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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Results KSSG • Adherence at 10y related to OSAS severity and symptoms (ESS) • BMI does not perdict adherence (n=1756) unpublished CPAP for OSAS: Adherence • • • • • • • Psychological factors: Stepwise approach Type of mask, mask fit, face masks Technical: Humidification Expiratory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) • • • • • 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 • • • • • 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 • • • • „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 • • • • • 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