“ Bi-Level and Non-invasive Intermittent Postive Pressure Ventilation ”.

1. “Bi-Level and Non-invasive Intermittent Postive Pressure Ventilation”. M.A . King Respiratory Support & Sleep Centre, Papworth Hospital, Cambridge, CB3 8RE, UK

2. Bi-level and NIPPV • Volumetric mechanical ventilation is usually reserved for the unconscious patient and is delivered by an endotracheal tube. • Non-invasive Intermittent Positive Pressure Ventilation is delivered by a mask. Bi-level and NIPPV

3. Plan • Avoid mentioning CPAP and Bi-Level in OSA ! • Focus in non-invasive ventilatory support. • What is ventilatory failure? • Who needs this treatment? • What do the machines do? • What are the outcomes? • Discusion • : Do Sleep Technologists need to be involved in these treatments?

4. Technological developments since the invention of CPAP Ventilatory insufficiency Ventilatory Failure OSA with lung problems OSA Bi-Level Bi-Level Bi-Level CPAP Pressure support ventilators Pressure support ventilators 1987 1990 1995 <1987 2000 <1987

5. Ventilatory Failure. Lung Function = Ventilation and gas exchange Minute Ventilation is a function of respiratory rateand tidal volume Ventilatory Failure causes a rise in CO2 and drop in O2 Gas Exchange (respiratory) failure causes hypoxia alone

6. “Pump” Failure. • Respiratory control centres. • Neurological system ( Nerves and synapses) • Muscle • Mechanics ( Thoracic cage). RESTRICTIVE VENTILATORY DEFECT

7. Restrictive defect. • Small lungs in a rigid chest cage. • Normal lungs which can not be expanded. • Lung mechanics are altered and efficiencey lost.

8. Ventilatory Pump. Cerebral cortex Brainstem WAKE Sleep-wake Respiratory muscles Airflow resistance Chemoreceptors Restrictive lung defect. Mechanoreceptors Ventilation Minute ventilation = MV

10. Respiratory Muscle Weakness Begin AJRCCM 1997 156 133-139

11. pump TV Control MV reduced work RR Prolonged hypoventilation + or – events (AHI), Desats, Arousals, WASO, poor sleep architecture. Muscle fatigue Hypoxia (hypersomnia) Hypercapnoea Progressive and insidious Acidosis Ventilatory Failure

12. TV Control MV reduced work RR Prolonged hypoventilation + or – events (AHI), Desats, Arousals, WASO, poor sleep architecture. Neuro-Muscle insult CVA Trauma Neuro’ disease Hypoxia Hypercapnoea Infection Acidosis Ventilatory Failure Acute

13. Obesity epidemic hits Europe (not France).

14. Nocturnal ventilatory insufficiency • Reduced tidal volume and reduced frequency. • Reduced minute volume = hypercapnoea and hypoxia.

15. Indications for NIPPV. • Ventilatory pump failure. • Chronic or acute. • Reduced MV, hypoxia with hypercapnoea. ( potential for normal gas exchange – single system failure).

16. Assessment. • Arterial blood gases (ABGs). • Overnight oximetry and CO2 • Lung Function.( volumes and muscle strength) • Medical exam ( cardio-vascular) • AHI and sleep stages have little diagnostic or prognostic value.

17. Simple overnight oximetry.

18. What do the machines do?

19. Non-invasive ventilation- objectives • Improve alveolar ventilation & oxygenation. • Reduction of work of breathing. • Airway support.

20. Objective:Improve alveolar ventilation & oxygenation. The physiological mechanism is complex & dependent upon the pathology/disease mechanism. • paO2=[(Pb-SWVP)xFiO2]-PaCO2/RQ • Increased Tidal volume and rate = minute Ventilation.

21. Work of breathing Work increases when FRC reduced or when TV = VC

22. Work of breathing When FRC and lung compliance are reduced more work is required to inflate the lung. By applying PEEP, the lung volume at the end of exhalation is increased. The already partially inflated lung requires less pressure and energy than before for full inflation TV

23. FiO2 & improved MV ( TV & RR) Te FiO2 Ti TV rco RR

24. Mechanical Ventilatory Support Invasive – endo-tracheal tube. Non- invasive ventilation (NIV). • Negative Pressure NIV • Positive Pressure NIV *

25. Negative Pressure NIV precedes positive pressure ventilation by 100 years. • - Patient lays inside a rigid cylinder with neck and head outside cylinder. • A vacuum pump creates a negative pressure within the chamber (outside of chest) • - this causes expansion of the patient's chest. This change in chest geometry reduces intrapulmonary pressure and ambient air flows into the lungs. • When the vacuum ends, the negative pressure applied to the chest drops to zero, and the elastic recoil of the chest and lungs results in passive exhalation. • Pump – Adjustable rate and adjustable negative pressure.

26. Iron lung.

28. Limitations of Negative Pressure NIV • Unsupported upper airway- obstruction induced with high transluminal pressure gradients. • Can reduce cardiac OP and peripheral oedema. • CONTROLLED ventilation. • Limited technologies.

30. Positive Pressure NIV 1. Delivery of positive pressure to lungs without intubation. 2. Delivery of air is patient controlled (with machine back up delivery). 3. Air is delivered via a nasal mask or oro-naso mask ( full face mask). NIPPV

31. Nomenclature of Positive pressure systems • CPAP • Bi-level • NIPPV • IPAP • EPAP • PEEP • Ventilating – peak pressure (pressure support) • Triggers - Cycling • Ti. Te, I/E ratio • Mode S, ST, T • Rise Time • Ramps

32. FiO2, tidal volume & rate. • FiO2 – room air 20.8%, facility to add oxygen. O2 % not measured. • TV – Patient controlled breath enhanced by delivery of air to a target pressure level. Missed breaths recognised. • RR- apnoea recognised. Back up rate.delivered. Tachypnea reduced by controlof inspiratory time and expiratory time.

33. Improved alveolar ventilation & oxygenation. The physiological mechanism is dependent upon the pathology/disease mechanism. • paO2=[(Pb-SWVP)xFiO2]-PaCO2/RQ • Increased Tidal volume and rate = minute Ventilation.

34. Basic summary • Trigger level= spontaneous patient effort to trigger a machine “breath”. • IPAP = expands the lungs more. • EPAP = supports small airways and allows for PEEP. • PEEP= increases the volume held in the lungs after passive recoil. Holds open alveoli & improves gas exchange.Reduces work. • T or back up rate- ensures machine breaths if the patient does not trigger. Status/progress measured with CO2 & O2 measurements

35. FiO2 & improved MV ( TV & RR) Te FiO2 Ti TV rco RR

36. Bi-level • Technology has developed from CPAP over several years. • Splints upper airway. • Supplements Spontaneous breathing, synchronisation, improves comfort. • Reduces work of breathing. • Time. Missed breaths delivered. • Range of features and settings added in recent times. Alarms – essentially a ventilator.NIPPV

38. Unrecognised ventilatory insufficiency leads to big problems

39. Problems with Home nocturnal NIV • Cost of ventilator. • Choice of ventilator- locked settings. • Mask problems. • Compliance ( nights and hrs used) • Need to monitor efficacy and share medical care with local doctor. • Rare diseases, physical disability, mental disability, agitation, poor sleep.

40. Clinical Outcomes & observational studies. Physiology – ABGs, TcCO2, SpO2. Lung Function. Psg – AHI little value. WASO and better sleep. Quality of Life – Activities of Living. Health care utility (cost) Survival

41. Post NIV

42. Sleep Study 100.0 Baseline Mean O2 95.0 Discharge Mean O2 90.0 85.0 80.0 75.0 70.0 elective Post exacerbation Mode of Referral Mean overnight oximetry before and after NIV

43. NIV : Wake ABGs in Myotonic Dystrophy Nugent Chest 2002 121 459-464

44. Numerous publications: NIV in Restrictive lung and neuromuscular disease • No prospective randomised controlled trials • Multiple case series and 2 withdrawal trials all showing similar treatment effects

45. Should NIV be used in COPD?

46. 600,000 patients diagnosed with COPD in the UK UK: 30,000 COPD deaths each year · By 2020 COPD is predicted to be the third biggest killer in the world and will be responsible for the deaths of over six million people · COPD is a major cause of medical admissions, particular in winter. 308,355 emergency hospital admissions per year. · Of those that are admitted to hospital for COPD, 1 in 10 will die in hospital, one in three will die within six months, and 43% will die within twelve months of their admission to hospital ·

47. Cochrane Systematic Review Nocturnal NIPPV for at least 3 months in hypercapnic patients with stable COPD had no consistent clinically or statistically significant effect on lung function, gas exchange, respiratory muscle strength, sleep efficiency or exercise tolerance. The small sample sizes of these studies precludes a definite conclusion regarding the effects of NIPPV in COPD. More evidence is required.

48. Summary • Bi Level is needed for some OSA patients. • Bi-Level machines have some features of pressure support ventilators but may not be appropriate for all patients. • Ventilatory Failure is common in some diseases. • Long term NIV is more effective for some patient groups than others. • Potential for dramatic increase of Obesity Hypopnoea Syndrome across Europe.

49. Should Psg technologists be involved in NIV services? • Nocturnal (sleep related) Ventilatory insufficiency. • Diagnostics. (type of abnormality) • Ventilatory Failure is not determined by events (AHI) • Treatment – medical speciality. • Outcomes. (efficacy of NIV)

50. Is our speciality led by technologies ? Bi-level machines CPAP (OSA is one of 87 sleep disorders) Ventilatory Failure ?