Ward-based NIV in the Respiratory Care Unit at Northern Health

1. Ward-based NIV in the Respiratory Care Unit at Northern Health DrKatharine See Respiratory and Sleep Physician

2. Overview • RCU at Northern Health • Patient selection • Evaluation of response • Ward-based vs critical care locations

3. Background to development of RCU • Limited capacity within ICU to offer NIV • Bed-block for patients stabilized on NIV (both ED and ICU) • Likely some patients missing out on NIV – potential impact on LOS

4. RCU • 4-bed room on T2 • Able to offer NIV or HFOT • Non-invasive monitoring • 1:2 nursing ratio • Not an experienced ward (yet) • Confidence • Capability/resourcing

7. Patient selection NIV may be appropriate for many indications associated with acute respiratory failure in a critical care setting Ward-based acute NIV (within RCU) is more limited • Hypercapnic respiratory failure due to AECOPD And • Not much else (step-down for NMD, OHS)

8. Why won’t ward-based NIV work? • Not a respiratory ICU or HDU • Limited (non-invasive) monitoring • Relatively inexperienced nursing staff • No medical staff at location • False reassurance of NIV (evidence demonstrates delays in escalating care) • No ability to escalate care

9. RCU isn’t ICU (or ED)

11. What is a respiratory care unit (RCU)? • Geography • Location of medical support • Ability to escalate care • Limited monitoring capability – non-invasive That means that patient safety (and therefore patient selection) is critical • Those likely to benefit from RCU interventions • Those likely to require ICU care

12. Who benefits from ward-based acute NIV? COPD

13. Hypercapnoea • Elevation of the arterial carbon dioxide tension • Directly proportional to CO2 production • Indirectly proportional to rate of elimination by lungs PaCO2 = K x VCO2/[Ve(1-Vd/Vt)] • PaCO2 rises with:  production (fever) • Minute ventilation (sedatives)  Dead space ventilation (COPD)

14. Decreased minute ventilation / global hypoventilation MV = RR x TV Mechanism: • Central: respiratory centre in medulla responds to chemoreceptors (H+ and PaCO2 and PaO2) and mechanoreceptors (stretch in upper airway and lungs). Drive is also responsive to cognitive and behavioural inputs (anxiety/pain) • Peripheral muscle: (diaphragm, intercostalsetc) alter RR, depth and duration of inspiration. Shallow breathing increased VD/VT • Thoracic cage dysfunction: post operatively. RR may increase to compensate but fatigue ensues. Also increases VD/VT

15. Examples Won’t breathe (the brain): Can’t breathe (nerves, muscles, thoracic cage) C spine injury (diaphragmatic paresis/paralysis) MND Polio GuillianBarre Phrenic nerve injury Myasthenia Polymyositis Myopathy (critical illness, secondary to thyroid) Kyphoscoliosis Ankylosing spondylitis Pectusexcavatum • Sedatives • Encephalitis • major stroke • central sleep apnoea • brain stem disease • metabolic alkalosis • hypothermia

16. Increased dead spaceThe non-gas exchanging part of the lung Anatomical dead space: upper airways to terminal bronchioles • Anatomical dead space is a fixed volume Alveolar dead space: reduced perfusion to ventilated alveoli • pulmonary capillary compression (extrinsic obstruction) from overinflated lungs (too much positive pressure) • destruction of pulmonary capillaries (emphysema, interstitial fibrosis, pulmonary vasculitis) It is the proportion of the tidal volume that is dead space that we can change

17. COPD • Increased VD main mechanism of hypercapnoea in COPD • Some compensate: MV or redistribute perfusion to improve V/Q matching (pink puffers) • Some cannot and develop chronic hypercapnoea (blue bloaters)

18. Mechanism • Destruction of capillaries by emphysema • Airflow obstruction leading to hyperinflation • Reduced lung compliance at high lung volumes • Breathing pattern in COPD: lower tidal volumes, higher RR which increases VD/VT • Drive is high, inspiratory time in short (VT) expiratory time in long (RR)

19. Oxygen induced hypercapnoea • Always aim for normoxia • Don’t kill someone with untreated hypoxia for fear of hypercapnoea. • Don’t believe that everyone needs oxygen and that oxygen is good – it can kill people

21. Oxygen induced hypercapnoea • Some COPD pts given oxygen will develop hypercapnoea • This is NOT due to loss of hypoxic drive (it’s only a small part) • Increased dead space: worsening of V/Q mismatch due to loss of hypoxic pulmonary vasoconstriction (HPV improves matching between blood flow and ventilation which improves V/Q and decreases physiologic dead space). Worse in more hypoxic patients • Haldane effect: Right shift of CO2-Hb dissociation curve in presence of increased oxygen

22. Effects of hypercapnoea • Cerebral: depressed conscious state and reduced respiratory drive, increased cerebral blood flow and intracranial pressure • Cardiorespiratory: dyspnoea (increased drive), reduced myocardial and diaphragmatic contractility • Physiologic: shift in oxy-haemoglobin dissociation curve to right, acidosis and associated problems • Metabolic: buffering with bicarbonate

23. What to do with AECOPD • Blood gas – if abnormal VBG MUST have ABG • Bronchodilator – MDI with spacer • Conservative oxygen therapy – sats 88-92% • Prednisolone at 0.75mg/kg • Send sputum • Single agent abx – checking for previous organisms and sensitivities • DVT prophylaxis • GOPC

24. Case 1: Mrs C • 72F from retirement village • “AECOPD” • Complicated by T2RF • FEV1 0.90L (38%), smoker • OSA? • Weight 120kg, BMI 36 • Examination: • RR 24 • SpO2 85% RA • BP 130/69, HR 100 • T 37.2 • GCS 14-15

25. Challenge the diagnosis:Not all ventilatory failure = AECOPD CO2 Capacity Load Chest wall Lung compliance Upper airway Drive Strength CNS disorders Sleep Drugs Neuromuscular disorders Obesity Chest wall restriction COPD

26. Case 1: Mrs C Commenced on NIV on arrival Initial VBG: pH 7.25

27. Case 1: Mrs C Commenced on NIV on arrival Initial VBG: pH 7.25 • What should happen next? • Can we stop there?

28. Venous blood gases • Useful screening test for acidaemia in someone with AECOPD • Valuable to confirm a clinical decision that NIV is notrequired • Results are redundant once a clinical decision to institute NIV has been made (Opinion: Should refute this decision with the gold standard test) Example: Empirical anticoagulation for PE – wouldn’t cease therapy on the basis of a negative D-dimer • PvCO2 is (often) misleading • Unable to use serial results to titrate ventilator settings

30. Venous pH in AECOPD • Venous pH cut-off of 7.34 correctly classified 87% of arterial pH≥7.35 (mean difference is 0.03) • Arguably a higher cut-point is sensible (7.38-7.40) • The aim is not perfect diagnostic accuracy – a sensitive screening test should be preferred in this situation • A false negative VBG means potentially withholding an evidenced based therapy (NIV) from a patient that can benefit from it

31. Case 1: Mrs C ABG on NIV (IPAP 10, EPAP 5, FiO2 21%): pH 7.25 pCO2 88 pO2 47 HCO3 38

32. Case 1: Mrs C ABG on NIV (IPAP 10, EPAP 5, FiO2 21%): pH 7.25 pCO2 88 pO2 47 HCO3 38 • What should happen next? • Transfer to ward for ongoing NIV • Repeat ABG • Refer to ICU • Adjust NIV settings • Review the mask • All of the above

33. Case 1: Mrs C ABG on NIV (IPAP 10, EPAP 5, FiO2 21%): pH 7.25 pCO2 88 pO2 47 HCO3 38 These don’t look right

34. Case 1: Mrs C • 72F from retirement village • “AECOPD” • Complicated by T2RF • FEV1 0.90L (38%), smoker • OSA? • Weight 120kg, BMI 36 • Examination: • RR 24 • SpO2 71% RA • BP 130/69, HR 100 • T 37.2 • GCS 14-15

35. Case 1: Mrs C • Settings adjusted: • IPAP 20cmH2O, EPAP 10cmH2O • Bronchodilators, Prednisolone, Antibiotics • Repeat ABG pH 7.32, pCO2 62, pO2 61, HCO3 31 • Improving -> transfer to RCU for ongoing NIV

36. Considerations with NIV settings • Which mask? • What pressures (IPAP and EPAP)? • How is a breath triggered and how sensitive should the trigger be? • How long should a breath be?

37. NIV masks Non-vented masks – ED/ICU/HDU • Separate exhalation line or valve that avoids re-breathing of expired air Vented masks – used in RCU (and all home CPAP or NIV devices) • Mask has in-built vents which intentionally leak and allow expulsion of expired air Using a non-vented mask on a ward ventilator (or CPAP device) can result in re-breathing If in doubt – please contact on of our Respiratory CNCs or registrars for advice

38. Vented Vents Non-vented Oxygen ports – not vents! Don’t use ICU/ED/theatre masks anywhere but ICU/ED/theatre with ICU/ED/theatre machines

39. NIV pressures EPAP – typically set to overcome upper airway resistance (and to vent CO2 from the mask) IPAP – provides the driving pressure to increase alveolar ventilation • Rule of thumb: EPAP should be ~1cmH2O for every 10-15kg of body weight • 120kg person: EPAP ~10cmH2O

40. Titrating pressures • Aiming for the lowest effective pressures • Increase IPAP-EPAP difference (=pressure support) to increase tidal volume • Increase EPAP if O2 low or possible upper airway obstruction • Serial ABG (fall in PaCO2, rise in pH) allows titration • Improvement confirms adequate settings and high probability that ward-based NIV will be successful • Lack of change or deterioration implies incorrect settings, incorrect mask, incorrect patient?

41. Admission criteria for RCU ED referrals • Acute exacerbations of COPD • Mild to moderate hypoxaemic respiratory failure ICU referrals (step-down care) • OHS/NMD/other – on NIV • Stable patients requiring ongoing respiratory monitoring (single organ dysfunction) Ward referrals

42. Contraindications to ward-based NIV (RCU admission) • High likelihood of failure of NIV • Invasive ventilation (via tracheostomy) • Acute severe asthma • Acute coronary syndromes • Acute pulmonary oedema • Severe hypoxaemic respiratory failure • Massive or submassive PE • Trauma • Haemodynamic instability • Confusion/need for iv sedation • Acute surgical pathology or complex post-op care

43. Written by critical care physicians (Society of Critical Care Medicine)

44. From Ergan et al, ERS, 2018

45. Problems with this approach • Too restrictive/prescriptive • Doesn’t consider response to Rx or likelihood of failure • Frequent ABGs!??! (every 8hrs) • Reality is that RCU sits above the ‘general ward’ but below the HDU in this paper

46. Venous blood gases • Good screening test for acidaemia in AECOPD • Should confirm abnormal result with an ABG (arguably any VBG <7.40) • Once a clinical decision is made to commence NIV -> ABG (should refute your clinical judgement with an accurate test) Ignore the PvCO2 – it is misleading and can’t be used to titrate settings

47. Clinical parameters • Comfort and tolerance • Respiratory rate • Oxygen saturation • Conscious state Once you are considering sedation to improve NIV tolerance you have an HDU/ICU patient in front of you

48. Comfort and tolerance • Mask choice (size) is critical • Zero leak is not the goal • Starting pressures may be low (for tolerance) but should not necessarily stay low • Respiratory rate should fall with application • Coordination with the device can be clinically assessed

49. NIV starting pressures • IPAP 10 and EPAP 5 will not work for most Reasonable to start but expect to increase • EPAP to overcome upper airway resistance • If on CPAP use this as a guide (EPAP generally ~2-4cmH2O below CPAP) • Roughly 1cmH2O for every 10-15kg body weight • IPAP (or pressure support level) titrated to PaCO2 level (but can use tidal volume as interim marker)

50. Gas exchange • Continuous pulse oximetry • No data to support a particular target range but no value in SpO2 >94-95% • A lower target (88-92%) has been recommended but this should be the unsupported target range in my view • On NIV I think 90-94% is adequate