Beyond Traditional PAP therapy

Brian Gaden BSRT, RRT, RPSGT

Sleep Consultant Philips Home Healthcare

Solutions

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

Sleep Impact on

the Respiratory

System

Cerebrum

Brain Stem

Spinal Cord

Controller

MechanicoreceptorsChemorecptors

Sensors/Feedback

Effector

Respiratory Muscles

Airway Vessels and Function

Gas ExchangeResult

Sleep Disordered Breathing- Physiology review

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

CerebrumBrain StemSpinal Cord

Controller

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

EffectorRespiratory

MusclesAirway Vessels

Function

Problems with Gas Exchange during sleep Gas ExchangeResult

• 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

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

MechanicoreceptorsChemorecptors

Sensors/Feedback

What happens in the lungs?

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

Effect of Sleep on Normal Respiration

McNicholas, Chest 2000; 117:488-538

20 – 50%

ABG changes due to Decrease in Min. V

0.5 – 1.5 LPM

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 PaCO2 - 2 – 8 mmHg Decrease PaO2 - 3 – 10 mmHg Decrease SaO2 - by 2%McNicholas, Chest 2000; 117:488-538

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

OSAIdiopathic/PBComplex

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

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 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

Apnea Apnea 1 Webster,et al. American Academy of Pain Medicine 2007

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

Remember:<2% of SDB

What is complex apnea?Complex apnea occurs with

the application of PAP therapy

Central apneas occurRelative CO2 drop from

application of PAP therapyREMEMBER: 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

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?

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

1 Interview with Dr. Younes & Dr. Sanders2 Moganthaler, et.al. Sleep 2006

Complex

~35 sec

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

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

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)

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

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

~60 sec1 Thomas, et. al. Curr. Opin Pulm Med. 2005

A B

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

1 Javaheri, et. al. Curr Treatment Option in CV Med: 2005:7:295-3062 Kasi, et. al. Circ. J.; 200569:913-9213 Teschler et al, AJRCCM, 164:614-419, 2001

Complicated Patients Patients have

complicated and variable breathing

Auto PAP treats OSA

Auto Backup rate treats CSA

Variable IPAP (PS) treats periodic breathing

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?

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

Absolute Hypoventilation Overlap disease Obesity

Hypoventilation Syndrome

Neuromuscular Disease

CO2 retention

Strategy: Improve ventilation

Provide consistent Tidal Volume (Vt)

Volume targeted pressure ventilation (AVAPS)

Consistent CO2 elimination

Improving Quality of Life

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

The COPD patient

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

Obesity Hypoventilation Patient

Neuromuscular disease 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

OSA Central/ Periodic

SDB

Neuro-Muscular Disorders

COPD – Overlap

Obesity Hypo-

Ventilation

Restrictive Thoracic Disorder

Complex SDB

How do we help patients to breathe when they cannot?

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

How AVAPS works

The AVAPS Initial Settings

Parameters Range

EPAP Start low. Adjust for Apnea

IPAP min 4 above EPAPIPAP max 10 above IPAP

minTidal Volume 8ml/kg IBW. Use

chart

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

* If applicable

Be Patient! Break old habits!

AVAPS Strategy Be patient! Titrate EPAP to

overcome obstructive apnea

Set Tidal Volume properly

Monitor patient and document

Control leak

Two Different patient groups

Absolute Hypoventilation patients

AVAPS Overlap disease Neuromuscular

disease OHS

Central Sleep Apnea

Periodic Breathing

Idiopathic CSA Complex CSA Servo

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!

You might be feeling like this..

Resources Brian, Jerry,

Tom, Jeff Andrew and Ben

Matt, Brian, Dax Mark, Tom,

Darryl The TEXAS

team!

Thank you