Acute Respiratory Emergencies. Martin Johnson Consultant Physician Gartnavel / Western

Transcription

1 Acute Respiratory Emergencies Martin Johnson Consultant Physician Gartnavel / Western

2 Summary What to expect - what are the common respiratory emergencies? How to recognise the problem? How to manage the problem?

3 Relative Frequency of Medical Emergencies The burden of lung disease. 2 nd Edition BTS 2006

4 Relative Frequency of Respiratory Emergencies The burden of lung disease. 2 nd Edition BTS 2006

5 Immediate Assessment

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

7 Symptoms Dyspnoea Chest pain Haemoptysis

8 Symptoms Dyspnoea Chest pain Haemoptysis

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

10 Symptoms Dyspnoea Chest pain Haemoptysis

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

12 Chest Pain Myocardial ischaemia Pericardial pain retrosternal pleuritic relieved by sitting forward worse on swallowing, twisting and with sternal pressure

13 Chest Pain Myocardial ischaemia Pericardial pain Respiratory typically not central pleuritic

14 Chest Pain Myocardial ischaemia Pericardial pain Respiratory Oesophageal retrosternal heart burn can be indistinguishable from cardiac pain

15 Chest Pain Myocardial ischaemia Pericardial pain Respiratory Oesophageal Musculoskeletal localised associated with tenderness

16 Symptoms Dyspnoea Chest pain Haemoptysis

17 Haemoptysis Percentage of cases Neoplasms Bronchiectasis Miscellaneous Bronchitis Bacterial pneumonia Tuberculosis Cryptogenic Misc PTE, LVF, aspergilloma, lung abscess, atypical mycobacteria

18 Other Points from the History Don t overlook the rest of the history PMH - e.g. previous DVT Drug history - e.g. new medications Smoking Occupation e.g. baker, asbestos exposure Pets especially birds FH

19 Examination Do not make the diagnosis from the history alone It is negligent not to examine a patient with new symptoms E.g. arrhythmia (esp AF / flutter) pneumothorax pericardial effusion

20 Observations HR BP Temp S p O 2 F I O 2 RR

21 Examination of the Chest Expansion Percussion Auscultation Air entry Quality of breath sounds Added sounds Vocal resonance

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

23 Investigations Blood FBC, U&Es, (D-dimer, Tn, CRP) ABGs ECG CXR

24 ABGs Normal values P a O kpa P a CO kpa H HCO mmol/l Do Write the results in the notes Document oxygen prescription

25 Interpretation of Arterial Blood Gases H+ PaCO2 PaCO2 respiratory acidosis metabolic acidosis respiratory alkalosis metabolic alkalosis

26 ABGs P a O P a CO H + 37 HCO3-25 Type 1 respiratory failure What are the physiological mechanisms for hypoxia?

27 ABGs P a O P a CO H + 55 HCO3-26 Decompensated Type 2 respiratory failure What is the physiological mechanisms for hypercapnia?

28 ABGs P a O P a CO H + 41 HCO3-34 Compensated Type 2 respiratory failure

29 ABGs P a O P a CO H + 22 HCO3-15 Hyperventilation

30 ABGs P a O P a CO H + 60 HCO3-10 Metabolic acidosis

31 ECGs When can they be helpful? Arrhythmia Cardiac ischaemia LVF Pericardial effusion P.E. RVF / pulmonary hypertension

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33 CXR

34 Case 1 62 Ex-smoker Progressive SOB over 18 months Now 4/7 SOB with productive cough O/E S p O 2 85% on air RR 30/min AE, minor wheeze, hyperinflated

35 Ix: Bloods - WCC ECG normal ABGs - P a O 2 5.5, P a CO 2 7.8, H + 50, HCO 3-26 CXR -

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37 Diagnosis Exacerbation of COPD Decompensated type 2 respiratory failure

38 Outcome from Exacerbation of COPD Exacerbation of COPD 100% Uncomplicated exacerbation 79% Immediate intubation 1% Resolve with nebuliser, controlled oxygen, etc 4% Acidotic 20% NIV 16% Men: 75/100,000/yr Women: 57/100,000/yr Plant 2000

39 Treatment O N A P

40 Treatment O Oxygen N Nebulised bronchodilators A Antibiotics P Prednisolone

41 Treatment Nebulised Bronchodilators Salbutamol 2.5 5mg as often as needed Ipratropium bromide 500mcg 6 hourly If patient is hypercapnic, the nebuliser should be driven by compressed air, not oxygen (to avoid worsening hypercapnia). If oxygen therapy is needed during the nebuliser, it should be administered simultaneously by nasal cannulae. Evidence Level D

42 Treatment Antibiotics should be used in exacerbations with purulent sputum How many? One combination of amoxycillin / macrolide only used in pneumonia First-line and second-line choices dictated by likely organism - S. pneumoniae, H. influenza, M. catarrhalis aminopenicillin or macrolide or tetracycline (NICE) (Coamoxiclav is a pretty safe first choice, Levofloxacin a useful second choice)

43 Prednisolone consider in patients admitted to hospital Treatment Cochrane Review 2005

44 Treatment Prednisolone How much & for how long? 30mg for 7-14 days (NICE) mg for 1/52 (local practice) Should you taper? Not if course less than 2-3 weeks Patients MUST be given clear instructions about why, when and how to stop their steroids

45 Treatment Other Options IV aminophylline no evidence but often used in most severe cases Doxapram remarkably effective in short term (hours) but mostly superseded by NIV ITU in this country rationed by limited provision of beds

46 Principles of Treatment of Respiratory Failure 1. Hypoxia will kill you first 2. Acidosis will kill you later

47 Principles of Treatment of Respiratory Failure 1. Correct Hypoxia to acceptable levels O 2 if Type 1 RF - aim for P a O 2 > 10 if Type 2 RF give controlled O 2 - aim for P a O If respiratory acidosis develops, support the respiratory muscles NIV (BiPAP) - on medical ward intubation and IPPV - ICU (respiratory stimulants e.g. doxapram)

48 Oxygen Toxicity in COPD

49 Oxygen Toxicity in COPD

50 Oxygen Nasal cannula Standard mask Mask with reservoir bag 2-4L/min 25-40% 5-15L/min <50% 15L/min <70% Inspired oxygen concentration depends on patient s minute ventilation patient also breathes in an unknown amount of air

51 Controlled Oxygen Therapy Venturi (Valve) Masks Deliver a high flow of a mixture of oxygen and entrained air of known composition provided flow rate of oxygen is set correctly (specified on mask)

52 Controlled Oxygen Therapy Venturi (Valve) Masks Works by Bernoulli s principle if oxygen speeds up its pressure drops and a large quantity of air is sucked in

53 Controlled Oxygen Therapy Venturi (Valve) Masks Works by Bernoulli s principle if oxygen speeds up its pressure drops and a large quantity of air is sucked in The patient is surrounded by a bubble of air/oxygen of known concentration 40% O 2

54 Non-invasive Ventilation = ventilation without an ET tube avoids ventilator associated pneumonia need for an ITU bed allows intermittent support normal eating, drinking, communication

55 How is it given? NIV/BiPAP

56 NIV/BiPAP non-invasive ventilation/bilevel positive airway pressure What is it? Pressure 12cmH 2 O Inspiration Expiration 4cmH 2 O Time

57 NIV/BiPAP How is it given? By a tight-fitting mask attached to an NIV machine. Typically an air compressor BiPAP with O 2 supply direct to mask (%O 2 would then be limited to ~45-50%) but can be an ICU type ventilator (up to 100% O 2 )

58 Case 2 65 PMH: IPF Sudden onset of left-sided pleuritic chest pain O/E Dyspnoeic at rest RR 30/min Bibasal crackles R>L

59 Case 2 Ix: Bloods Normal including D-dimer ABGs P a O 2 7, P a CO 2 4.5, ECG normal CXR -

60 Case 1

61 Pneumothorax Defn: Air in the pleural space Primary no associated lung disease (subpleural bleb) Secondary associated lung disease (typically fibrosis or emphysema) No of hospital admissions: Men 16.7 / / yr (approx 250 in Greater Glasgow) Women 5.8 / /yr Smoking is the greatest risk factor 12% lifetime risk in smokers (cf 0.1% in nonsmokers) Half recur within 4 years BTS Guidelines 2003

62 Volume of Pneumothorax

63 Volume of Pneumothorax Small visible rim of < 2cm Large visible rim of 2cm

64 Treatment 1

65 Treatment 2

66 Aspiration + + X

67 Chest Drain

68 Chest Drain X

69 Chest Drain

70 Complications of Chest Drain Penetration of lung, stomach, spleen, liver, heart, great vessels Pleural infection (1%) Surgical emphysema (malpositioned tube or kinked/blocked tube)

71 Myths Debunked Are expiratory films useful? Does high flow oxygen work? Should we clamp drains before removal? Are large drains better than small drains? What is first-line management of a tension pneumothorax? No Yes No (?) No

72 Tension Pneumothorax Intrapleural pressure exceeds atmospheric due to one-way valve effect results in venous return, cardiac output, BP Patient rapidly distressed sweating, cyanosis, HR, RR, EMD/PEA arrest

73 Tension Pneumothorax Not dependent on the size of the pneumothorax

74 Tension Pneumothorax Treatment Cannula of at least 4.5cm length in 2 nd ICS MCL X

75 Tension Pneumothorax Treatment Cannula of at least 4.5cm length in 2 nd ICS MCL then Chest drain

76 Case 3 35 PMH: UC Sudden onset of SOB 3/7 ago Productive cough and left sided pleurisy for 2/7 O/E pyrexial Left basal crackles and dullness

77 Ix: Bloods - WCC; D-dimer ECG normal ABGs - P a O 2 9.0, P a CO 2 5.3, CXR

78

79 Diff Δ:- PTE Pneumonia

80 Pulmonary Embolism Annual incidence / / yr 1000 in Greater Glasgow Typically PTE is present in 15 40% of cases where the diagnosis is considered Modern diagnostic pathway uses:- clinical probability D-dimer assay CTPA

81 Pulmonary Embolism Diagnostic Pathway PIOPED II AJM 2006

82 Clinical Probability Risk of PTE BTS Guidelines 2003

83 Clinical Probability Scores PIOPED II AJM 2006

84 Revised Geneva Score

85 D-dimer Assay Quantitative ELISA based assays (e.g. VIDAS) have sensitivity of ~ 95% But specificity poor The only useful D-dimer result is a negative one Chance of having had a PTE with negative D- dimer is low clinical probability 0.7 2% moderate clinical probability 5% high clinical probability >15% PIOPED II AJM 2006

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

87 Imaging CTPA rapidly becoming the first line test sensitivity may be as low as 83% (PIOPED II NEJM 2006) however, safe to withhold anticoagulation if CTPA negative (prevalence of further event by 3/12 ~ 1.5%) in low/moderate risk debate as to best practice in CTPA ve / high risk patients very useful for revealing alternative diagnoses V/Q a useful alternative where CT contraindicated (e.g. iodine allergy) generally only useful if CXR normal and no chronic cardiorespiratory disease

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90 LMW heparin Treatment Difficulties arise with - obese patients - renal failure - rapid reversal Oral anticoagulation with warfarin Aim for INR of 2 3 Duration of anticoagulation Temporary risk factors 4-6/52 Idiopathic 3-6/12 Risk of major bleeding 3% at 3/12 mortality 0.5% Investigation for cancer usually unnecessary BTS Guidelines 2003

91 Massive PTE A pulmonary embolism so large as to cause circulatory collapse Usually the patient has presented with clear acute event often with syncope and is in extremis Signs of right heart failure with hypoxia i.e. BP, JVP, RV gallop, clear chest

92 Investigation of massive PTE If patient peri-arrest, do not delay treatment for investigations If patient unstable, consider a cardiac echo (looking for RV dilatation) as first-line test If patient stabilises, proceed to CTPA

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95 Treatment of Massive PTE Thrombolysis BTS Guidelines 2003

96 Other Treatment Options Clot fragmentation by pulmonary artery catheter / interventional radiology Embolectomy

97

98 How does a PE make you hypoxic? When would you give iv heparin? thrombolysis? an IVC filter? How long should you anticoagulate? Should you investigate for cancer?

99 D-dimer Sensitive but not specific test for VTE Allows you to rule out PTE or DVT in patients with low / moderate clinical probability (VIDAS assay) It should not be done:- As a screening test on all general medical patients In high probability cases Only useful if negative

100 Clinical Probability In a patient with clinical features of PTE (sudden onset SOB, chest pain, haemoptysis..) a) Is there no other reasonable clinical explanation? b) Is there a major risk factor? a AND b HIGH a OR b but not both MEDIUM neither a nor b LOW

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102 Case 2 45 SOB over several months Worse at night, disturbing sleep Wheezy at times with productive cough Son recently acquired pet rat O/E Speaking in short sentences HR 120/min RR 30/min PEF not recorded Sp02 93% on air Widespread wheeze

103 Ix: Bloods normal ECG normal ABGs P a O 2 8, P a CO 2 3.9, CXR

104 CXR

105 How severe?

106 Severity of Acute Asthma

107 Treatment of Acute Asthma

108 Treatment of Acute Asthma

109 Anaphylaxis case

110 Correction of Hypoxia and Hypercapnia Correct hypercapnia by increasing alveolar ventilation Correct hypoxia by reducing shunt i.e. you need to improve O 2 delivery or decrease blood supply to diseased areas

111 Uncontrolled Oxygen Flow 2L/min by nasal cannula does not necesssarily give 28% Time

112 Uncontrolled Oxygen Flow 2L/min by nasal cannula does not necesssarily give 28% 20 24% 35% Time