Acute noninvasive ventilation what s the evidence? Respiratory Medicine Update: Royal College of Physicians & BTS Thu 28 th January 2016

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1 Acute noninvasive ventilation what s the evidence? Respiratory Medicine Update: Royal College of Physicians & BTS Thu 28 th January 2016 Annabel Nickol Consultant in Respiratory Medicine, Sleep & Ventilation and Lung Function Leads Oxford Centre for Respiratory Medicine, Churchill Hospital Site, OUH NHS Foundation Trust Department of Physiology, Anatomy and Genetics, University of Oxford

2 NIV helps restore the balance between load, capacity and drive Drive Renal compensation blunting ventilatory responses Oxygen supplementation Opiates Adequate ventilation Load Increased airways resistance Airway secretions and hyperinflation Obesity Kyphoscoliosis Capacity Functional or actual diaphragmatic weakness Respiratory failure Cardiac impairment & Metabolic factors

3 How does NIV work? IPAP Increases alveolar ventilation by increasing tidal volume Decreases PaCO 2 (and also bicarbonate, so restoring ventilatory sensitivity) Decreases work of breathing EPAP Increases oxygenation by increasing FRC Recruits under-ventilated lung units Offsets intrinsic PEEP Reduces CO 2 rebreathing (favourable RR: V T ) Splints upper airway

4 The Copenhagen poliomyelitis epidemic, 1952 West (2005) J Appl Physiol 99:

5 The renaissance in clinical physiology! West (2005) J Appl Physiol 99: Bjorn Ibsen Danish anaesethist Manual positive pressure ventilation Poul Astrup father of modern acid-base physiology

6 Non-Invasive Negative Pressure Ventilation

7 Early NIV Negative pressure Cumbersome Poor mobility Upper airway obstruction Positive pressure driven by CPAP treatment from 80s Used for long-term ventilation first, then acute Progressive comfort of masks & ventilator synchrony

8 NIV initially used in the home setting Respiratory failure due to heterogenous causes N = 180 Followed for 5 years Simonds and Elliott Thorax (1995) 50: 604-9

9 NIV use in AE COPD

10 n=60 PCO 2 > 6 kpa PO 2 < 7.5 kpa Lancet 1993; 341: NIV Control Reduced 30 day mortality: 1/26 cf 9/30 (excluded those NIV intol) Breathlessness ph Control NIV

11 Time at which intubation was performed n=85 pt AE COPD In ICU Patients intubated: 11/43 NIV 31/42 standard care Mortality: 4/43 NIV (9%) 12/ 42 standard (29%)

12 Lancet 255: (2000) UK multi-centre (13), ward based; delivered by clinical staff 22 of 25 wards had no experience of NIV Nurse: patient = 1: 11 Acute exacerbations COPD (n = 236) RR > 23 ph PaCO 2 > 6kPa Usual medical care v NIV + usual medical care Simple bi-level devise + written protocol EPAP 4 cmh 2 O IPAP 10 to 20 cmh 2 O or max tolerated in 1hr

13 Plant et al, Lancet 2000 Results Need for intubation BSC 32/ 118 (27%) NIV 18/ 118 (15%) (p<0.05) Mortality BSC 24/118 (20%) NIV 12/ 118 (10%) (p<0.05) Staff workload by 26 mins in 1 st 8 hrs Training 7.6 hrs/ 3M hrs/ M ongoing

14 Overall benefit of NIV: But no significant benefit of acute NIV if pre-niv ph < 7.30:

15 Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and metaanalysis JVJ Lightowler, JA Wedzicha, MW Elliott and FSF Ram BMJ 326, Jan 2003 Objective To determine the effectiveness of NPPV in the management of patients with respiratory failure due to an acute exacerbation of COPD

16 Treatment Failure Results

17 Endotracheal Intubation Results

18 Mortality Results

19 Results: Summary of Primary Outcome Measures Outcome measure Relative risk NNT Rx Failure 0.51 ( ) 5 (4 7) Mortality 0.41 ( ) 8 (6 13) Intubation 0.42 ( ) 5 (4 7) Complications 0.32 ( ) 3 (2 4) BMJ 2003;326:

20 Results: Secondary Outcome Measures NPPV group: length of hospital stay by 3 days Improvements in Respiratory rate at one hour ph PaCO 2

21 In AE COPD NIV is better than intubation Compared to invasive ventilation Same short term outcome, but fewer readmissions & lower LTOT requirements. Conti et al. Int Care Med (2002) 28: Lower mortality rates (decreased incidence of pneumonia) Brochard et al. N Engl J Med (1990) 323:

22 CPAP 5cmH 2 O Use?hrs/night Time to first readmission 56 days NIV cmH 2 O Use 7-9hrs/night Time to first readmission 71 days

23 UK multicentre RCT HOT HMV COPD Trial Global Medical Excellence Cluster, NIHR Portfolio (UKCRN) Patrick Murphy & Nicholas Hart St Thomas Primary Outcome Admission free survival PaCO 2 still >7 kpa 2 wks post acute hypercapnic COPD exacerbat n Enrolment Randomisation to HOT or HOT + HMV with titrated IPAP Assessments Secondary Outcome Compliance with NIV HRQL PaCO 2 PaO 2 ph HCO 3 - Lung function BMI FFMI 6-MWT HCVR COPD-related admissions Compliance with LTOT Withdrawal of LTOT Courses of antibiotics Courses of steroids Follow up at 6 wks, then 3, 6 & 12 mnths

24 NIV use in acute cardiogenic pulmonary oedema

25 359; 2 (2008) Multicentre (26), open RCT Standard oxygen therapy, CPAP or NIV Primary end points: 1,000 ph < 7.35: actually mean = 7.22 O2 alone vs resp support: death within 7 days CPAP vs NIV: death or intubation within 7 days

26 Oxyge n Suppor t OR; 95% CI D Dyspnoea at 1 hr* ; * D HR at 1 hr* ; * D ph at 1 hr* ; <0.001* Mortality at 7 days 9.8% 9.5% 0.97; p Mortality or intubation at 7 days CPAP NIV Stats 11.7% 11.1%

27 30 day mortality difference NS 16.4% vs 15.2%; CI (pp = 0.64)

28 30 day mortality difference NS 15.4% vs 15.1%; (p = 0.92)

29 Conclusion: Consider CPAP/ NIV in acute pulmonary oedema with severe respiratory distress as an adjunct to therapy, or for patients whose condition does not improve with pharmacologic therapy Results supported by Cochrane Collaboration database (2013)

30 Where are we now: current BTS guidelines

31 Indications for NIV PaCO 2 > 6kPa and ph <7.35 Despite maximal medical therapy for 1 hr+ ph < 7.26 should be managed on the HDU/ ICU

32 NIV advantages Morbidity of intubation avoided Avoids sedation Applied intermittently Allows patient to eat, drink and mobilise Able to talk Upper airway defence mechanisms preserved - decreased risk of VAP

33 NIV disadvantages No airway control Airway suctioning/ lavage difficult Leak compromises efficiency of ventilation Mask claustrophia Facial skin necrosis (2 18%) Gastric distension (2%)

34 NIV disadvantages Not always successful: failure rates 9 50% May delay intubation Workload of staff increased Not universally tolerated by patients

35 Relative contraindications to NIV GCS<13 Inability to protect airway Recent upper airway surgery Copious secretions Weak cough Vomiting Life-threatening hypoxaemia Haemodynamic instability Bowel obstruction and patient choice (assuming capacity)

36 Levels at which NIV may be used As a holding measure to assist ventilation at an earlier stage than NIV would be considered As a therapeutic trial with a view to intubation if NIV fails As a ceiling of treatment o o Decide prior to starting NIV Document discussions with family

37 How do we do in the UK in the real life situation? Data compiled by Michael Davies, Consultant Chest Physician, Papworth

38 NHS Atlas of Variation Proportion of patients admitted with COPD receiving NIV Death rate at 30 days post admission in COPD

39 BTS audits 2010, 2011, 2012 and 2013 Substantial comorbidities Performance status limited in 36%; v limited 43% CXR consolidation in 40% Indication for NIV o COPD 61% o Pulmonary oedema 8% o Obesity 8% o Chest wall/ neuromuscular weakness 4%

40 BTS audits 2010, 2011, 2012 and 2013 Oxygen toxicity contributed to respiratory failure in 17% Progressive reduction in pre-niv ph values 7.30 to 7.24 in successive years Prior to NIV 47% COPD pt had ph < % had ward-based treatment despite low ph Recommendation is for these patients to receive care in an HDU/ ICU setting

41 Safe oxygen use Beware excessive oxygen for the patient who is not working hard (unless planning to intubate) Titrate to SaO 2 usually 85 92%

42 CO 2 sensitivity is blunted in ventilatory failure V (l/ min) PetCO 2 (kpa)

43 V (l/ min) Post-NIV Pre-NIV PetCO 2 (kpa)

44 Increased ventilatory drive post-niv mirrors that post altitude exposure V (l/min) 80 D21 60 D1 SL 40 D0 20 Adapted from Kellog (1963) P et CO 2 (kpa)

45 Oxygen dissociation curve SaO PaO 2 kpa

47 BTS audits 2010, 2011, 2012 and 2013 PaCO kpa fell by 1.3 kpa at 1 hr 1.9 kpa at 4-6hrs Acidosis resolved in 45% cases 66% achieved success (ph > 7.3 and reduced PaCO 2 by 0.5kPa)

48 BTS audits 2010, 2011, 2012 and % failed to achieve benefit 3% went on to intubation Failure was due to general deterioration, intolerance or agitation Ceiling of therapy in 67%

49 High hospital mortality

50 Outcome worse in patients with consolidation on CXR (also with patients with the lowest ph values)

51 What are the barriers to excellent outcomes? Doctor and nurse training: rolling programme essential Patient selection: morbidities and ph outside trial criteria Limited HDU and ICU resource Nihilistic attitudes Patients often have NIV as ceiling of care What next? NCEPOD study focusing upon delivery an acute NIV service in 2016

Acute NIV in COPD and what happens next. Dr Rachael Evans PhD Associate Professor, Respiratory Medicine, Glenfield Hospital

Acute NIV in COPD and what happens next Dr Rachael Evans PhD Associate Professor, Respiratory Medicine, Glenfield Hospital Content Scenarios Evidence based medicine for the first 24 hrs Who should we refer