OSA and Obesity Hypoventilation Syndrome

OSA and Obesity
Hypoventilation Syndrome –
a clinician’s guide
Andrea Loewen MD, FRCPC,
DABIM (sleep medicine)
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No conflict of interest to declare
Obstructive Sleep Apnea
Obstructive Sleep Apnea
Syndrome
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Obstructive apneas, hypopneas or
respiratory related arousals
Daytime somnolence
Signs of sleep disturbance
Prevalence OSAS 4% men, 2% women
Obesity levels rising
Stats Can Catalogue 82-003
Consequences of OSA
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Excessive daytime sleepiness,
cognitive dysfunction, impaired work
performance, decreased HRQL, driving
Systemic hypertension
Cardiovascular disease
Abnormalities in glucose metabolism
Obesity Hypoventilation Syndrome
Obesity Hypoventilation
Syndrome
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Definition
– BMI ≥ 30 kg/m2
– PaCO2 > 45 mmHg
– Absence of other causes
(hypothyroid, muscle weakness,
airway disease, medications)
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Pickwickian syndrome
OSA is present in 90% of
people with OHS (OSAHS)
10% have pure obesity
hypoventilation (SHVS)
AASM Sleep 1999;22:667-689
CTS HMV guideline CRJ 18(4): 2011
Clinical scenarios
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Severe OSA and significant nocturnal
desaturation
Hypoxic, hypercapnic respiratory
failure, right heart failure
Post operative respiratory failure
Screening prior to bariatric surgery
Pulmonary hypertension and hypoxia
Polycythemia
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Hypoventilation = ↑ PaCO2 from
decreased total ventilation
Total ventilation (VE) = Tidal volume (Vt) x frequency (RR)
Restrictive lung disease
“can’t breathe”
CNS factors
“won’t breathe”
Total ventilation (VE) = alveolar ventilation + deadspace
ventilation
Physiologic deadspace
(V/Q mismatching)
Prevalence hypercapnia in obese
subjects – medical I/P
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Inpatients
BMI >35
ABG (PaCO2 >43)
Sleep questionnaire
Mortality followup
Nowbar AJM 2004
Prevalence OHS – OSAS
<30
Prevalence of Daytime Hypercapnia
Patients with OSAS
(n=1141, normal spirometry)
BMI
PaCO2 >45mmHg
(% of patients)
7.2
30-40
9.8
>40
23.6
Laaban, JP chest 2005
Economic and Health Impact
Snorers/control
OSA/control
OHS/control
Jennum
Thorax
2011;66
Mortality
Nowbar AJM 2004
Is OHS Under recognized?
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Only 13% of patients discharged had
therapy for hypoventilation started
Nowbar AJM 2004
Pathophysiology OHS
Central
respiratory
control
Pulmonary
mechanics
Sleepdisordered
breathing
Pulmonary Function
Pulmonary Function and
Obesity
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Preserved TLC
↓ FRC ↓ ERV
Wheeze
VQ mismatch hypoxia
Jones RL Chest 2006
Pathophysiology OHS
Central
respiratory
control
Pulmonary
mechanics
Sleepdisordered
breathing
Sleep-disordered
breathing
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90% OHS have OSA
10% have pure hypoventilation (no
flow limitation)
Kessler R Chest 2001
Berger KI Semin Resp Crit Care 2009
Pathophysiology OHS
Central
respiratory
control
Pulmonary
mechanics
Sleepdisordered
breathing
Feedback Control
Chemoreceptors
O2, CO2, H+
Mechanoreceptors
Benditt JO Resp Care Aug 2006 51(8)
Ventilatory response to hypercapnea during sleep
•Ventilation increases in
response to increases in PCO2
•Sleep dampens the ventilatory
response
•Below a certain PCO2 level
(apneic threshold), breathing
effort ceases.
Central chemoreceptors: medulla (sensitized to pH)
Ventilatory Response to hypoxia during sleep
• Ventilation increases in a linear
fashion to drops in oxygen
saturation
• Sleep depresses the response =
dampening of controller gain
Peripheral chemoreceptors: carotid body and aortic arch
• During the wake state, cortical activation
(speaking, eating, walking) tends to
override automatic control
• During sleep, the body is dependent on
autonomic control of breathing
(in a state where the chemoreceptor
responses are already dampened).
During sleep relative hypoventilation: ∆PaCO2 = ↑3-9 mmHG
This process is particularly pronounced during REM sleep
Ventilatory Control
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Eucapnic obesity = increased drive
compared to normal
OHS = lack sufficiently augmented
drive
Ventilatory Control
Pretreatment
Severe OSA (mean AHI 55 +/- 25)
Hypercapnic  BIPAP
Eucapnic  CPAP
Han F Chest 2001
Return to eucapnia with
treatment
Han F Chest 2001
Ventilatory Control Posttreatment
Han F Chest 2001
Diagnosis OSA/OHS
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Clinical suspicion
– History compatible with OSAS
– Hypoxia, right heart failure
– Level III OSA, SaO2<90% for more than
40% of the night
– Elevated HCO3
– Elevated awake PaCO2
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Polysomnography
Kaw R Chest 2009
Case
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BMI 35.4, NC 47 cm (18.5 inches)
Treated hypothyroidism, DM2
Non-smoker, no airways disease
Epworth Sleepiness Score 22/24
Level III
– RDI 94 per hour,
– mean oxygen saturation 80%
– 85% of the night <90% SaO2
Level III study
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Oximetry
Heart rate
Nasal flow
Snoring/position
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ABG (RA) : pH 7.38/ PaCO2 45/ PaO2
67/ HCO3 27
TSH normal
Level I Polysomongraphy
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3 channel EEG
Electrooculogram (2 channel)
Chin EMG
EKG
Airflow sensor
– Thermistor
– Pressure transducer
– Pneumotachometer
Respiratory effort sensors
– Ribcage/ abdominal strain gages
– Ribcage/ abdominal IPG (Respitrace)
Leg EMG
Oxygen saturation
(transcutaneous CO2)
Treatment
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CPAP
BiPAP /Noninvasive ventilation
Oxygen
Weight loss
CPAP/BiPAP interfaces
Continuous Positive
Airway Pressure
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Can deliver a range
of pressure
(autoCPAP) or fixed
(standard) CPAP
Pneumatic splint for
the airway
Delivered via nasal,
full face or total
face interface
Bilevel positive airway
pressure
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Set IPAP and EPAP,
back up rate
Tidal volume
(VT)variable
VT proportional to
– IPAP – EPAP
– Compliance
– Resistance (airway,
tubing)
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Delivered via nasal, full
face or total face
interface
BiPAP improves ventilation
Total ventilation (VE) = Tidal volume (Vt) x frequency (RR)
CPAP or BiPAP for OHS?
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BiPAP effective in most cases
CPAP effective in some cases
Positive Airway Pressure
therapy in OSA/OHS
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Prospective, observational
OHS: BMI >35, mean PaCO2 62 mmHg
Nocturnal nasal noninvasive ventilation
(VCV)
7-18 days significant increase PaO2,
decrease PaCO2
9/13 switched to CPAP after initial NIV
Attributed to change in chemosensitivity
Piper AJ Chest 1994
Piper AJ Chest 1994
CPAP
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CPAP in hypercapnic OSA
Improve PaCO2
Improve ventilatory response to CO2
Ameliorate symptoms
Improve quality of life
BiPAP
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However in a subset…
CPAP titrated to eliminate obstruction
Persistent desaturation despite
maximal CPAP  BiPAP
43% of those with BMI >50 required
BiPAP
Banerjee, D Chest 2007
CanadianThoracic Society Home
Mechanical Ventilation guidelines,
Canadian Respiratory Journal 2011
CPAP or BiPAP – how
much?
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Daily hours PAP
FEV1 %
Baseline PaCO2
Minimum daily
recommended 5-7
hours
Conclusions – OSA/OHS
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Maintain high index of suspicion
Testing: Level III  Level I
polysomnogram, ABG, PFT, TSH,
echocardiogram
Referral to Pulmonary/Sleep MD and
CPAP clinic
Generally BiPAP is indicated +/oxygen  improvement over time
Thank you! Foothills Medical Centre Sleep Centre
Pulmonary function and
obesity
Preserved TLC ↓ FRC ↓ ERV
Jones RL Chest 2006
EEG
CO2
PAW
FLOW
VOLUME
VE=6.1
VE=6.1
Respitrace
EEG
CO2
PAW
FLOW
VOLUME
VE=16.8
VE=6.5
Respitrace
1.0 sec/div
Control of Breathing during wakefulness
Cortical control of breathing
Medullary Respiratory controller
Lung, chest wall,
Airway receptors
Respiratory Muscle Activation
Airflow into the lungs
Gas Exchange
Chemoreceptors
Control of Breathing during sleep
↓ Cortical control of breathing
Medullary Respiratory controller
Lung, chest wall,
Airway receptors
Respiratory Muscle Activation
Airflow into the lungs
Gas Exchange
Chemoreceptors
Sleep-disordered
breathing
Hypercapnic OSA
Eucapnic OSA
Intervention: nasal CPAP
Lin ERJ 1994
Sleep-disordered
breathing
Sleep-disordered
breathing
Leptin
O’Donnell CP Respiration Phys 2000
Leptin
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Leptin deficiency rare in humans
Central resistance to leptin could
explain alterations in ventilatory
control in OHS
Ventilatory response to
CO2 post-treatment
De Lucas Ramos
Respiratory Medicine
2004
Renal compensation
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Renal bicarbonate excretion necessary
as increased bicarb blunts change in
H+ for a given change in CO2 and
blunts ventilatory drive
Renal compensation may be
compromised by diuretic induced
chloride deficiency, increased sodium
avidity (CHF, hypoxia)
Berger KI Semin Respir Crit Care 2009
AVAPS
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Average volume assured pressure
support
Hybrid mode of inspiratory assistance
Guarantees Vt despite varying chest
wall compliance and patient effort
RCT comparing BiPAP PS vs AVAPS no
difference in clinically significant
outcomes
Murphy, PB Thorax 2012
Pulmonary hypertension
Pulmonary hypertension in OSA/OHS
mild – treat the underlying cause
Kessler R Chest 2001