Presentation is loading. Please wait.

Presentation is loading. Please wait.

Otto Schoch, PD Dr. Leitender Arzt Pneumologie und Zentrum für Schlafmedizin Kantonsspital St.Gallen Obesity-Hypoventilation and Sleep-Apnea.

Similar presentations


Presentation on theme: "Otto Schoch, PD Dr. Leitender Arzt Pneumologie und Zentrum für Schlafmedizin Kantonsspital St.Gallen Obesity-Hypoventilation and Sleep-Apnea."— Presentation transcript:

1 Otto Schoch, PD Dr. Leitender Arzt Pneumologie und Zentrum für Schlafmedizin Kantonsspital St.Gallen Obesity-Hypoventilation and Sleep-Apnea

2 WHO Grad I = BMI 30-35 kg/m 2 WHO Grad II = BMI 35-40 kg/m 2 WHO Grad III = BMI >40 kg/m 2 Definition Obesity Stunkard: obese > Silhouette 6

3 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

4 Prevalence of BMI >30 kg/m 2 : 25% Switzerland 2010: 14% OSAS patients KSSG (1756): 51% European Sleep Apnea Database (5103): 50.7% (OSAS KSSG >35 kg/m 2 : 25%)

5 Otto Schoch Kantonsspital St.Gallen

6 Otto Schoch Kantonsspital St.Gallen AJRCCM 2012; 185: 241-3

7 Am J Respir Crit Care Med Vol 179. pp 320–327, 2009 Weight and AHI: Study from Finland mild OSAS, AHI 5-15/h 81 of 630 referrals weight reduction: if > -15 kg: 85% cured !

8 Sutherland K et al. Thorax 2011;66:797-803 ©2011 by BMJ Publishing Group Ltd and British Thoracic Society 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.

9 > Korrektur der Apnoen > CO 2 Anfall reduziert Sullivan CE, Berthon-Jones M, Issa F, Eves L. Obstructive Sleep Apnea: CPAP Keeps upper airway open Constant pressure during breath cycle http://www.nejm.org/doi/full/10.1056/NEJMicm1212352?query=TOC

10 CPAP for OSAS: Results KSSG Adherence at 10y related to OSAS severity and symptoms (ESS) BMI does not perdict adherence (n=1756) unpublished

11 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, CO 2

12 Obesity Hypoventilation OHS Hypoventilation = Wach-Pa CO2 > 6 kPa (>45mmHg) OHS = BMI > 30kg/m 2 + Hypoventilation No pulmonary or neuromuscular disease Increase in prevalence with increase in BMI BMI >50 kg/m 2 = > 50% OHS Prodromal stage: Nocturnal Hypoventilation Amanda Piper, Ronald Grunstein: AJCCM 2011,183: 292-8

13 AJCCM 2011,183: 292-8; Respirology 2012, 17: 402–411

14 J Appl Physiol 2010, 108: 199–205, AJCCM 2011, 183: 292-8 OHS Eucapnic Obesity Thorax 2009; 64: 719–25 Expiratory Flow Limitation and intrinsic PEEP. CPAP abolishes PEEPi and reduces neural respiratory drive

15 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 HCO 3- elevation Sleep deprivation: reduced ventilatory response to hypercapnia 2 weeks of CPAP improve VD Acetazolamide increases VD Respirology (2012) 17, 402–411

16 Respir Care 2010;55(11):1442–1448 BMI Terzilen: 30-36, 36-42, 42-60 kg/m 2 HCO 3 Terzilen: 26-31, 31-37, 37-44 mmol/L HCO 3- Mit / ohne Acetazolamid (Diamox) Ventilatory drive in OHS

17 Anesthesiology 2012; 117:188 –205

18

19

20 Prognosis of OHS

21

22

23 Screening for OHS OSAS patients at diagnosis BMI 30-40 kg/m 2 : 10% OHS BMI 40-50 kg/m 2 : 20% OHS BMI >50 kg/m 2 : 50% OHS Pulsoxy <92% aBGA in OHS: PaO 2 <70 mm Hg (10kPa) HCO 3 >27 mEq/L: Sensitivity 92%, specificity 50% continuous transcutaneous CO 2 Monitoring very sensitive > Prodromal stage of OHS (eg in REM)

24 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 paCO 2 decrease than CPAP vs bilevel NIV J Clin Sleep Med 2006;2:57–62

25 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

26 CPAP or bilevel NIV ? 1 Radomized controlled trial Thorax 2008;63:395–401.

27 CPAP or bilevel NIV ? Thorax 2008;63:395–401.

28 Supplemental O 2 for OHS Double-edged sword Risk of CO 2 increase with O 2 MV decreases considerably with 100% O 2 Assess reason for low O 2 –Pulmonary hypertension, CTEPH, COPD –Heart failure Monitor effect on CO 2 and HCO 3 Consider Acetazolamide if HCO 3 high CHEST / 139 / 5 / MAY, 2011: 975 f

29 Long term results: NIV for OHS CHEST 2010; 138(1):84–90

30 OHS with and without supplemental O2 CHEST 2010; 138(1):84–90

31 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

32 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

33 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

34 C- Mixed apnea under NPPV in Spontaneous mode. Two consecutive events associated with drops in SpO2. Total interruption of airflow, with cessation of thoraco- abdominal 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

35 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-SpO 2 <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?)

36

37 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


Download ppt "Otto Schoch, PD Dr. Leitender Arzt Pneumologie und Zentrum für Schlafmedizin Kantonsspital St.Gallen Obesity-Hypoventilation and Sleep-Apnea."

Similar presentations


Ads by Google