1. Respiratory Failure Dr Svitlana Zhelezna Clinical Teaching Fellow UHCW NHS Trust svitlana.zhelezna@uhcw.nhs.uk 2013/2014 academic year

2. Learning objectives: Describe the clinical features, potential causes and management of respiratory failure List indications/contraindications/complications of non invasive ventilation and understand its set up and monitoring

3. Definition: Acute respiratory failure occurs when pulmonary system is no longer able to meet the metabolic demands of the body

4. Type 1 Respiratory Failure Hypoxaemic pO2 < 8 kPa ON AIR pCO2 < 6.0 kPa Type 2 Respiratory Failure Hypercapnic pO2 < 8 kPa ON AIR pCO2 > 6.0 kPa

5. Clinical signs: 1. Respiratory compensation Tachypnoea Accessory muscles Recession Nasal flaring 2. Sympathetic stimulation  HR  BP (early) sweating 3. Tissue hypoxia Altered mental state  HR and  BP (late signs) 4. Haemoglobin desaturation: (SpO2 < 90%)

6. Case 1 70 year old man referred to A&E by his GP PC: SOB and productive cough 4/7 HPC: gradual onset over 4-6/12 but worse over the last 3-4 days. SH: smoking 30 pack years. O/E: O2 sats are 91% on air, RR 26, temp 37.8, BP 130/75, HR 89. Pt’s chest shows widespread bilateral wheeze throughout, reduced air entry LLL. 1. List your differential diagnosis and investigation tests. 2. What would be your initial management of this patient?

7. ABG: pH 7.31 pO 2 8.4 kPa (on 6L O2) pCO 2 5.9 kPa, HCO 3- 21 mmol/l Lac 3.1 What is your interpretation?

8. Initial management: Investigations: ABG FBC, U&E, LFTs Peak flow CXR ECG Sputum and Blood culture Urine dip, Urine Microscopy Treatment: A-E - Sepsis! Oxygen – high flow initially, consider controlled to aim O2Sat 88-92% when stable Nebulised bronchodilators Steroids Antibiotics Fluids

9. COPD – Background: Definition: COPD is predominantly caused by smoking and is characterised by airflow obstruction that: is not fully reversible and is usually progressive in the long term COPD acute exacerbations: Increasing dyspnoea Increasing sputum volume Increasing sputum purulence (change in character)

10. Differentiating COPD from asthma Clinical featuresCOPDAsthma Smoker or ex-smoker Nearly allPossibly Symptoms under age 35Rare Often Chronic productive coughCommon Uncommon BreathlessnessPersistent and progressive Variable/Intermittent Night time waking with breathlessness and or wheeze Uncommon Common Significant diurnal or day to day variability of symptoms Uncommon Common

11. Asthma – Background: More than one of the following symptoms: Wheeze, cough, difficulty breathing, frequent and recurrent chest tightness, worse at night and in the early morning; Occur in response to, or are worse after, exercise or other triggers, Personal/ Family history of atopic disorder and/or asthma Widespread wheeze heard on auscultation History of improvement in symptoms or lung function in response to adequate therapy.

12. Severe Asthma LIFE THREATENING PEF <33% best or predicted SpO2 <92% PaO2 <8 kPa normal PaCO2 (4.6-6.0 kPa) silent chest cyanosis poor respiratory effort arrhythmia exhaustion, altered conscious level BP low NEAR FATAL Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

13. Criteria for Referral to ITU Refer any patient: requiring ventilatory support with acute severe or life threatening asthma, failing to respond to therapy, evidenced by: - deteriorating PEF - persisting or worsening hypoxia - hypercapnea - ABG analysis showing low pH - exhaustion, feeble respiration - drowsiness, confusion, altered conscious state - respiratory arrest

14. Case 2 17 y.o. female student PC: severe SOB, can not speak in full sentences HPC: woke up at 4 am feeling SOB and started coughing, her housemate called ambulance PMH: too breathless to give O/E: Pt agitated, wide spread audible wheeze bilaterally, poor chest expansion, using accessory muscles, HR 100, BP 130/85, T 36,6, O2 sat 93% What would be your differential diagnosis and initial management?

15. ABG: pH 7.46 pO 2 8.2 kPa (on 15L O2) pCO 2 2.8 kPa, HCO 3- 18 mmol/l What is your interpretation?

16. Initial Management Oxygen – high flow 15L Nebulised bronchodilators Peak flow ABG FBC, U&E, LFTs, Steroids

17. Case 3 76 year old male PC: SOB, 7/7 productive cough with phlegm PMH: known COPD, LTOT at home 2L for 16/24. On admission: RR 18, sats 85% on 2L oxygen, HR 110, BP 134/68, temp 38.5. RLL crackles, but widespread wheeze throughout both lung fields. The paramedics gave him 5ml salbutamol nebs and 100mg IV hydrocortisone an hour ago, he was given IV abx first dose, but he is not improving as yet, but become drowsy

18. What would be your management? ABG: pH 7.23 pO 2 8.3kPa pCO 2 8.4kPa, HCO 3- 24 mmol/l Lac 4 Vitals: RR 12 O 2 Sats 90% on 4L oxygen HR 115 BP 115/68 FBC: Hb 16 g/dL WCC: 18 × 10 9 /L Neutrophils 80% U&E: Na 143 mmol/ K 4.6 mmol/L Creat 120 μmol/L Urea 8.2 mmol/L

19. What next? Continue Nebulised Salbutamol NIV (non-invasive ventilation)

21. NIV – non-invasive ventilation Definition: Definition: NIV is the delivery of mechanical ventilation to the lungs using techniques that do not require an endotracheal airway

22. Types: Continuous Positive Airway Pressure CPAP Treating Hypoxia Type 1 RF Bi-level Positive Airway Pressure (VPAP/Stellar) Treating Hypercapnia Type 2 RF

23. Main goals of NIV Correction of abnormalities in ABG’s (hypoxia and hypercapnia) Maintaining alveolar ventilation and lung volume Reduce the work of breathing Avoiding respiratory muscle fatigue NIV does not correct underlying disorder or condition!

24. Medical conditions/Indications : Acute exacerbation of COPD (pH 7.26 – 7.35 or patients with NIV as ceiling of care and considered not suitable for HDU/ITU care) Morbid Obesity / Severe OSA / Alveolar Hypoventilation Syndrome Chronic Neuromuscular Disease Kyphoscoliosis / Chest wall deformity.

25. NIV contraindications: Respiratory arrest Undrained pneumothorax Impaired consciousness/confusion/aggressive behaviour Chest wall trauma Uncontrolled vomiting/distended abdomen/ excessive secretions Facial trauma/surgery, burns or facial abnormalities that are likely to cause difficulty with appropriate mask fit. Recent upper abdominal surgery or intestinal obstruction.

26. Starting NIV: Locations: HDU/ITU, Respiratory ward A+E resus ( Not usually on a general ward – the nursing staff will not know how to deal with it) Settings: Should be prescribed by a consultant

27. Monitoring NIV: Main actions: Baseline ABG, RR, HR Repeat ABG after one hour of starting After every setting change, repeat ABG at 1 hour Otherwise, every 4 hours, or if not well Key points: Aim minimum 6 hours treatment Most people better by 24 hours on NIV Weaning thereafter

28. Complications of NIV: Pneumothorax, Decreased pre-load – may drop BP Increased risk of aspiration Face mask discomfort Anxiety + confusion

29. Key message Common contributors to RF Type 1 (↓O2): Asthma and COPD Type 2 (↓O2 and ↑CO2): COPD and life threatening asthma NIV is effective in treating ↑CO2

30. Summary worry if RR > 30/min (or < 8/min) unable to speak 1/2 sentence without pausing agitated, confused or comatose cyanosed or SpO 2 < 90% deteriorating despite therapy remember normal SpO 2 does not mean severe ventilatory problems are not present

31. Thank you! Any questions?