2.  Definition
 Why do we use NIV?
 Indications for BiPAP use
 Contraindications to use
 Patient selection
 Set up
 Monitoring
 Escalation
 Duration of treatment
 Weaning
 Palliation
 Clinical scenarios

3.  To gain a more in depth knowledge of BiPAP
and it’s clinical indications

4.  To state the definition of NIV
 To list 3 clinical indications to commence
BiPAP
 To list 3 contraindications for its use
 To discuss patient selection considerations
 To be able to correctly describe set up
 To be able to give clear instructions on
monitoring
 To be able to relay that an escalation plan
should be documented at commencement

5.  Non invasive ventilation – ‘the provision of
ventilatory support through the patient’s
upper airway using a mask or similar device’.
 CPAP – continuous positive airway pressure
 BiPAP – bilevel positive airway pressure.

6.  NIV in T2RF in COPD - reduction in mortality
~50%
 Reduces intubation rates in COPD pts with
decompensated respiratory acidosis
 Reduction in need for ICU admission and
reduced hospital costs compared to standard
medical therapy

7.  Acute exacerbation of COPD
 Persistent respiratory acidosis :
PaCO2 > 6kPa, 7.26 < pH <7.35
- despite immediate maximal
standard medical treatment on
controlled oxygen therapy for no
more than one hour

8. Standard medical therapy:
 Controlled oxygen to maintain SaO2 88-92%
 Nebulised salbutamol 2.5 – 5mg
 Nebulised ipratropium 0.5 mg
 Prednisolone 30 mg
 Antibiotics (when indicated)

9.  Acute / acute on chronic hypercapnic
respiratory failure - chest wall deformity /
neuromuscular disease.
 Decompensated OSA (esp if respiratory
acidosis)
 ?Acute exacerbation of bronchiectasis
 ARDS / postoperative, post-transplantation
respiratory failure
 Weaning from invasive ventilation
 ?Heart failure / pneumonia

10.  Facial burns / trauma / recent facial or upper airway
surgery
 Vomiting
 Fixed upper airway obstruction
 Undrained pneumothorax
 Upper gastrointestinal surgery
 Inability to protect the airway
 Copious respiratory secretions
 Life threatening hypoxaemia
 Haemodynamically unstable requiring inotropes / pressors
(unless in a critical care unit)
 Severe co-morbidity
 Confusion / agitation
 Bowel obstruction
 Patient declines treatment

11.  Place in one of 5 groups:
 Immediate intubation and ventilation
 Suitable for NIV and escalation to ICU /
intubation if required
 Suitable for NIV but not suitable for escalation
 Not suitable for NIV but for full active
management
 Palliative care most appropriate

12.  Premorbid state
 Severity of physiological disturbance
 Reversibility of acute illness
 Presence of relative contraindications
 Patients wishes (if possible)

13.  Inclusion criteria
 Sick but not moribund
 Able to protect airway
 Conscious and cooperative
 No excessive respiratory secretions
 Potential for recovery to quality of life
acceptable to the patient
 Patient’s wishes considered

14.  Decision to start – CT2 or above
 Patient consent
 Trained staff
 Initial settings
 IPAP – 10 cms H2O
 2-5cms increments
 5cms every 10 mins
 target 20 cms or until therapeutic response
achieved / pt tolerability reached
 EPAP – 4-5 cms H20.
 Oxygen (when required) – sats 88 – 92 %

15.  Continuous sats, cardiac monitoring (first 12
hours) RR, HR, BP and GCS
 ABGs – minimum 1, 4 and 12 hours (1 hour
after further changes)
 Management plan – within first 4 hours of NIV
– ?intubation
 Compliance with NIV, patient-ventilator
synchrony and mask comfort – KEY FACTORS
IN DETERMINING OUTCOME!
 Appropriately trained staff

16.  Management plan in event of NIV failure
should be made at outset!
 Uncertainty / not for escalation - discuss
with a consultant
 Escalation appropriate – discuss with ICU
team early (ideally intubate first 4 hours)
 In late NIV failure (>48 hours) intubation is
mx of choice

17.  Benefit during first hours - NIV for as long as
possible during first 24 hours
 Tx should last until the acute cause has
resolved, commonly 2 – 3 days
 If NIV successful (pH> 7.35, resolution of
underlying cause and sx, RR normalized) –
appropriate to start weaning

18.  Tx reduction – daytime periods first
 After withdrawal in the day, a further night
of NIV is recommended
 Documentation of weaning strategy in
nursing and medical records

19.  When NIV failed, not for escalation – need
proactive approach to palliation

20.  NIV works! – evidence based
 Indicated in AECOPD – respiratory acidosis
(PaCO2>6kPa, pH<7.35 , >7.26) despite 1
hour medical therapy
 Select your patients with thought!
 Ensure no contraindications
 Think of long term plan when starting

22.  67 yo man with known moderate to
severe COPD
 Multiple admissions with IECOPD, no ITU
admissions
 3/7 hx of productive cough, increasing
SOB & wheeze
 ABG (on non rebreathe mask put on by
ambulance):
 pH 7.28, pCO2 9.1, pO2 58
 HCO3 29.2, BE -2, lactate 1.9
 MANAGEMENT?

23.  Salbutamol neb 2.5–5 mg
 Ipratroprium neb 500μg
 Prednisolone 30mg PO or hydrocortisone
200mg IV (for minimum of 5 days)
 Antibiotic (if evidence of infection)
 CXR
 Consider IV aminophylline
 Most importantly controlled oxygen

24. Initial ABG (100% non
re-breathe mask)
ABG at 1 hour (28%
venturi mask)
pH 7.28 7.37
pO2 58 26.5
pCO2 9.1 8.1
HCO3 29.2 32
BE -2 -1.5
Sats 98 88

25.  67 yo man with known moderate to
severe COPD
 Multiple admissions with IECOPD, no ITU
admissions
 3/7 hx of productive cough, increasing
SOB & wheeze
 ABG (on non rebreathe mask put on by
ambulance):
 pH 7.28, pCO2 9.1, pO2 58
 HCO3 29.2, BE -2, lactate 1.9
 Initial management as before

26. Initial ABG (100% non
rebreathe)
ABG at 1 hour (28%
venturi)
pH 7.28 7.21
pO2 58 26.2
pCO2 9.1 11.3
HCO3 29.2 28
BE -2
Sats 98 86
• What now?

27.  NIV should be considered in all patients with
an acute exacerbation of COPD in whom a:
 respiratory acidosis (pH <7.35, PaCO2 > 6kPa)
persists despite immediate maximum standard
medical treatment on controlled oxygen therapy
for no more than 1 hour

28.  NIV started at
 EPAP 4cm H20 (improves O2)
 IPAP 10cm H20 (reduces PCO2)
 O2 level to maintain 88-92% sats
 Titrate up to therapeutic setting over 1
hour
 IPAP by 2–5cm increments at ~ 5cm H20/10
mins, with usual target of 20 cm H20 or until
therapeutic response achieved or patient
tolerability reached
 Within 1 hour, IPAP target of 18-22cm H20

29. Initial ABG (100%
non rebreathe)
ABG at 1 hour
(28% venturi)
ABG 2 hrs post
starting NIV
pH 7.28 7.21 7.36
pO2 58 26.2 18.1
pCO2 9.1 11.3 7.2
HCO3 29.2 28 24
BE -2
Sats 98 86 90
• What now?

30.  ABG at 2 hours showing improved pH &
decreasing pCO2
 What next?
 If no longer acidotic and pCO2 normalising then
don’t stop immediately!
 Remain on present settings, repeat ABG in 4-6hrs
 Need to wean down the BiPAP over several days –
e.g. D1 24hr, D2 16hr, D3 8hr then stop

31. Initial ABG (100%
non rebreathe)
ABG at 1 hour
(28% venturi)
ABG 2 hrs post
starting NIV
pH 7.28 7.21 7.15
pO2 58 26.2 23.1
pCO2 9.1 11.3 13.5
HCO3 29.2 28 27
BE -2
Sats 98 86 82
• What now?

32.  Still acidotic & pCO2 not improving despite
therapeutic settings
 Is this person an ITU candidate?
 Consider if development of complication
 E.g. pneumothorax, mucus plugging, aspiration
pneumonia
 Poor fitting mask, tubing disconnection

33.  57 yo lady with IHD and severe LV
dysfunction
 Acute onset SOB 2 hours previously
 Brought to resus – wheezy ++, accessory
muscle use ++, RR 40
 ABG:
 pH 7.23, pCO2 7.9, pO2 7.1, lactate 3.8, HCO3 18
on 15L non-rebreathe mask
 Likely diagnosis?
 Management?

34.  Management:
 O2, morphine, furosemide, GTN
 CPAP
 Reduces preload and afterload through positive
intrathoracic pressure, increases SV, decreases HR
 Standard is not BiPAP
 Studies show does improve pH/pCO2/HR/RR/SOB and
intubation rate
 BUT possible increased MI rate (Mehta S et al,Crit Care
Med 1997; 25:620-628)

35.  Acute exacerbation of COPD
 Firstly 1 hour of maximum standard medical
treatment
 ABG at 1 hour
 If NIV started then ABG at 1-2 hours
 Slow wean down of NIV if improvement
 Consider complications/ITU if deterioration
 BiPAP not standard for pulmonary oedema

36.  Mehta S, Jay GD, Woolard RH, Hipona RA, Connolly EM, Cimini DM, Drinkwine JH,
Hill NS. “Randomized, prospective trial of bilevel versus continuous positive airway
pressure in acute pulmonary edema” Critical Care Medicine 1997; 25:620–628
 http://www.brit-thoracic.org.uk
 “Non-invasive ventilation in chronic obstructive pulmonary disorder: management of
acute type 2 respiratory failure” RCP/BTS Concise guideline, October 2008
 “NIPPV Non-Invasive Ventilation in Acute Respiratory Failure” British Thoracic
Society Standards of Care Committee; Thorax 2002; 57:192-211
 “The Use of Non-Invasive Ventilation in the management of patients with chronic
obstructive pulmonary disease admitted to hospital with acute type II respiratory
failure (with particular reference to Bilevel positive pressure ventilation)” British
Thoracic Society/Royal College of Physicians London/Intensive Care Society
guideline, October 2008
 Lightowler JV, Wedzicha JA, Elliott MW et al; “Non-invasive positive pressure
ventilation to treat respiratory failure resulting from exacerbations of chronic
obstructive pulmonary disease: Cochrane systematic review and meta-
analysis.” BMJ 2003; 326:185–7.
 Ram FSF, Picot J, Lighthowler J et al. “Non-invasive positive pressure ventilation for
treatment of respiratory failure due to exacerbations of chronic obstructive
pulmonary disease.” Cochrane Database Syst Rev 2004; 3.