrosine kinase § Breathlessness inhibitor) § Non-productive cough • Lung transplantationMedical History u Inhaled substance u Mould u Exposure to bird/avian proteins u Pets u Dusty environments u Occupational history u Medication u Pulmonary infectionsHistology Usual interstitial pneumonia (UIP): heterogenous areas of lung fibrosis with areas of relatively normal lung architecture Non-specific intersitial pneumonia (NSIP): Homogenous pattern of diffuse inflammation +/- fibrosis of the lung interstitium Organising Pneumonia (OP): areas of focal abnormalityHypersensitivity Connective Tissue Associated Pneumonitis u Also referred as extrinsic ILD allergic alveolitis • Rheumatoid arthritis • SLE u Excessive immune response of an • Sjogren’s syndrome environmental antigen • Systemic sclerosis (e.g avian proteins, mold • Mixed connective tissue or farming) disease u A detailed environmental and occupational history • Polymyositis • Dermatomyositis needs to be taken u Usually presents as upper lobe fibrosis on imagingPulmonary Function Tests u Restrictive pattern in Pulmonary fibrosis u Reduced FEV1 and FVC u However the FEV1/FVC ratio is normal/high u The lung volumes are reduced but the proportions are persevered i.e total lung capacity, functional residual capacity and residual volume u The fibrous tissue reduces lung compliance u However airway resistance at a specific lung volume is normal or reduced due to increased radial traction due to fibrosisPulmonary Tuberculosis Symptoms: Investigations: Management: 1. Fever 1. Sputum AFB x 3 1. 6 months treatment 2. Night sweats 2. HIV test 3. Hepatitis B, C Rifampicin: 6 months 3. Weight loss 4. CT chest (in some cases Isoniazid: 6 months 4. Productive abdomen and pelvis) Ethambutol: 2 months cough/haemoptysis 5. Bronchoscopy (if unable to Pyrazinamide: 2 months Signs get diagnosis from sputum Pyridoxine (Vitamin B6): 6 months AFB 1. Phrenic nerve crush scar 2. Crackles (secondary bronchiectasis) 3. Cervical lymphadenopathy (can be generalised)Q7 u 40 year old African American gentleman found to have bilateral hilar lymphadenopathy on CT chest. Endobronchial Biopsy of hilar lymph nodes shows non caseating granulomas on histology. He is asymptomatic. What is the likely diagnosis?Lung Cancer History Examination 1. Persistent cough 1. Clubbing 2. Haemoptysis 2. Tar staining 3. Increased SOB 3. Engorged neck veins and facial swelling 4. Weight/Appetite loss 5. Hoarseness of voice 4. Assess for pleural effusion 6. Bone pain 5. Lymphadenopathy 6. Cachexia 7. Smoking history 7. Scars (thoracotomy) 8. Family historyInvestigations: Small cell lung cancer 1. Limited vs Extensive disease 1. CXR 2. Bloods including clotting 3. CT Chest Treatment: 4. PET CT scan 1. Surgical resection 5. Pulmonary function tests 2. Chemotherapy 3. Radiotherapy 6. Bronchoscopy/EBUS (mediastinal 4. Immunotherapy lymph nodes/central masses) 5. Palliative treatment 7. CT guided biopsy (peripheral lesions) Non small cell lung cancer 1. Squamous cell lung cancer 2. Adenocarcinoma Treatment: 1. Depends on TNM staging, performance status and lung functionObstructive Sleep Apnoea History Examination Investigations 1. Excessive daytime 1. High BMI 1. Sleep Study sleepiness 2. Hypertension 2. Echocardiogram 2. Unrefreshed sleep 3. Pulmonary 3. Early Morning ABG 3. Snoring hypertension/right 4. Morning headache 5. Poor concentration Treatment: 6. Obesity 1. CPAP 2. Avoiding smoking and alcohol 3. Surgery Sarcoidosis Aetiology: Signs 1. Multisystem granulomatous 1. Papules and papulonodules disease 2. Affects lungs in 90% of cases 2. Lupus pernio 3. More common in African 3. Subcutaneous nodules Americans and Scandinavians 4. Scleritis Symptoms 1. Asymptomatic 5. Episcleritis 2. Increased SOB 3. Lethargy 6. Lymphadenopathy 4. Cough 5. Chest pain 7. Optic neuritisInvestigations: Treatment: 1. CXR 1. Corticosteroids 2. CT chest scan 2. Azathioprine 3. Pulmonary function tests 3. Hydroxychloroquine 4. Endobronchial ultrasound 4. Anti-TNF therapy 5. BronchoscopyAcute Respiratory Distress Syndrome (ARDS) Aetiology: PaO2/FiO2 ratio Acute Treatment: • End result of intrinsic and u Mild ARDS: 201 - 300 mmHg 1. Treat underlying cause extrinsic insults to lung • Interstitial and alveolar (≤ 39.9 kPa) 2. Mechanical ventilation u Moderate ARDS: 101 - 200 oedema 3. Inhaled pulmonary • Pro-inflammatory state mmHg (≤ 26.6 kPa) vasodilators leading to increased capillary permeability u Severe ARDS: ≤ 100 mmHg (≤ 4. Proning 13.3 kPa) 5. Neuromuscular blockade Clinical Features: • Worsening hypoxaemia 6. ECMO • Bilateral alveolar opacification • Poor lung compliance • Decreased PaO2/FIO2 ratioPleural Effusion Pathology: Exudative: Symptoms • Transudate vs Exudative • Pneumonia • Increasing • Malignancy Breathlessness • Transudative: Usually (lung/metastasis) • Associated caused by increased • TB features hydrostatic pressure or depending on reduced oncotic cause pressure Light’s criteria • Exudative: Increased 1. Pleural protein: capillary permeability serum protein Signs: due to >0.5 • Tracheal inflammation/infection deviation 2. Pleural LDH: • Decreased chest Serum LDH >0.6 expansion on Transudative: 3. Pleural LDH affected side • Heart failure >2/3rds upper limit of blood LDH • Stony dull • Liver failure percussion note • Nephrotic syndrome • Decreased vocal resonanceInvestigations: Management: 1. CXR 1. Treat underlying cause 2. ABG 2. Hold 3. Bloods including clotting antiplatelets/anticoagulants 4. Pleural fluid pH, protein, 3. Check platelets and clotting LDH, glucose, AFB, 4. Diagnostic tap/chest drain cytology, amylase (if pancreatitis suspected), triglycerides (chylothorax) 5. CT CAPQ8. This patient presents with sudden onset increased SOB with background of COPD. Requiring 2Litres oxygen via nasal cannula and haemodynamically stable. What’s the next appropriate management? Pneumothorax Traumatic Spontaneous Pneumothorax 1. Primary Pneumothorax (bullae rupture in 1. Iatrogenic 2. Non-iatrogenic (blunt or healthy patients) penetrating chest injury 2. Secondary Pneumothorax (rupture of damaged pulmonary tissue) Pathology u Pleural pressure negative throughout respiratory cycle u pressure difference between the alveoli and pleural cavity is the transpulmonary u In pneumothorax pulmonary alveoli or airway becomes connected to the intrapleural cavity u Usually pressure between alveoli and pleural cavity equalises u In tension pneumothorax there is a one way valve between the alveoli and the pleural cavityThank youReferences 1. Chest radiograph | Radiology Reference Article | Radiopaedia.org 2. Saddle Pulmonary Embolus - radRounds Radiology Network 3. Pulmonary Embolism (PE) Workup: Approach Considerations, Clinical Scoring Systems, D-Dimer Follow-Up on Low-to-Moderate Pretest Probability (medscape.com) 4. 59 – Pulmonary Hypertension Due to Lung Disease | Semantic Scholar 5. CV Physiology | Pulmonary Capillary Wedge Pressure 6. CE Article: BiPAP Essentials for Prehospital Providers (hmpgloballearningnetwork.com) 7. Right middle lobe pneumonia | Radiology Case | Radiopaedia.org 8. Structure and function of the alveolus | Deranged Physiology 9. Hypersensitivity Pneumonitis: A Historical, Clinical, and Radiologic Review | RadioGraphics (rsna.org) 10. J. Clin. Med., EISSN 2077-0383, Published by MDPI 11. Flow Volume Loops: A Critical Analysis – Stepwards 12. http://dx.doi.org/10.1136/thx.2010.136986