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Chronic Obstructive Pulmonary Disease(COPD) Nadine Soliman Year 3 Teaching 3rdyearteaching@gmail.comWhatwewillcovertoday! – ABGs – Pathophysiology of COPD – Signs & Symptoms – Investigation – Management (including LTOT) – Complications – Practice Questions/OSCEABGs Step by step interpretation guideOverallcontext – When interpreting an ABG, you want to be aware of the clinical context. – What signs and symptoms is the patient presenting with, does the patient seem unwell, breathless, are they vomiting, what are your differentials, etc. – All these points can give you an idea as to what you’re expecting to see on their ABG!PaO2 – Hypoxia will be the most immediate threat to your patients life, so make sure you’re assessing their PaO2 – You want to make sure you’re also checking their FiO2 if your patient is on oxygen – If they are on oxygen, a rule of thumb that can help you out is that their PaO2 should be approximately 10kPa less than the % inspired concentration FiO2 – Forexampleif your patient on 40% oxygen, you expect their PaO2 to be around 30 kPa. So if their PaO2 was for example 15kPa, although that is in the normal ranges, it is considered abnormal because their PaO2 should be a lot higher on that amount of oxygenpH – Is this patient acidotic or alkalotic – A low pH, about < 7.35 indicates ACIDOSIS – A high pH, about > 7.45 indicates ALKALOSIS – To identify the cause of either the acidosis or alkalosis, you then want to look at the PaCO2 and HCO3-PaCO2 and HCO3 - – PaCO2 – HCO3- – The main respiratory component – The main metabolic component that that affects acid-base balance affects acid base balance – Raised CO2 results in acidosis as the – Raised HCO3- results in alkalosis as CO2 dissociated, releasing H+ ions it picks up the free H+ ions – Low CO2 results in alkalosis – A low HCO3- results in acidosis as – If CO2 is normal, and there’s a pH there isn’t enough HCO3- to pick up abnormality, you know it’s metabolic the H+ ionsCompensation – When there is an acid-base imbalance, sometimes what can happen is the other system can try to compensate to try to normalize the pH. – So if there is a respiratory cause to the pH derangement, your kidneys will try to produce more/less HCO3- to oppose the effects of the CO2 – And if there’s a metabolic cause to the pH derangement, your body’s respiratory rate will change to either breathe out more or retain more CO2 to oppose the effected of the HCO3- imbalance – Key point is, respiratory compensation occurs quite quickly whereas metabolic compensation takes time to develop, therefore, when you see a metabolic compensation, there is likely a chronic CO2 retention issue.Baseexcess – Base excess essentially is a marker of the total serum base, mainly HCO3-. – If it’s >2 it suggests high HCO3- either because there is a metabolic alkalosis or metabolic compensation for a respiratory acidosis – If it’s <2 then there’s too little HCO3-, either due to a metabolic acidosis or a metabolic compensation for respiratory alkalosisType of respiratory failure – Type 1 respiratory failure – Type 2 respiratory failure – Remember type 1 is due to an issue – Type 2 is due to issue in 2 things, the in only 1 thing, the oxygen oxygen and the CO2 – So the patient is hypoxic (low PaO2) – The patient is hypoxic and they have but their CO2 is not raised raised PaCO2 – Caused by VQ mismatch, causes – Caused by alveolar hypoventilation, include: causes include: – Asthma, ARDS, pulmonary edema, – COPD, sedative drugs, respiratory PE, pneumonia failure, severe asthma, etc. Normal values: • pH: 7.35 – 7.45 • PO2 : 10-14 kPa • PCO2 : 4.5 – 6 kPa Question1 • HCO3- : 22-28 mmol/l – Which of the following best describes her ABG – A 45 year old female presents to A&E due 1. Respiratory acidosis with partial to an asthma attack. The patient is metabolic compensation currently on 8% oxygen and her chest is silent. The following is seen on her ABG 2. Mixed metabolic and respiratory acidosis 3. Repository acidosis with full metabolic – pH : 7.32 compensation – PO2 : 6.5 kPa 4. Respiratory alkalosis with no metabolic – PCO2 : 7.6 kPa compensation – HCO3- : 24 mmol/l 5. Respiratory acidosis with no metabolic compensation Normal values: • pH: 7.35 – 7.45 • PO2 : 10-14 kPa • PCO2 : 4.5 – 6 kPa Question2 • HCO3- : 22-28 mmol/l – A 68 year old male has been admitted – Which of the following describes his ABG onto the ward following an infective best? exacerbation of his COPD. He’s currently 1. Fully compensated metabolic alkalosis, on a 24% venturi mask at 4l/minute to type 2 respiratory failure keep his oxygen sats between 88-92% 2. Partially compensated respiratory alkalosis, type 1 respiratory failure – His ABG is as follows: 3. Partially compensated metabolic – pH : 7.38 acidosis, type 2 respiratory failure – PaO2 : 7.9 kPa 4. Fully compensated respiratory acidosis, – PaCO2 : 7.8 kPa type 2 respiratory failure – HCO3- : 34.1 mmol/l 5. Fully compensated respiratory acidosis, type 1 respiratory failure – Base excess : 5.1 Normal values: • pH: 7.35 – 7.45 • PO2 : 10-14 kPa • PCO2 : 4.5 – 6 kPa Question3 • HCO3- : 22-28 mmol/l – A 28 year old female presents to A&E – Which of the following best describes complaining of abdominal pain, nausea this ABG? and vomiting. 1. Respiratory acidosis with partial – Her ABG is as follows: metabolic compensation 2. Metabolic acidosis with partial – pH: 7.3 respiratory compensation – PO2 : 6 kPa 3. Metabolic alkalosis with full respiratory – PCO2 : 4.3 kPa compensation – HCO3- : 14 mmol/l 4. Respiratory alkalosis with no metabolic compensation 5. Metabolic acidosis with no respiratory compensationCase1 A 55 year old male presents to the GP surgery you work at, complaining of shortness of breath and having to stop to catch his breath when he goes for a walk at his own pace. He’s also been having a chronic cough over the last 3 months. He sometimes brings up white sputum when he coughs but does not feel unwell particularly. He has been smoking 30 cigarettes a day over the past 30 years. There are no red flags such as haemoptysis or weight loss. – What do you suspect? – COPD – What’s your diagnostic investigation? – Spirometry – How many pack years is this? – 1.5x30= 45 pack years – What would this patient be scoring on the MRC dyspnoea scale? – Grade 3WhatisCOPD? ➔Progressive airway obstruction with very little to no reversibility ➔A combination of chronic bronchitis and emphysema ◆ Chronic bronchitis ◆ Inflammation of airways with goblet cell hyperplasia and excessive mucous production -> fibrosis & airway narrowing ◆ Most days for 3 months of 2 successive years ◆ Emphysema alveoli destroyed -> enlarged air spaces/bullae -> reduced surface area for gas exchange ➔No daily variation, or diurnal variationCauses? –Smoking! (90% of cases) – A 35 year old patient who is a non-smoker presents with symptoms classical of COPD. What is the most likely diagnosis? – Alpha-1-antitrypsin Deficiency – Alpha 1 antitrypsin is a protease inhibitor produced by the liver. If it is reduced, there is no elastase inhibition which leads to breakdown of elastin in both the lungs and liver and thereby, a compromise of the alveolar structure plus cirrhosis. – Diagnosis – ↓ serum-alpha 1-antitrypsin – Liver biopsy shows cirrhosis and acid-Schiff-positive staining globules – Genetic testing for the A1AT gene – High resolution CT thorax diagnoses bronchiectasis and emphysemaDiagnosis? – How do you diagnose COPD? – Spirometry – FEV1- maximum expiration (forced expiratory volume) in 1 second - reduced – FVC- maximum expiration following full inspiration (forced vital capacity) – normal or slightly reduced • COPD • Asthma Symptoms/ HistoryT aking • Lung cancer • Bronchiectasis • TB ➔ As with any history: • HF • GORD ➔ ICE ➔ Presenting complaint -> ongoing cough, shortness of breath ➔ SOCRATES any symptoms ◆ Red flags! Haemoptysis, weight loss, night sweats, lymphadenopathy – could they have cancer too? ➔ PMH -> childhood asthma? HTN?, Ischaemic heart disease? ➔ MH -> any allergies? Any reactions to NSAIDs? ➔ FH -> any history of atopy? ➔ Social history: need to get their smoking pack years! Need to ask about their job and exposure to asbestos! ➔ Other good things to ask: pets (birds in particular), and travel? (TB) ➔ Think about differentials too: are you sure your breathless patient doesn't have heart failure? ➔ What would you ask about to rule out heart failure? ➔ Paroxysmal nocturnal dyspnoea (waking up at night breathless) ➔ Sleeping propped up on a few pillows, ➔ Orthopnoea ➔ CVD: HTN or a previous MI? ➔ Ankle swelling?SpecificSymptoms • Any sputum ? What colour? Typically the COPD patient will: - have a significant pack year • Any diurnal variation? history • Breathless -> what makes them breathless? -> MRC dyspnoea - have shortness of breath - bring up clear sputum score - cough • Wheeze? - have no diurnal variation - recurrent RTIs • Frequent chest infections? Examination • General inspection- •Chest • look at the bedside (any cigarettes? Any inhalers? Any oxygen?); ØPosition Ølying at 45 degrees • muscle use? Pursed lip breathing? Tripod position?)ccessory ØInspection ØScars • Hands- ØBarrel chest • tar staining? ØPalpation- • Fine tremor? ØDecreased chest expansion • Flapping tremor? • Tachycardia or tachypnoea? ØParasternal heave (or pulmonale) ØDisplaced apex beat • Face– ØTactile vocal fremitus (or vocal resonance) • flushing? ØPercussion • central cyanosis? ØHyperresonance? • Poor dentition/tar staining? ØAuscultation • Neck – Øreduced breath sounds • tracheal deviation? Øpossibly coarse crackles (start of inspiration) • tracheal tug? (should be 5cm or more ( ~3 finger breaths) ØRhonci (snore-like sounds over inspiration and • Reduced cricosternal distance? expiration due to secretions or obstructions) • Raised JVP (Pulmonary HTN/ or pulmonale)? Øwheeze (what type?) ØPolyphonic Have you practised a resp exam? One thing I'd advise is after you do palpation, go directly to the back and say, "as signs are best ØCheck for peripheral oedema elicited on the back, I'm going to continue the rest of the exam on ØDo your lymph node examination!!! the back only, in the interests of time." Tar staining Examination Pitting oedema Use of accessory muscles Measuring cricosternal distanceCorpulmonale • Right sided heart failure secondary to What are some ECG changes you might see? pulmonary disease • Alveolar damage and obstruction of the airways -> raised CO2 in the alveoli -> reduced blood • P pulmonale (sign of right atrial enlargement) flow to those alveoli -> vasoconstriction of the • Right ventricular hypertrophy pulmonary arteries -> pulmonary hypertension if • Dominant R wave in V1 (R/S ratio >1) widespread • Dominant S wave in V5/V6 (R/S ratio < 1) • Signs: • RAD of 110 degrees or more • Raised JVP • RBBB may be present (MARROW) • Parasternal heave • Peripheral oedema • HepatomegalyExamination – COMPLETE THE EXAMINATION: – ‘To complete my examination, I would like to do a set of obs, a lymph node RSHF)’ation (if you run out of time) and a cardiovascular examination (if signs of – PRESENT YOUR FINDINGS – ‘I examined Mr Brook who is a 64 year old gentleman. On general inspection, he appeared slightly out of breath and seemed to have a lower than normal body habitus. His hands showed marked tar staining and he was tachypnoeic. He also had some tar staining around the lips. There was a reduced cricosternal distance and raised JVP on neck examination. Examination of the chest showed reduced chest expansion, hyperresonance on percussion and some bilateral course crackles in the upper lobes. He had some peripheral leg oedema up to his ankles. Overall, my findings are consistent with a diagnosis of COPD.’ PEEP - Positive End Expiratory Pressure Inside the lungs of COPD patients, breathing through pursed lips keeps a bit of positive pressure inside the lungs at the end of expiration, which stops the alveoli from PinkPuffers,BlueBloaters collapsing, and makes them easier to inflate. ➔ Pink puffers: breathless but not cyanosed. They use pursed lip breathing. Their ABG is normal or near-enough. They may progress to type 1 respiratory failure. ➔ Blue bloaters: they now rely on their hypoxic drive, so they are cyanosed. They have chronic CO2 retention and are therefore in type 2 respiratory failure. They may also develop cor pulmonale.HypoxicDrive ➔ In someone with healthy lungs, the stimulation to breathe comes from detection of high enough levels of CO2. Oxygen has nothing to do with it. ➔ However, when someone has been living on such high levels of CO2 for so long without it being corrected, the body stops using the hypercapnic drive, and starts to use the hypoxic drive – which everyone has. This kicks in when oxygen levels are very very low, which is why people with hypoxic drives have O2 sats of around 92%. So, when managing a COPD patient, if we know they are a CO2 retainer, and therefore rely on their hypoxic drive, we don't want to keep them on 100% oxygen on fear of removing their drive to breathe so we keep them at 88-92% SatsFingerClubbing(NOTFOUNDINCOPD) - Respiratory - Fibrotic lung disease e.g. idiopathic pulmonary fibrosis - Cystic fibrosis, lung disease (bronchiectasis, chronic abscesses) - Lung cancer (all except small cell which tends to progress too fast to induce clubbing) - Cardiac - Infective endocarditis, - Atrial myxoma - Congenital cyanotic heart disease - Gastro - IBD, Coeliac disease, Cirrhosis - Other - Thyroid acropachy, Idiopathic/familiallStable COPD -investigations – Bedside- – Imaging- • Obs • CXR • BMI • CT scan if spirometry results don’t match the symptoms or other • Sputum culture (if purulent) diagnosis suspected • ECG (if signs of cor pulmonale) • ABG (respiratory failure (hypoxaemia with or without hypercapnia) - Bloods- • FBC (polycythaemia?) What would you see on a CXR? • haematocrit. The low levels of oxygen lead to increased EPO secretion from the kidneys. This can • Hyperexpansion predispose a person to a DVT among other • More than 10 posterior ribs present symptoms. • Serum A1AT • Flattened hemidiaphragms • Reduced peripheral lung markings • TLCO • Saber sheath trachea • Transfer factor for carbon monoxide(TLCO) is about the severity of the disease and may be increased in other conditions such as asthma.OxygenDeliverysystems Every bed has 100% oxygen hooked up behind it. We can attach different devices to it to adjust how much the patient is getting. It can mix with air to reduce the concentration. Common devices: - Nasal cannula: use in non-acute situations. Just because a patient has one doesn’t mean they’re breathing through their nose! [range = 24-30%] (we say patients get around 4-5L) - Venturi maskhas many different coloured nozzles which we can use to decide how much oxygen to use. We often use these for COPD patients where we want to avoid over oxygenation (target sats are 88-92% rather than 94-98%) [range = 24-60% O2] - Non-rebreathe mask:special valves ensure that air breathed out on expiration is not breathed back in. This device delivers almost 100% oxygen at a flow rate of 15L/min. For any patient, over oxygenation is bad and they should not be kept on this for prolonged period. We can also put patients on CPAP (sleep apnoea, acute pulmonary oedema) or BiPAP (COPD exacerbation), or fully ventilate them to give oxygen. NonInvasiveVentilation:BiPAPvsCPAP Non-Invasive Positive Pressure Ventilation is used when patients are still hypoxaemic despite best medical management. ➔ CPAP stands for continuous positive ➔ BiPAP stands for bilevel positive airway airway pressure. This can be used pressure. In the inhalation phase, when the airway needs to be “splinted” open. For example, in the pressure is higher than in the exhalation chronic setting people with sleep phase. This helps to recruit alveoli that apnoea have symptoms because their are normally under ventilated or airway collapses (Scored using the collapsed. Mallampati score). ➔ BiPAP used in type II failure typically ➔ CPAP used for Obstructive Sleep COPD exacerbation, having respiratory Apnoea, Congestive Cardiac Failure, acidosis Acute Pulmonary OedemaStable COPD -management OSCE station example: This patient has COPD. Explain the diagnosis and management of their condition Smoking cessation - What is the most important step in management? - Smoking cessation -> local support groups, medications- do youotine know what they are? • Varenicline • One off pneumococcal • Bupropion - Vaccines -> which ones are offered? • Annual flu jab - Pulmonary rehabilitation – exercise, breathing techniques - Inhaler therapy -> what is first lineSABA or SAMA - Self management ie rescue packs (antibiotics and steroids) - Optimisation of any co-existing conditions eg heart failureStable COPD -management – Inhaler therapy 1. SABA/SAMA – Other management options: • Mucolytics not routinely given (according to NICE) to prevent 2. Does not 2. Responds to exacerbations. May help if chronic respond to steroids: cough with thick phlegm or sputum steroids: LABA + ICS LABA + LAMA • Prophylatic antibiotics if frequent exacerbations • Long-term Oxygen Therapy (LTOT) 3. LABA + LAMA + ICS Surgical management: • Lung volume reduction surgery/Bullectomy • Lung transplant ( g in alpha 1 antitrypsin deficiency patients)SurgicalManagement:MoreInfo The empty spaces are giant bullae. Bullae are focal areas of emphysema. Smaller ones are called blebs. They can encroach on lung tissue and worsen symptoms. They may also burst and cause pneumothoraces. Connective tissue disease can cause them too.LTOT-LongT erm OxygenTherapy ➔ Research has shown that when COPD Patients are kept on PaO2 above 8 for 15 hours a day, 3 year survival increases by 50%. 1. MUST BE Non-smoker on maximal treatment with consistent pO2 below 7.3 2. Consistent pO2 in between 7.3 and 8.0 with one of: ◆ Secondary polycythaemia ◆ Peripheral oedema ◆ Nocturnal hypoxia ➔ Can also consider if patient is being palliated (end of life).ComplicationsofCOPD • Exacerbation- infective or non-infective • Respiratory failure (Type 1 or Type 2) ->ow do they differ from each other? • Pneumothorax due to rupture of bullae Type 2-> hypoxia plus hypercapnia • Polycythaemia • DepressionAcute Exacerbation of COPDWhatisit? ➔ One of the most common reasons for hospital admissions. ➔ Can be infective or non-infective. ➔ It’s technically a sustained but temporary worsening of someone's baseline. ➔ Non-infective causes can be poor adherence, pollutants, allergens, toxins, ➔ If infective: ◆ Most common ◆ Haemophilusinfluenzae ◆ Pneumococcus (streptococcus pneumoniae) ◆ Moraxella catarrhalis ◆ Rhinovirus ◆ Pseudomonas aeruginosaAcute Exacerbations:SignsandSymptoms Ø SOB Ø Cough ± wheeze Ø Increased sputum/purulent (Usually a change in colour from colourless sputum to more yellow/green) Ø Hypoxia and related confusion Ø Possible Differentials? Ø Asthma Ø Pulmonary oedema (heart failure related) Ø LRTI or pneumonia Ø Pneumothorax (not a very close differential but can happen concurrently!) Acute Exacerbation of COPD: Investigations and why? Bedside: Bloods: Imaging: ➔ CXR ➔ Obs ➔ FBC ➔ ECG ➔ U&E ➔ ABG ➔ CRP ➔ Sputum cultures if purulent ➔ Blood cultures if fever – Sample ABG: pH 7.27 PaO2 7.6 kPa Respiratory acidosis with partial Normal ranges: PaCO2 6.8 kPa metabolic compensation pH 7.35-7.45 Bicarb 35.8 mmol/l PaO2 11-13 kPa BE -5 mmol/l Type 2 respiratory failure PaCO2 4.7-6.0 kPa HCO3 24-30 mmol/l What does this ABG show? BE -2 to +2 mmol/lAcute Exacerbation of COPD: Treatment retention either due to previous records or signs of CO2 Retention (Which are?) you would start on lower doses of O2 Very similar to asthma: using a venturi mask to aim for sats of - Salbutamol and ipratropium via nebulizer 88-92% Keep in mind whenever you start/change oxygen, do an ABG in an - Oxygen hour to check for changes. - Steroids – extremely important aspect of management, we give IV hydrocortisone and oral prednisolone (5 day course 30 mg continued afterwards) - Antibiotics (IV) (commonly amoxicillin, doxycycline, or clarithromycin – in OSCEs always say you’d consult your local trust’s guidelines). - Only use antibiotics if there is evidence of an infection! - If nebulizers and steroids don’t help, add IV aminophylline/theophylline (PDEi)Whatifthepatientdeterioratesfurther? ➔ Consider ICU ADMISSION + NIPPV if: ◆ RR > 30 or, ◆ pH < 7.35 or, ◆ PaCO2 continuing to rise ➔ If NIPPV is not effective and pH drops below 7.26 and PaCO2 is still rising, then consider intubation and ventilation but this is managed by ICURescue Packs! ➔ Exacerbations, or flare-ups, can be managed at home sometimes so COPD patients are often given rescue packs. ➔ This can stop patients from coming in to hospital, provided the exacerbation isn‘t too severe. ➔ May need to counsel a COPD patient, so you can mention this but don’t forget to safety net them on what is considered severe and needs immediate hospital admission!ProgressstylequestionsQuestion1 – A 70 year old female who has been smoking 20 cigarettes/day for the last 40 years comes to see the GP with worsening shortness of breath on exertion over the last year. She also notes that she gets wheezy and struggles to catch her breath when she gets a URTI in winter. She has no weight loss or othe red flags. She is not breathless at rest. COPD is suspected and diagnosed on spirometry. Which of the following is most likely to improve the patient’s prognosis? – A. Pulmonary rehab – B. SABA inhaler – C. Smoking cessation – D. SAMA inhaler – E. Oxygen therapyQuestion2 – A 64-year-old man attends his general practitioner for a review of his chronic obstructive pulmonary disease (COPD). – His current treatment is limited to a salbutamol inhaler when required, and he reports using this at least 5-times daily and twice overnight, as he wakes up feeling breathless. He reports that, since his diagnosis, he has stopped smoking. – Further questioning reveals that the his other past medical history includes asthma, hypertension and hayfever. – Based on the above information, what is the most appropriate additional therapy to initial in this patient? A. LABA + LAMA + ICS B. LABA + ICS C. LABA + LAMA D. LAMA + ICS E. SAMAQuestion3 The hyper-expansion and asterixis suggests – A 70 year oldmale patient presents to the emergency department with shortness of this patient is a CO2 breath and cough productive of sputum. – He has a 50 pack year history. On physical examination he is hyper-expanded and retainer, so his targets will be 88-92% there is asterixis. The respiratory rate is 24/minute, and the oxygen saturations are The reason it’s a Venturi 85% on room air. mask and not a nasal cannula is that the – Which of the following is the most appropriate oxygen therapy for this patient? Venturimask allows you A. 2L/min via nasal cannula, target oxygen saturations 88-92% to deliver controlled B. 4L/min via Venturi mask, target oxygen sats 94-98% C. Non-invasive ventilation oxygen while the nasal cannula does not. D. 15L/min via a non-rebreathe mask E. 4L/min via Venturi mask, target oxygen saturations 88-92%Question4 – A 60 year old male has recently been diagnosed with Chronic Obstructive Pulmonary Disease (COPD) after being admitted to hospital with breathlessness. He was not suffering from any complications of this condition and after being stabilised on first line medical management, was discharged home. – Which of these chest x-ray (CXR) findings was most likely seen in this patient? A. Consolidation B. Pleural calcification C. Tracheal deviation D. A peri-hilar mass E. Flattened hemi-diaphragmsQuestion5 Normal values: • pH: 7.35 – 7.45 • PO2 : 10-14 kPa • PCO2 : 4.5 – 6 kPa – A 58-year-old-man with a known diagnosis of chronic obstructive pulmonary • HCO3- : 22-28 mmol/l disease (COPD) presents to the emergency department with worsening breathlessness and purulent sputum production. His respiratory rate is 26 and his oxygen saturations 85%. The pH is < 7.35 so we know it’s an – The admitting doctor suspects an infective exacerbation of his COPD and takes an acidosis arterial blood gas (ABG) which shows a pH 7.32, pO2 7 kPa, pCO2 7.5 kPa, Because the CO2 is raised, we know it’s a respiratory acidosis bicarbonate 45 mmol/l. We know that metabolic – What is the correct interpretation of the ABG results? compensation takes time to develop. Because this patient has A. Acute on chronic respiratory alkalosis high HCO3- to compensate B. Metabolic acidosis with partial respiratory compensation thereforeit suggests a CO2 C. Acute respiratory acidosis chronic retention picture. And it’s acute on chronic because D. Acute respiratory alkalosis we can see he’s having an acute E. Acute on chronic respiratory acidosis exacerbation from the history.Question6 – A 40 year old mal presents to the GP as he has noticed that his sclera appeared yellow this morning. He has a long term history of shortness of breath and cough and the inhaler (salbutamol and salmeterol) that were previously prescribed to him do not seem to be working. He has no smoking history. – Which of the following would be the diagnostic investigation for this patient? – A. Spirometry – B. Liver ultrasound – C. Serum alpha 1 antitrypsin – D. Chest X ray – E. Viral hepatitis screenQuestion7 Normal Values pH 7.35- 7.45 CO2 4.6 - 6.0 O2 11 - 13 Base excess -2 - +2 HCO3 22 - 26Question8 A 67 year old male comes to clinic for a follow up of his COPD. He has years ago. His medications are optimal and cannot be increasedaround 2 anymore. Which of the following would make him a good candidate for LTOT? A. PaO2 8.2 plus peripheral oedema B. PaO2 8.0 on its own C. PaO2 7.6 plus polycythaemia D. PaO2 7.5 on its own E. PaO2 7.8 plus cough with purulent sputumThanksforlistening Any questions?