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Obesity-Hypoventilation and
Sleep-Apnea
Otto Schoch, PD Dr.
Leitender Arzt
Pneumologie und Zentrum für Schlafmedizin
Kantonsspital St.Gallen
Definition Obesity
• WHO Grad I = BMI 30-35 kg/m2
• WHO Grad II = BMI 35-40 kg/m2
• WHO Grad III = BMI >40 kg/m2
Stunkard: obese > Silhouette 6
Obesity 2012
• Major ‚public health‘ Problem
• Since1980 > Adipositas has dobbeled:
more CV Diseases, Diabetes, Arthrosis,
Carcinoma
• 5. frequent cause of death world wide
• Risks increase with BMI
• Energy imbalance between calories
consumed and calories expended
WHO facts sheet 5/ 2012
Prevalence of BMI >30 kg/m2: <1% to >25%
Switzerland 2010: 14%
OSAS patients KSSG (1756): 51%
European Sleep Apnea Database (5103): 50.7%
(OSAS KSSG >35 kg/m2: 25%)
Otto Schoch
Kantonsspital St.Gallen
AJRCCM 2012; 185: 241-3
Otto Schoch
Kantonsspital St.Gallen
Weight and AHI: Study from Finland
mild OSAS, AHI 5-15/h
81 of 630 referrals
weight reduction: if > -15 kg: 85% cured !
Am J Respir Crit Care Med Vol 179. pp 320–327, 2009
Surface reconstructions
(CT scans)
before and after weight
loss
(A) head and neck region
(B) the upper airway.
-19 kg Gewicht (18% KG)
+ 5.1 cm3 Volumen Pharynx
AHI: 55.9 /h auf 15.1 /h.
Sutherland K et al.
Thorax 2011;66:797-803
©2011 by BMJ Publishing Group Ltd and British Thoracic Society
Sullivan CE, Berthon-Jones M, Issa F, Eves L.
Obstructive Sleep Apnea: CPAP
Keeps upper airway open
Constant pressure during breath cycle
> Korrektur der Apnoen
> CO2 Anfall reduziert
http://www.nejm.org/doi/full/10.1056/NEJMicm1212352?query=TOC
CPAP for OSAS:
Results KSSG
• Adherence at 10y
related to OSAS
severity and symptoms
(ESS)
• BMI does not perdict
adherence
(n=1756)
unpublished
CPAP for OSAS: Adherence
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Psychological factors: Stepwise approach
Type of mask, mask fit, face masks
Technical: Humidification
Expiratory pressure release
Support interventions, eg Telemedicine
Regular follow-up checks, technical
Effectivity: Pulse oximetry, CO2
Obesity Hypoventilation OHS
Hypoventilation =
Wach-PaCO2 > 6 kPa (>45mmHg)
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OHS = BMI > 30kg/m2 + Hypoventilation
No pulmonary or neuromuscular disease
Increase in prevalence with increase in BMI
BMI >50 kg/m2 = > 50% OHS
Prodromal stage: Nocturnal Hypoventilation
Amanda Piper, Ronald Grunstein: AJCCM 2011,183: 292-8
AJCCM 2011,183: 292-8; Respirology 2012, 17: 402–411
Eucapnic Obesity
OHS
AJCCM 2011,
183: 292-8
J Appl Physiol 2010,
108: 199–205,
Expiratory Flow Limitation and intrinsic PEEP.
CPAP abolishes PEEPi and reduces neural respiratory drive Thorax 2009;
64: 719–25
Ventilatory drive (VD) in OHS
• VD in increased in obesity vs normal weight
• No correlation of VD with BMI
• OHS: hypercapnic & hypoxic VD markedly
reduced (wake)
• Reduction parallels HCO3- elevation
• Sleep deprivation: reduced ventilatory response
to hypercapnia
• 2 weeks of CPAP improve VD
• Acetazolamide increases VD
Respirology (2012) 17, 402–411
Ventilatory drive in OHS
BMI Terzilen:
30-36, 36-42, 42-60 kg/m2
HCO3 Terzilen:
26-31, 31-37, 37-44
mmol/L HCO3-
Mit / ohne Acetazolamid
(Diamox)
Respir Care 2010;55(11):1442–1448
Anesthesiology 2012; 117:188 –205
Anesthesiology 2012; 117:188 –205
Anesthesiology 2012; 117:188 –205
Prognosis of OHS
Screening for OHS
OSAS patients at diagnosis
BMI 30-40 kg/m2: 10% OHS
BMI 40-50 kg/m2: 20% OHS
BMI >50 kg/m2: 50% OHS
Pulsoxy <92%
aBGA in OHS: PaO2 <70 mm Hg (10kPa)
HCO3 >27 mEq/L: Sensitivity 92%, specificity 50%
continuous transcutaneous CO2 Monitoring
very sensitive > Prodromal stage of OHS (eg in REM)
Positive Airway Pressure for OHS
• CPAP: High pressure levels to overcome
‚upper airway resistance‘
• Oxymetry in the first night: 30-50% of OHS
still at SpO2 <90%
• Adherence is a better predictor of paCO2
decrease than CPAP vs bilevel NIV
J Clin Sleep Med 2006;2:57–62
NIV for OHS: Technical issues
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CPAP vs NIV
Supplemental Oxygen
NIV Mode: S / ST / T
How to define optimal frequency ?
How to define optimal EPAP level /
Automatic EPAP?
• Role of Average Volume Assured PS with
IPAP range (Storre, Chest 2006)
> Need for measuring PSG / PG / ptCO2
CPAP or bilevel NIV ?
1 Radomized controlled trial
Thorax 2008;63:395–401.
CPAP or bilevel NIV ?
Thorax 2008;63:395–401.
Supplemental O2 for OHS
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„Double-edged sword“
Risk of CO2 increase with O2
MV decreases considerably with 100% O2
Assess reason for low O2
– Pulmonary hypertension, CTEPH, COPD
– Heart failure
• Monitor effect on CO2 and HCO3
• Consider Acetazolamide if HCO3 high
CHEST / 139 / 5 / MAY, 2011: 975 f
Long term results: NIV for OHS
CHEST 2010; 138(1):84–90
OHS with and without
supplemental O2
CHEST 2010; 138(1):84–90
S-Mode / ST-Mode low back-up / ST-Mode high back-up ?
A: Central Apnea Hypopnea Index (N/hour); B: Mixed Apnea Hypopnea Index
Chest 2012, e-pub
A- Central hypopnea under NPPV in “S/T” mode with high BURR (RR: 20/min).
Note disappearance of thoraco-abdominal movements during the event and
resumption of flow with resumption of respiratory movements; ventilator switches to
BURR and continues to pressurise, inducing small spikes on the flow curve. Drop in
SpO2 ensues.
Chest 2012, e-pub
B- Obstructive hypopnea under NPPV in “S/T” mode with low BURR (RR: 11/min.).
Flow decreases drastically in spite of persistent pressurisations by the ventilator,
which has switched to BURR. Thoracic and abdominal movements show phase
opposition and a gradual increase in inspiratory efforts until airflow resumes. The
event induces a drop in SpO2.
Chest 2012, e-pub
C- Mixed apnea under NPPV in “Spontaneous mode”. Two consecutive events
associated with drops in SpO2. Total interruption of airflow, with cessation of thoracoabdominal movements during the initial part of the event (central component), followed
by resumption of thoraco-abdominal movements with phase opposition (obstructive
component). No pressurisation occurs during the event because ventilator is in “S”
mode.
Chest 2012, e-pub
Treating chronic OHS: how I do it
• Always start with nasal or oronasal CPAP
• Re-assess after 1 month of treatment:
adherence and night-time oximetry
• If night-SpO2 <92%: aBGA, LuFu, 6MWT,
PG/PSG under CPAP with ptCO2, Echo
• Refractory OHS: Switch to NIV, Consider
Acetazolamide
• PAH suspected: Right heart catheter,
antikoagulation, (specific treatment?)
Haemodynamic effects of non-invasive
ventilation in patients with OHS
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30 OHS patients
Echo: 43% systolic pulmonary hypertension
6 months NIV
sPAP from 58±11 to 44±12 mmHg (p<0.05)
6MWT from 350±110 to 426±78m (p<0.01)
Respirology. 2012 Nov;17(8):1269-74