Top Tips on Respiratory On-Calls

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1 Top Tips on Respiratory n-calls Dr Manish Pagaria Consultant Respiratory and Critical Care Medicine Royal College Tutor for Medicine Dudley Group of Hospitals NHS FT 22 nd July 2017, Fast Bleep the Doctor, RCP, London

2 bjectives Burden of disease How to recognise the problem? How to manage the problem?

3 Percentage of hospital admissions

4 Percentage of death

5 Immediate Assessment

6 How to recognise the problem? History Symptoms Importance of the HPC Examination Investigation

7 Symptoms Dyspnoea Chest pain Haemoptysis

8 Symptoms Dyspnoea Chest pain Haemoptysis

9 Dyspnoea: Pattern of nset Sudden Pneumothorax PTE Aspiration Cardiac event arrhythmia, MI ver hours / days Asthma Pneumonia Pulmonary oedema Intermittent Asthma Hyperventilation Progressive CPD IPF Pleural effusion Anaemia LVF Pulmonary hypertension

10 Symptoms Dyspnoea Chest pain Haemoptysis

11 Chest pain Myocardial ischaemia Pericardial pain Respiratory esophageal Musculoskeletal

12 Chest pain - 1 Myocardial ischaemia central radiating to the jaw / arm(s) squeezing / crushing / heavy weight aggravated by exertion relieved by rest / GTN associated autonomic features

13 Chest pain - 2 Myocardial ischaemia Pericardial pain Retrosternal Pleuritic relieved by sitting forward worse on swallowing, twisting and with sternal pressure

14 Chest pain - 3 Myocardial ischaemia Pericardial pain Respiratory typically not central pleuritic

15 Chest pain - 4 Myocardial ischaemia Pericardial pain Respiratory esophageal Retrosternal heart burn can be indistinguishable from cardiac pain

16 Chest pain - 4 Myocardial ischaemia Pericardial pain Respiratory esophageal Musculoskeletal Localised associated with tenderness

17 Symptoms Dyspnoea Chest pain Haemoptysis

18 Haemoptysis

19 ther Points from History Don t overlook the rest of the history PMH -e.g. previous DVT Drug history -e.g. new medications Smoking ccupation e.g. baker, farmer, asbestos exposure Pets especially birds Family History

20 Examination Do not make the diagnosis from the history alone It is negligent not to examine a patient with new symptoms Follow the gold guide of inspection, palpation, percussion and auscultation

21 Examination Wheeze Stridor Asthma / CPD Heart failure Anaphylaxis Foreign body Foreign body Epiglottitis Anaphylaxis Crackles Pulmonary oedema Fibrosis Pneumonia Bronchiectasis Clear chest PTE Pneumothorax Hyperventilation Metabolic acidosis Anaemia Drug overdose

22 Investigation Bloods ABG CXR ECG FBC, U&E, CRP Trop, Ddimer

23 D-dimer Assay (Pulmonary Embolism) Quantitative ELISA based assays have sensitivity of ~ 95% But specificity is poor The only useful D-dimer result is a negative one Chance of having had a PE with negative D-dimer is low clinical probability 0.7 2% moderate clinical probability5% high clinical probability >15% PIPED II AJM 2006

24 D-dimer Assay It should not be done:- As a screening test on all general medical patients In high probability cases

25 Arterial Blood Gases NRMAL VALUES ph: p 2 : 10 14kPa pc 2 : 4.5 6kPa Base excess (BE): (-2) (+2) mmol/l HC 3 : mmol/l

26 How to interpret an ABG Look at the patient!!! Review history and examination findings. What is the p 2 mention Fi 2 What is the ph? - determine acid/base state What is the pc 2? determine resp/metabolic What is the HC 3 and base excess? Is the patient compensating? What are the other values? Ensure that you look at all other figures on the gas.

27 How to present an ABG State that this is an arterial blood gas sample (rather than venous). State the patients name and outline history/pertinent examination findings. State the time the sample was taken and how much oxygen the patient was on at the time. Present your findings: e.g. this showed type one respiratory failure with a p0 2 of 7 Present any abnormal findings or important negatives from the rest of the values. A one line summary of your findings. ABG done on 2l 2 for Mr JS with CPD who came in with SB, it shows partially compensated T2RF with ph 7.21, pc , p 2 8.5, HC 3 45.

28 Question 1 An increase in ventilation leads to: (a) a rise in pc 2 and p 2 (b) a fall in pc 2 and p 2 (c) a rise in pc 2 and a fall in p 2 (d) a fall in pc 2 and a rise in p 2 (e) a rise in pc 2 and no change in p 2

29 Answer 1 D (a fall in pc 2 and a rise in p 2 ) Increase in ventilation blows off more C 2 (leading to a fall in pc 2 ) and replenishes the alveolar oxygen, leading to an increase in alveolar 2 and therefore arterial p 2, although the 2 saturation of the blood may alter very little.

30 Question 2 VQ mismatching leads to: (a) a rise in pc 2 and p 2 (b) a fall in pc 2 and p 2 (c) a rise in pc 2 and a fall in p 2 (d) a fall in pc 2 and a rise in p 2 (e) no change in pc 2 and a fall in p 2

31 Answer 2 E (no change in pc 2 and a fall in p 2 ) In VQ mismatch with respect to C 2 content, the high content of blood from underventilated areas is balanced by the low content from overventilated areas. However in the case of 2, the low content of blood from underventilated areas cannot be compensated for by an equivalent increase in the 2 content of blood from the overventilated areas.

32 Question 3 A 24, day 3 post cholecystectomy complaining of SB. What is the most likely diagnosis ABG on Room Air: ph: 7.49 (a) Pulmonary embolism pc 2 : 3.9 kpa (b) Anxiety p 2 : 7.5 kpa (c) piate overdose shc 3 : 22 mmol/l (d) Excessive vomiting BE: -1 (e) pneumonia 2 sats: 97%

33 Answer 3 A (Pulmonary embolism) This is type 1 respiratory failure. The P2 is low with a low C2. The accompanying alkalosis is a response due to the patient blowing off C2 due to her likely high respiratory rate. The (A-a) gradient is increased(7.6), implying a problem within the lungs (affecting V/Q matching) which anxiety cannot explain. (A-a) gradient = P A 2 P a 2 = P I 2 (P a C 2 /0.8) P a 2 Normal (A-a) gradient is < 2

34 Question 4 A 75 with CPD, admitted with SB. What does the ABG show ABG on 2l 2 : ph: 7.25 pc 2 : kpa p 2 : 7.8 kpa shc 3 : 40.3 mmol/l BE: +9 (a) Metabolic acidosis (b) Respiratory Acidosis (c) Compensated Respiratory Acidosis (d) Partially compensated Respiratory Acidosis

35 Answer 4 D (Partially compensated Respiratory Acidosis) This is Acute on Chronic Type 2 respiratory failure. Note that the HC 3 is raised in this patient despite the abnormal ph. This would indicate that the patient normally retains C 2 and has a chronically raised HC 3. The drop in ph represents the normal mechanisms of compensation being over whelmed. This is one of the cases where having an old ABG from a previous admission can be useful. xygen administration in this group is a complicated issue. 100% oxygen makes subsets of CPD patients retain C 2, decreasing respiratory drive and worsening hypoxia and hypercapnia.

36 NIV in Acute Hypercapnic Respiratory failure May complicate a number of conditions that affect lungs and/or impair the function of respiratory pump Airway disease : CPD, asthma, Cystic fibrosis and non-cf bronchiectasis Respiratory pump : neuromuscular disease, chest wall deformity and morbid obesity AHRF may be acute or acute on chronic Commonest cause of AHRF : 20% AECPD In CPD signals advanced disease, high risk of future hospitalisations and limited long term prognosis In CPD mortality 8% without AHRF and up to 30% with AHRF depending on the degree of acidosis

37 Recommendations Target oxygen saturation range of 88-92% Consider starting NIV when ph < 7.35, PC2 > 6.5 kpa and respiratory rate > 23 NIV should not be used in acute hypercapnic asthma Do not delay starting NIV or continue with it when the patient is deteriorating as both increase mortality. The use of NIV should not delay escalation to IMV when this is more appropriate

38 NIV and ecpd Initial management should be optimal medical therapy and targeting an oxygen saturation of 88 92% (Grade A). NIV should be started when ph<7.35 and pc2 >6.5 kpa persist or develop despite optimal medical therapy (Grade A). Arterial blood gas (ABG) measurement is needed prior to and following starting NIV. Chest radiography is recommended but should not delay initiation of NIV in severe acidosis. Reversible causes for respiratory failure should be sought and treated appropriately. At the start of treatment, an individualised patient plan (involving the patient wherever possible) should document agreed measures to be taken in the event of NIV failure.

39 Chest drain FAQ Patients should be assessed regularly for pain, breathlessness, drop in 2 saturations (Sp2) and subcutaneous emphysema. The chest drain must always be kept upright and below the level of the chest Daily observational recording of the chest drain site, volume and amount of any drainage. Swinging Continuous bubbling Flushing Suction Removal of drain

40 Chest drain - clamping There is no evidence to suggest that clamping the drain prior to its removal prevents pneumothorax re-occurrence (Laws et al, 2003). The only indications for clamping are: Following rapid initial drainage of >1000ml in the first hour When changing the drainage bottle If the tube becomes accidental disconnected While transferring a patient where the tubing does not reach Following intra-pleural fibrinolytic or talc instillation Before removal only if instructed to do so by a senior member of the medical team For large effusion, drain a maximum of 1000mls at a time and clamping for minutes before further drainage prevents the potential complication of re-expansion pulmonary oedema

41

42 CXR White CXR Pneumonia Pulmonary oedema Pleural effusion Pulmonary fibrosis Pulmonary hge Black CXR CPD Asthma Pneumothorax Pulmonary embolism normal

43 RLL Consolidation

44 Pleural Effusion

45 Pulmonary edema

46 LUL Collapse

47 LUL collapse

48 LLL Collapse

49 Situs Inversus

50 Pulmonary Haemorrhage

51 LLL abscess

52 Bullous emphysema

53 Bullous emphysema

54

55 Pneumothorax

56 Hiatus Hernia

57 Pneumomediastinum

58 CPD

59 TB Thoracoplasty

60 Summary Most common respiratory problems faced during oncall Assessment of the sick patient Recognizing the problem Some aspects of management

61 Any Questions?

62 Complex is easy, Simple is much harder to achieve but much more important

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