Transcript TSSP-NIV-presentation

Beyond Traditional PAP
therapy
Brian Gaden BSRT, RRT, RPSGT
Sleep Consultant
Philips Home Healthcare Solutions
Objectives
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Review of pathology behind the need for ventilation
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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
Cerebrum
Sleep
Impact on
the
Respiratory
System
Controller
Brain Stem
Spinal Cord
Respiratory Muscles
Effector
Result
Sensors/Feedback
Airway Vessels and Function
Gas Exchange
Mechanicoreceptors
Chemorecptors
Sleep Disordered BreathingPhysiology review
Controller
Cerebrum
Brain Stem
Spinal Cord
Factors that may impact the function of the brain during sleep
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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
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
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
Gas Exchange
Sensors/
Feedback
Mechanicoreceptors
Chemorecptors
Systemic monitoring systems that influence ventilation and
• Central
Chemoreceptors
oxygenation
– 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
What happens in the lungs?
One thing to remember
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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
Effect of Sleep on Normal Respiration
20 – 50%
McNicholas, Chest 2000;
117:488-538
ABG changes due to
Decrease in Min. V
0.5 – 1.5 LPM
Normal Changes During Sleep
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Decrease in chemoreceptor sensitivity
 Both oxygen and CO2 by 20 – 50%
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Reduction in Alveolar Ventilation due to decrease in Reticular
Activation Center activity
 Body position & increased airway resistance
 Decrease in tidal and minute volume
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Sum total of physical change causes the following for a normal
patient :
 Increase PaCO2 - 2 – 8 mmHg
 Decrease PaO2 - 3 – 10 mmHg
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Decrease SaO2 - by 2%
McNicholas, Chest 2000; 117:488-538
The complicated world of sleep disordered breathing
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Vast majority of SDB patients typical
OSA profile
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80 – 90% OSA
AHI controlled by CPAP therapy
Central Sleep Apnea
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Idiopathic Central Sleep Apnea
Complex Sleep Apnea
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Periodic Breathing (such as CSR)
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“CPAP Emergent events”
CO2 and Chemoreceptor issue
Usually secondary to CHF
Pulmonary Disorders: CO2 retention
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Overlap Syndrome (OSA and COPD)
Restrictive Disorders
Neuromuscular Disorders
Obesity Hypoventilation Syndrome
OSA
Idiopathic/PB
Complex
Idiopathic Central Sleep Apnea
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Problem is with the
controller mechanism
(the brain)
Can be secondary to
stroke, brain injury
Cause not always
known
Treatment is the same
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
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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
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Apnea
1 Webster,et al. American Academy of Pain Medicine 2007
Apnea
Treatment recommendations for
idiopathic central sleep apnea
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Oxygen therapy
Respiratory Stimulant medications
NIV
BiPAP S/T
Must be able to differentiate between
Idiopathic CSA and Complex Apnea
Remember:
<2% of SDB
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!
•Complex
Apneas
on CPAP
7 cm
H2O
•Cycle
time for
events is
~30
seconds
Pittman Slides
Complex Sleep Apnea Characteristics
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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. 60-90 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):1203-1209
Possible Cause of Complex Sleep Apnea?
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Theory of Complex Apnea is due to a combination of airway resistance and respiratory drive 12
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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
Complex
~35
sec
1
Interview with Dr. Younes & Dr. Sanders
2 Moganthaler, et.al. Sleep 2006
Treatment Strategies for Complex Sleep
Apnea
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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
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No improvement, try alternatives below
Medications + CPAP
 Auto Servo Ventilation
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RAD policy for Complex Sleep Apnea
Key Strategy
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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
Periodic Breathing (such as
CSR)
What is the population mix?
What do they look like on PSG?
What is the treatment strategy for PB?
Periodic Breathing
(such as Cheyne Stokes)
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Prevalence normally about 5% of patients
Increase in prevalence with special populations
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Heart Failure (~40%-50%)
Neurologic disorders (stroke)
Altitude
Renal Failure, Dialysis patients
Characteristics
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Emerges in non REM sleep
May resolve in REM sleep
May be seen prior to study and during diagnostic study
Periodic Breathing
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Characteristics: waxing and waning breathing pattern
Length is based on disease process causing the breathing pattern
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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
A
1 Thomas, et. al. Curr. Opin Pulm Med. 2005
B
~60
sec
Treatment Recommendations for PB
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If patient has PB due to disease process, medical
management of disease will help with management of
PB
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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
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If the patient has predominately OSA (<50% CSR),
CPAP should be prescribed
1 Javaheri, et. al. Curr Treatment Option in CV Med: 2005:7:295-306
2 Kasi, et. al. Circ. J.; 200569:913-921
3 Teschler et al, AJRCCM, 164:614-419, 2001
Complicated Patients
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Patients have
complicated and
variable breathing
Auto PAP treats OSA
Auto Backup rate
treats CSA
Variable IPAP (PS)
treats periodic
breathing
ASV Initial Settings
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EPAP min - ??
EPAP max -20cwp
PS min – 0
PS max- 10
Backup rate- Auto
Max pressure - 25
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Be patient
Document
Must control leak
How much leak is too
much?
Central Sleep Apnea Summary
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Idiopathic CSA: BiLevel PAP with Backup rate
Complex Apnea: PAP with patience. Servo if
needed
Periodic Breathing: Servo Ventilation. BiPAP
Auto SV Advanced
Absolute Hypoventilation
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Overlap disease
Obesity
Hypoventilation
Syndrome
Neuromuscular
Disease
CO2 retention
Strategy: Improve ventilation
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Provide consistent
Tidal Volume (Vt)
Volume targeted
pressure ventilation
(AVAPS)
Consistent CO2
elimination
Improving Quality of Life
COPD Overlap Syndrome
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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
The COPD patient
Obesity Hypoventilation
Syndrome
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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
Obesity Hypoventilation Patient
Neuromuscular disease
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Progressive muscle weakness that increases over
time
Patient cannot ventilate adequately
Example: ALS
NIV required to help patient ventilate
Retains CO2
Neuromuscular Disease
Pathology Overlaps coming from the
Sleep Lab
Obesity
HypoVentilation
NeuroMuscular
Disorders
COPD –
Overlap
OSA
Restrictive
Thoracic
Disorder
Central/
Periodic
SDB
Complex
SDB
How do we help patients to
breathe when they cannot?
Average Volume Assured Pressure
Support (AVAPS)
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Acts primarily as a bilevel pressure support ventilator that is able
to provide a constant tidal volume
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Automatically adjusts the pressure support level to maintain a
consistent tidal volume
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Progressive Ventilatory Insufficiency
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IPAP will automatically increase or decrease to maintain set tidal volume
Volume targeted Pressure Ventilation
Neuromuscular Disease
Amyotrophic Lateral Sclerosis
COPD
Positional Compromised Ventilation
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Obesity Hypoventilation Syndrome
How AVAPS works
The AVAPS Initial Settings
Parameters
EPAP
IPAP min
IPAP max
Tidal Volume
Range
Start low. Adjust
for Apnea
4 above EPAP
10 above IPAP
min
8ml/kg IBW. Use
chart
Titration Method for Patient on
BiPAP AVAPS
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Continually assess ventilation through the following areas:
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Continually assess oxygenation through
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Respiratory Rate
Tidal volume (ratio between EPAP and IPAPmax but must have a large enough
delta between IPAPmin and IPAPmax to maintain)
CO2 levels*
SaO2
EPAP settings
Try to maintain baseline CO2 levels throughout the night if
possible
* If applicable
Be Patient! Break old habits!
AVAPS Strategy
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Be patient!
Titrate EPAP to
overcome obstructive
apnea
Set Tidal Volume
properly
Monitor patient and
document
Control leak
Two Different patient groups
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Absolute
Hypoventilation
patients
AVAPS
Overlap disease
Neuromuscular
disease
OHS
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Central Sleep Apnea
Periodic Breathing
Idiopathic CSA
Complex CSA
Servo
Take Away Points
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AVAPS- you must
titrate EPAP
Monitor ventilation
IPAP min 4 above
EPAP
Must control leak!
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Servo- EPAP is auto
titration
Be patient!
PS min is 0
Must control leak!
You might be feeling like this..
Resources
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Brian, Jerry, Tom, Jeff
Andrew and Ben
Matt, Brian, Dax
Mark, Tom, Darryl
The TEXAS team!
Thank you