Brian Gaden BSRT, RRT, RPSGT
Sleep Consultant
Philips Home Healthcare Solutions

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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

Controller
Effector
Result
Cerebrum
Brain Stem
Spinal Cord
Respiratory Muscles
Airway Vessels and Function
Gas Exchange
Sensors/Feedback Mechanicoreceptors
Chemorecptors

Sleep Disordered Breathing-
Physiology review

Controller
Cerebrum
Brain Stem
Spinal Cord
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
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

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The primary drive to breathe is based upon the
CO2 level in the blood.
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The secondary drive to breathe is based upon the O2 level in the blood.
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If CO2 levels are too high , the body responds by increasing ventilation to get rid of excess CO2
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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

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Normal Changes During Sleep
Decrease in chemoreceptor sensitivity
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Both oxygen and CO2 by 20 – 50%
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Reduction in Alveolar Ventilation due to decrease in Reticular
Activation Center activity
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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 :
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Increase PaCO
2
- 2 – 8 mmHg
Decrease PaO
2
- 3 – 10 mmHg
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Decrease SaO
2 -
McNicholas, Chest 2000; 117:488-538 by 2%

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
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AHI controlled by CPAP therapy
Central Sleep Apnea
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Idiopathic Central Sleep Apnea
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Complex Sleep Apnea
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“CPAP Emergent events”
Periodic Breathing (such as CSR)
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CO2 and Chemoreceptor issue
Usually secondary to CHF
Pulmonary Disorders: CO2 retention
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Overlap Syndrome (OSA and COPD)
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Restrictive Disorders
Neuromuscular Disorders
Obesity Hypoventilation Syndrome
OSA
Idiopathic/PB
Complex

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Problem is with the controller mechanism
(the brain)
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Can be secondary to stroke, brain injury
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Cause not always known
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Treatment is the same

• No output from respiratory center of the brain causing lack of movement of the thorax.
• No movement of thorax & abdomen causes apnea

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Cause of Idiopathic Central Apnea:
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The respiratory center of the brain does not fire during sleep causing periodic apnea (see below)
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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 apnea 1
Impacts very small population of people
Apnea
1 Webster,et al. American Academy of Pain Medicine 2007
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

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

•Complex
Apneas on CPAP
7 cm
H2O
•Cycle time for events is
~30 seconds
Pittman Slides

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Characteristics of Complex Sleep Apnea
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Typically emerges
PSG during titration not during diagnostic
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Emerges with the implementation of CPAP to alleviate OSA events 1
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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
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Estimated prevalence 1/7 or ~15% of the SDB population
1 Morganthaler, et. al. Sleep 2006; 29 (9):1203-1209

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Possible Cause of Complex Sleep Apnea
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)
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Hyperventilation then leads to development of central apneas causing complex breathing events
Chemoreceptor issues unmasked when OSA is eliminated
Complex
~35 sec
1
2
Interview with Dr. Younes & Dr. Sanders
Moganthaler, et.al. Sleep 2006

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

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

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

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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)
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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)
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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
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CPAP Therapy 1
Auto Servo Ventilation 3
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

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

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

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

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Overlap disease
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Obesity
Hypoventilation
Syndrome
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Neuromuscular
Disease
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CO2 retention

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Provide consistent
Tidal Volume (Vt)
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Volume targeted pressure ventilation
(AVAPS)
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Consistent CO2 elimination

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

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

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

Pathology Overlaps coming from the
Sleep Lab
Neuro-
Muscular
Disorders
Obesity
Hypo-
Ventilation
OSA
COPD –
Overlap
Central/
Periodic
SDB
Restrictive
Thoracic
Disorder
Complex
SDB

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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IPAP will automatically increase or decrease to maintain set tidal volume
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Volume targeted Pressure Ventilation
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Progressive Ventilatory Insufficiency
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Neuromuscular Disease
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Amyotrophic Lateral Sclerosis
COPD
Positional Compromised Ventilation
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Obesity Hypoventilation Syndrome

Parameters
EPAP
IPAP min
Range
Start low. Adjust for Apnea
4 above EPAP
IPAP max 10 above IPAP min
Tidal Volume 8ml/kg IBW. Use chart

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Continually assess ventilation through the following areas:
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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)
CO
2 levels*
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Continually assess oxygenation through
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SaO
2
EPAP settings
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Try to maintain baseline CO
2 possible levels throughout the night if
* If applicable

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

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Absolute
Hypoventilation patients
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AVAPS
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Overlap disease
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Neuromuscular disease
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OHS
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Central Sleep Apnea
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Periodic Breathing
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Idiopathic CSA
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Complex CSA
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Servo

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

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