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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
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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
Cerebrum Brain Stem Spinal Cord Controller Respiratory Muscles Effector Airway Vessels and Function Result Gas Exchange Mechanicoreceptors Chemorecptors Sensors/Feedback Sleep Impact on the Respiratory System
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
Respiratory Muscles Effector 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 Gas Exchange 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
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
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 20 – 50% ABG changes due to Decrease in Min. V 0.5 – 1.5 LPM McNicholas, Chest 2000; 117:488-538
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
OSA Idiopathic/PB Complex 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
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 1Webster,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 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 • Characteristics of Complex Sleep Apnea • Typically emerges during titrationnot 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 1Morganthaler, et. al. Sleep 2006; 29 (9):1203-1209
Complex ~35 sec 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 1Interview with Dr. Younes & Dr. Sanders 2 Moganthaler, et.al. Sleep 2006
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
~60 sec 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 A B 1Thomas, et. al. Curr. Opin Pulm Med. 2005
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: 2005:7:295-306 2 Kasi, et. al. Circ. J.; 200569:913-921 3 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
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
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
Neuromuscular disease Progressive muscle weakness that increases over time Patient cannot ventilate adequately Example: ALS NIV required to help patient ventilate Retains CO2
Pathology Overlaps coming from the Sleep Lab Obesity Hypo-Ventilation Neuro- Muscular Disorders OSA COPD – Overlap Central/ Periodic SDB Restrictive Thoracic Disorder Complex SDB
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
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
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!