1. Beyond Traditional PAP therapy
Brian Gaden BSRT, RRT, RPSGT
Sleep Consultant
Philips Home Healthcare Solutions

2. Objectives Review of pathology behind the need for ventilation
Central Sleep Apnea
Overlap Disease
Obesity Hypoventilation
Neuromuscular Disorder
Describe the use of Servo ventilation for patients with Complex and Central Apnea
Describe the use of BiPAP S/T with AVAPS for patients with pulmonary disorders
Describe the titration methods for patients requiring NIV

3. Sleep Impact on the Respiratory System
Cerebrum
Brain Stem
Spinal Cord
Controller
Sleep Impact on the Respiratory System
Effector
Respiratory Muscles
Airway Vessels and Function
Gas Exchange
Result
This introductory slide highlights the major factors that may be impacting the respiratory system. The brainstem and the ability to fire an impulse to stimulate breathing. This maybe a problem with patients who have idiopathic central apnea, patients who are on high levels of pain medications or patients with a history of stroke.
The area the brain impacts is the respiratory system including airway diameter as well as muscles that move the system. If the system is diseased (due to airway destruction or restriction, muscle function negatively impacted due to REM sleep paralysis or neurological disorders like ALS) as a result it impacts Gas Exchange.
Once gas exchange is impacted, then a feedback loop to the brain thru the chemorecptors or mechanicoreceptors in the body will impact the feedback to the brain. This may also be the problem with patients who have complex apnea.
You will cover this further.
Mechanicoreceptors
Chemorecptors
Sensors/Feedback

4. Sleep Disordered Breathing- Physiology review

5. Factors that may impact the function of the brain during sleep
Cerebrum
Brain Stem
Spinal Cord
Controller
Factors that may impact the function of the brain during sleep
Change in blood flow
Drug administration
Change in cortical inputs
Disease of the Cerebrum/Brain Stem/Spinal cord
Loss of motor neurons due to disease
Severing of the motor neurons
This graphic outlines the factors that may impact the way the brain functions and fires at night while the patient sleeps: changes in blood flow due to perfusion and postional changes in the patient as they sleep. Drug administration thru pain medications or medications they patient may change, can impact the respiratory drive while the paitent sleeps. Changes or damage to the brain due to disease (ALS, dementia, stoke) or loss of motor neurons going to the peripheral

6. Impact of the respiratory muscles and airway vessels during sleep
Effector
Respiratory Muscles
Airway Vessels
Function
Impact of the respiratory muscles and airway vessels during sleep
Any change can directly impact the respiratory system
Positional changes
Damage or loss of the respiratory muscles will
Damage to the airway support system
Damage to the airway vessels
Damage or loss of blood supply
This area is focuses on the site which is moving by the brain stem stimuli which is movement of gas into the lungs thru the airway and also movement of the muscles to pull air into the lungs. During sleep muscle fucntion will change as well as positioning of the lungs and blood supply can impact the patient.
Patients with ALS have issues with this area due to loss of muscle strength due to interrupted signals from the brain, also COPD and restrictive disorders may also have problems here due changes in the airway support and airway vessels.

7. Problems with Gas Exchange during sleep
Result
Problems with Gas Exchange during sleep
There can be several reasons for gas exchange to not occur:
Poor perfusion of the pulmonary system
Positional changes in perfusion
Destruction of the alveolar sacs due to underlying disease
Lack of ability to move gas into the alveolar sacs
Muscle loss
Conduction problem with nervous system impulse
Eventually changes in the respiratory mechanic’s, respiratory system or brian system will negatively impact gas exchange. The impact on gas exchange is what arouses a patient from sleep as well as stimulates the nervous system to respond to stimuli. The way it does that is thru the feedback system known as the chemoreceptors and mechanico receptors.

8. Systemic monitoring systems that influence ventilation and oxygenation
Mechanicoreceptors
Chemorecptors
Sensors/
Feedback
Systemic monitoring systems that influence ventilation and oxygenation
Central Chemoreceptors
Found inside of the brain to regulate and stimulate the respiratory system in the brain stem
Feedback system is thru acid/ carbon dioxide levels in the brain and body
Peripheral Chemorecptors
Chemical Receptors found on the aortic arch and carotid artery
Send impulses to the brain stem to change the respiratory rate and pattern
Respond to both oxygen and carbon dioxide levels
There are 2 main systems for responses back to the brain to regulate breathing is thru central and peripheral chemoreceptors. There are also stretch receptors in the lungs that need to be activated as well to maintain stable breathing. IF any of the feedback systems are not triggered the patient will increase their rate. On the other hand, if the feedback system is over stimulated, the patient may stop breathing or may start cycling breathing (hypoventilation to hyperventilation).

9. What happens in the lungs?

10. One thing to remember
The primary drive to breathe is based upon the CO2 level in the blood.
The secondary drive to breathe is based upon the O2 level in the blood.
If CO2 levels are too high, the body responds by increasing ventilation to get rid of excess CO2
If CO2 levels are too low, the body responds by decreasing ( or stopping ) ventilation to allow CO2 to build back to normal levels

11. Effect of Sleep on Normal Respiration
20 – 50%
The following areas are normally impacted during the sleep process causing a slight variation of a patients breathing pattern, oxygen levels and carbon dioxide levels. For a normal patient, these drops can easily be compensated for over a night. For the patient with COPD or OSA or both, the effects are more compounded due causing an abnormal response by the body during sleep.
For a normal patient, cortical inputs to the Reticular activation center of the brain decreases, chemorecepotor sensitivity decreases by 20 – 50%, respiratory motor neurons transmit less impulses due to less activity by the respiratory muscles and brain activity, RR generally remains the same but tidal volumes will decrease due to either increased airway resistance may increase due to body position or drop in muscle stimulation, this causes ventilation to decrease by 0.5 – 1.5 LP.
ABG changes due to
Decrease in Min. V
0.5 – 1.5 LPM
McNicholas, Chest 2000; 117:

12. Normal Changes During Sleep
Decrease in chemoreceptor sensitivity
Both oxygen and CO2 by 20 – 50%
Reduction in Alveolar Ventilation due to decrease in Reticular Activation Center activity
Body position & increased airway resistance
Decrease in tidal and minute volume
Sum total of physical change causes the following for a normal patient :
Increase PaCO – 8 mmHg
Decrease PaO – 10 mmHg
Decrease SaO2 - by 2%
For a Normal Person during sleep the changes that occur are due to primarily 4 items:
Decreased activation of the brain center (Reticular Activation Center), increased airway resistance, decrease in metabolic rate (by 10 – 15%) and decreased chemosenstivity for oxygen and carbon dioxide (by 20 – 50%).
As a result of these 4 items, the body has a reduction in alveolar ventilation (by 0.5 – 1.5 LPM) causing a change in the patients areterial blood gases. For a patient with normal lungs and normal sleeping patterns, the effect is a drop in oxygen saturation by ~2%, a drop in oxygenation by 3 – 10 mmHg, and an increase in arterial carbon dioxide levels by 2 -8 mmHg.
McNicholas, Chest 2000; 117:

13. The complicated world of sleep disordered breathing
Vast majority of SDB patients typical OSA profile
80 – 90% OSA
AHI controlled by CPAP therapy
Central Sleep Apnea
Idiopathic Central Sleep Apnea
Complex Sleep Apnea
“CPAP Emergent events”
Periodic Breathing (such as CSR)
CO2 and Chemoreceptor issue
Usually secondary to CHF
Pulmonary Disorders: CO2 retention
Overlap Syndrome (OSA and COPD)
Restrictive Disorders
Neuromuscular Disorders
Obesity Hypoventilation Syndrome
OSA
Idiopathic/PB
Complex
So when talking about patients walking into the sleep laboratory, there are a variety of patients you may need to treat. This includes the majority of them being your standard OSA patient. In addition, patients may have central apnea including Complex Sleep Apnea which is OSA with emergent central apneas with treatment or periodic breathing such as Cheynne-Stokes Respiration.
Lastly, there is a growing number of patients coming into the sleep center who have underlying pulmonary disorders in addition to sleep disorders. This includes patients with Overlap syndrome which includes COPD and OSA, Restrictive Thoracic disorders like kyphosis and neuromuscular disorders like ALS.
Lets talk about each of them

14. Idiopathic Central Sleep Apnea
Problem is with the controller mechanism (the brain)
Can be secondary to stroke, brain injury
Cause not always known
Treatment is the same

15. Idiopathic central sleep apnea – PSG view
No output from respiratory center of the brain causing lack of movement of the thorax.
No movement of thorax & abdomen causes apnea
Idiopathic central sleep apnea is when there is no output from the respiratory center of the brain (the medullary center) which causes lack of movement of the thorax. As a result of no movement of the thorax and abdomen, the patient stops breathing. This is an Alice screen shot of a patient having a central event. Notice there is no movement of air, thorax and abdomen.

16. Idiopathic central sleep apnea
Cause of Idiopathic Central Apnea:
The respiratory center of the brain does not fire during sleep causing periodic apnea (see below)
Seen during the diagnostic night and titration night
Generally seen in non REM sleep clears during REM sleep
Generally seen in younger populations
May appear as part of a neurological disease process or injury
Relationship between chronic opioid therapy and central sleep apnea1
Impacts very small population of people
Cause of idiopathic central sleep apnea:
The respiratory center of the brain does not fire during sleep causing periodic apneas. This pattern is demonstrated on the PowerPoint. Notice how the patients have periods of breathing followed by times of complete cessation of breathing.
Idiopathic central sleep apnea can be seen during the diagnostic night as well as the titration night.
Generally seen in non REM sleep. It also has been shown to clear up during REM sleep..
Generally seen in younger populations
May appear as part of a neurological disease process or injury.
In a recent study, there was a direct relationship found between the central apnea index and daily dosage of methadone and benzodiazepines used for chronic pain management (Webster, et al. 2007)
Twenty-four percent of patients in the study were identified as having central sleep apnea.
Interestingly, Cheyne-Stokes Respiration was not observed in these patients, suggesting the mechanism for CSA due to opioid therapy is different and may be related to the direct effects of opioids on the respiratory controller.
Impacts a very small population of people, estimated to be 1-2% of those in the SDB population
Apnea
Apnea
1 Webster,et al. American Academy of Pain Medicine 2007

17. Treatment recommendations for idiopathic central sleep apnea
Oxygen therapy
Respiratory Stimulant medications
NIV
BiPAP S/T
Must be able to differentiate between Idiopathic CSA and Complex Apnea
Treatment of idiopathic central sleep apnea may include some or all of the following:
Oxygen therapy **
If the patient has significant desaturation during the night, the patient may qualify for oxygen therapy. The patient must have desaturation below 88% for 5 minutes or longer to qualify for oxygen therapy (CMS guidelines) OR 89% for 5 minutes with history of either Congestive Heart Failure (CHF), Pulmonary Hypertension (Pulm HTN), Cor Pulmonale or Increased Red Blood Cell (RBC) count. The use of oxygen therapy will help to prevent significant desaturation during central events.
Oxygen therapy and CPAP therapy
CPAP therapy may also be used for patients who are having a combination of central and obstructive events. The CPAP therapy may help with airway stability; the oxygen therapy will help with preventing desaturation during the night. In order to qualify, the patient must have desaturation + AHI >5 with EDS or AHI>15 without EDS (CMS guidelines).
Medications have been shown to be an effective method to help control and regulate breathing at night for the patient with central sleep apnea. Two common medications used are: Theophylline 1, 3 and Acetazolamide 2, 3. Additionally, Eckert, et al., reports that “gradual dose reduction of opioid medication may improve high-dose narcotic-induced CSA”3.
Remember:
<2% of SDB

18. What is complex apnea?
Complex apnea occurs with the application of PAP therapy
Central apneas occur
Relative CO2 drop from application of PAP therapy
REMEMBER: PAP does NOT fix central events!

19. Complex Apneas on CPAP 7 cm H2O
Cycle time for events is ~30 seconds
This slide demonstrates a second patient event with complex breathing. On a CPAP of 7 cmH20 they transition from OSA to CSA with cycling events that are occurring at 30 second intervals.
Pittman Slides

20. Complex Sleep Apnea - Characteristics
Characteristics of Complex Sleep Apnea
Typically emerges during titration not during diagnostic PSG
Emerges with the implementation of CPAP to alleviate OSA events1
Occur at ~ 30 second intervals vs second interval with CSR
Complex Sleep Apnea is a mixture of OSA which converts over to central apnea upon CPAP application and opening of the airway 1
Minimal data available
Estimated prevalence 1/7 or ~15% of the SDB population
1 Morganthaler, et. al. Sleep 2006; 29 (9):
The definition of Complex Sleep Apnea is Central Apneas that emerge during the application of CPAP therapy. This typically emerges during the titration night and not during the diagnostic night. As a result, complex sleep apnea is a mixture of both OSA and CSA with CPAP therapy.
Some general characteristic of Complex Apnea is that they can occur at 30 second intervals which is different from other types of periodic breathing that may occur at night.
Dr. Morganthalier from the Mayo Clinic identified the prevalence to be 1 in 7 patients or 15% of the sleep disordered breathing population.

21. Possible Cause of Complex Sleep Apnea?
Theory of Complex Apnea is due to a combination of airway resistance and respiratory drive 12
Theory: once airway open with low levels of CPAP, OSA is eliminated with CPAP. The airway now allows for normal RR causing instability of CO2 receptors.
With a “normal” breathing pattern, the patients brain function reads the change in CO2 and causes hypoventilation to occur. (slight change of 2 can cause instability)
Hyperventilation then leads to development of central apneas causing complex breathing events
Chemoreceptor issues unmasked when OSA is eliminated
Due to the limited amount of research done on this type of breathing pattern, there is limited information on the reasons why this may occur in the sleep population. Several leading researchers (Dr. Sanders who is a consultant with Respironics, Dr. Magdy Younes (u-ness) along with Dr. Morgathaler have several possible reasons why this may occur:
Complex
~35 sec
1 Interview with Dr. Younes & Dr. Sanders
2 Moganthaler, et.al. Sleep 2006

22. Treatment Strategies for Complex Sleep Apnea
CPAP + Time on Therapy to reset chemoreceptors for patient
Must qualify with AHI > 5 with EDS OR AHI >15
To move to AutoServo Ventilation must meet RAD criteria
No improvement, try alternatives below
Medications + CPAP
Auto Servo Ventilation
RAD policy for Complex Sleep Apnea
Acetylzolamide is the medication of treatment for stability of RR

23. Key Strategy
When performing a titration where complex apnea presents, patience is the key
Usually a difficult and tedious titration
In most cases, the CPAP emergent apnea will resolve with time to adjust to PAP pressure.
Servo may be required if CSA persists

24. Periodic Breathing (such as CSR)
What is the population mix?
What do they look like on PSG?
What is the treatment strategy for PB?

25. This is a sample of a patient with CSR
This is a sample of a patient with CSR. They have periods of hyperventilation followed by hypoventilation. They continue to cycle with a waxing and wanning pattern thru out the night.

26. Periodic Breathing (such as Cheyne Stokes)
Prevalence normally about 5% of patients
Increase in prevalence with special populations
Heart Failure (~40%-50%)
Neurologic disorders (stroke)
Altitude
Renal Failure, Dialysis patients
Characteristics
Emerges in non REM sleep
May resolve in REM sleep
May be seen prior to study and during diagnostic study

27. Periodic Breathing
Characteristics: waxing and waning breathing pattern
Length is based on disease process causing the breathing pattern
Longer events for patients in heart failure 1 (picture A)
50-70 second events of CSR then followed by normal respiration (waxing and waning of Respiration) in patients with Heart failure 1
Shorter events in those with preserved heart function 1 (picture B)
20 – 40 seconds on length with those with preserved heart function 1
Some of the characteristics of patients with periodic breathing like cheyne stokes breathing include waxing and waning breathing patterns. The event characteristic may change based on the underlying disease process. This includes patients with heart failure and cheyne stokes may have longer cycle events vs. patients with periodic breathing who have issues due to altitude, neurological disorders or renal failure
~60 sec A B
1 Thomas, et. al. Curr. Opin Pulm Med. 2005

28. Treatment Recommendations for PB
If patient has PB due to disease process, medical management of disease will help with management of PB
Medical Management of Heart Failure is KEY in treatment of CSR 1
If the patient has predominately CSR, (CSR >50%), CSA > 5, AHI
CPAP Therapy1
Auto Servo Ventilation3
Bi-Level Therapy with back up rate 2
If the patient has predominately OSA (<50% CSR), CPAP should be prescribed
If a patient has periodic breathing due to a specific disease process, medical management of that disease process is key in helping to stabilize or regulate the patients respiratory pattern. This is especially true for patients with heart failure.
However, if the patient has an AHI > 5 with EDS or AHI >15 without EDS, they can be treated with therapy to help with this sleep disorder. As the titration occurs, if the patient has predominately CSR or Central Apneas, which are greater than 50% of the hourly events and the AHI hits the required number there are options of CPAP therapy, Auto Servo Ventilation or Bilevel therapy with a back up rate to help control not only the OSA events but also regulate the patients respiratory pattern during the central events.
If the patient has predominately OSA, they should have CPAP or BiPAP S therapy prescribed to help with management of their obstructive events.
1 Javaheri, et. al. Curr Treatment Option in CV Med: 2005:7:
2 Kasi, et. al. Circ. J.; :
3 Teschler et al, AJRCCM, 164: , 2001

29. Complicated Patients Patients have complicated and variable breathing
Auto PAP treats OSA
Auto Backup rate treats CSA
Variable IPAP (PS) treats periodic breathing

30. ASV Initial Settings EPAP min - ?? EPAP max -20cwp PS min – 0
PS max- 10
Backup rate- Auto
Max pressure - 25
Be patient
Document
Must control leak
How much leak is too much?

31. Central Sleep Apnea Summary
Idiopathic CSA: BiLevel PAP with Backup rate
Complex Apnea: PAP with patience. Servo if needed
Periodic Breathing: Servo Ventilation. BiPAP Auto SV Advanced

32. Absolute Hypoventilation
Overlap disease
Obesity Hypoventilation Syndrome
Neuromuscular Disease
CO2 retention

33. Strategy: Improve ventilation
Provide consistent Tidal Volume (Vt)
Volume targeted pressure ventilation (AVAPS)
Consistent CO2 elimination

34. Improving Quality of Life

35. COPD Overlap Syndrome A combination of OSAHS and COPD
Patients with overlap disease usually have a more significant oxygen desaturation
More likely to develop pulmonary hypertension
CO2 retention due to hypoventilation
Decrease in O2 levels are very evident on PSG

36. The COPD patient

37. Obesity Hypoventilation Syndrome
Also known as “Pickwickian Syndrome”
Increase in CO2 during sleep (>10mmHg)
BMI usually greater than 30kg/m2.
No other reason for hypoventilation such as neuromuscluar disease, restrictive thoracic disease, obstructive lung disease or interstitial lung disease
Retains CO2

38. Obesity Hypoventilation Patient

39. Neuromuscular disease
Progressive muscle weakness that increases over time
Patient cannot ventilate adequately
Example: ALS
NIV required to help patient ventilate
Retains CO2

40. Neuromuscular Disease

41. Pathology Overlaps coming from the Sleep Lab
Obesity Hypo-Ventilation
Neuro-
Muscular
Disorders
OSA
COPD –
Overlap
Central/ Periodic SDB
The majority of patients entering the sleep lab for treatment and titration will have straight OSA. With the data from Dr. Morganthaler, 10 – 20% of patients entering with a possible diagnosis of OSA will end up with complex sleep disorders. That includes periodic breathing, and CPAP induced central apneas.
With the release of Neuromusuclar guidelines, patients with several forms of neuromuscular diseases will have issues with their sleep patterns as their disease progresses. As a result, they may enter the sleep lab for treatment of these sleep disorders. In addition, patients with COPD may also be sent to a sleep lab for treatment of a sleep condition.
Restrictive Thoracic Disorder
Complex SDB

42. How do we help patients to breathe when they cannot?

43. Average Volume Assured Pressure Support (AVAPS)
Acts primarily as a bilevel pressure support ventilator that is able to provide a constant tidal volume
Automatically adjusts the pressure support level to maintain a consistent tidal volume
IPAP will automatically increase or decrease to maintain set tidal volume
Volume targeted Pressure Ventilation
Progressive Ventilatory Insufficiency
Neuromuscular Disease
Amyotrophic Lateral Sclerosis
COPD
Positional Compromised Ventilation
Obesity Hypoventilation Syndrome
AVAPS is found in our BiPAP S/T platform and is a device with the ability the enable to feature that will alllow the machine to maintain a constant tidal volume if desired.
The BIPAP with AVAPS acts primarily as a bi-level pressure support ventilator fluctuating between IPAP and EPAP levels. However the machine is able to adjust itself if a constant tidal volume is requested. The machine will raise it self between an IPAP min and IPAP max setting to maintain a requested tidal volume
This device allows for constant ventilation for patients who may need ventilatory support with advancement of their pulmonary or neuromuscular disorder. This includes patients with COPD, restrictive disorders and obesity hypoventilation.

44. How AVAPS works
This provides a graphical representation on how AVAPS works. By setting an IPAP min and IPAP max and tidal volume the machine will fluctuate over time to maintain the desired tidal volume set by the practitioner.

45. The AVAPS Initial Settings
Parameters
Range
EPAP
Start low. Adjust for Apnea
IPAP min
4 above EPAP
IPAP max
10 above IPAP min
Tidal Volume
8ml/kg IBW. Use chart
AVAPS is not a mode, but a support function that is activated within the existing S, S/T, PA and timed modes of ventilation.
The Low Vte alarm indicates that the target Vte cannot be reached at the maximum IPAP. If the target tidal volume cannot be reached at the maximum pressure for a period of 1 minute, the low tidal volume alarm becomes active. Once active the alarm is reset when the target is reached for 30 seconds. It is a high priority alarm.

46. Titration Method for Patient on BiPAP AVAPS
Continually assess ventilation through the following areas:
Respiratory Rate
Tidal volume (ratio between EPAP and IPAPmax but must have a large enough delta between IPAPmin and IPAPmax to maintain)
CO2 levels*
Continually assess oxygenation through
SaO2
EPAP settings
Try to maintain baseline CO2 levels throughout the night if possible
When performing a BiPAP AVAPS titration, there are specific parameters you would want to monitor and adjust based on what parameter you would like to adjust. If the patient is having increases or decreases in their PaCO2, adjustment and monitoring of their respiratory rate and tidal volume (which can be impacted by the difference between EPAP, IPAPmin and IPAPmax) will help to assess ventilation along with patency of the upper airway. Make sure to maintain a large enough delta between the IPAPmin, EPAP and IPAPmax settings to allow the machine to fluctuate and provide a consistent tidal volume over time.
To assess oxygenation, monitor the upper airway patency along with lung volumes. Both of these can be addressed by monitoring the SaO2 or SpO2 settings along with EPAP levels or oxygen administration through the system.
* If applicable

47. Be Patient! Break old habits!

48. AVAPS Strategy Be patient! Titrate EPAP to overcome obstructive apnea
Set Tidal Volume properly
Monitor patient and document
Control leak

49. Two Different patient groups
Absolute Hypoventilation patients
AVAPS
Overlap disease
Neuromuscular disease
OHS
Central Sleep Apnea
Periodic Breathing
Idiopathic CSA
Complex CSA
Servo

50. Take Away Points AVAPS- you must titrate EPAP Monitor ventilation
IPAP min 4 above EPAP
Must control leak!
Servo- EPAP is auto titration
Be patient!
PS min is 0
Must control leak!

51. You might be feeling like this..

52. Resources Brian, Jerry, Tom, Jeff Andrew and Ben Matt, Brian, Dax
Mark, Tom, Darryl
The TEXAS team!

53. Thank you