NON INVASIVE VENTILATION IN OBESE HYPOVENTILATION SYNDROME: CPAP versus BIPAP? Antonio M. Esquinas MD, PhD, FCCP, Internacional Fellow AARC Intensive Care and Non Invasive Ventilatory Unit Hospital Morales Meseguer. Murcia, Spain Director  International School of Non-invasive mechanical Ventilation President International Association of NIV and Ibero American  Association of  Bioethics in NIV antmesquinas@gmail.com

Reasons for decisions Key determinants OHS-Pathophysiology determinants Interactions OHS-CPAP-BIPAP Determinants interactions: key methodology aspects Integration CPAP and BIPAP mode in OHS diseases Summary CPAP-BIPAP results Strategy CPAP-key factors Strategy BIPAP-key factors Recommendations for clinical practice decisions

Key aspect: OHS Health Care Resources CPAP vs BiPAP OHS-

Obesity Hypoventilation Syndrome Consequences

Key aspects Obesity Consequences CPAP vs BiPAP OHS-

Key aspect: OHS AND OSA Prevalence-2 CPAP vs BiPAP OHS-

OHS, OSA COPD, Obesity, Overlap Diseases

Key aspect: OHS, OSA COPD, Obesity, Overlap Diseases Clinical, methodology implications CPAP vs BiPAP OHS- COPD Obese Obesity Hypoventilation OSA

OHS Respiratory Failure Pathways-Influence

Obesity-Mechanism-Lung disease Key aspect: OHS Mechanisms CPAP vs BiPAP OHS-

Differences: normal, obesity and hypoventilation Key aspect: OHS Volume Failure: Pathways CPAP vs BiPAP OHS-

Pathways daytime hypercapnia Chronic Hypercapnia

Key aspect: OHS Lung-effects CPAP vs BiPAP OHS-

Hypoxemia during CPAP therapy

Key aspect: Obesity-OHS Hypoxemia during CPAP therapy CPAP vs BiPAP OHS-

Summary OHS-CPAP-vs BiPAP

Key aspect: Summary Studies OHS Prevalence-1 CPAP vs BiPAP OHS-

Key aspect: OHS Arterial Blood Gases Response-2 CPAP vs BiPAP OHS-

Key aspect: OHS Arterial Sleep Parameters-3 CPAP vs BiPAP OHS- NPPV-Short-term and long term positive airway pressure therapy improve AHI and oxygen saturation during Sleep in OHS

Key aspect: OHS PulmonaryFunction-4 CPAP vs BiPAP OHS- NPPV-Short-term and long term positive airway pressure therapy on Pulmonary Function Key aspect: OHS PulmonaryFunction-4 CPAP vs BiPAP OHS-

Key aspect: OHS %, TST response-5 SpO <90% CPAP vs BiPAP OHS- NPPV-Short-term and long term positive airway pressure therapy improve % TST response with SpO2 in OHS Key aspect: OHS %, TST response-5 SpO <90% CPAP vs BiPAP OHS-

Summary Results -1 CPAP vs BiPAP OHS-1

Summary Results -2 CPAP vs BiPAP OHS-2

Summary Results -3 CPAP vs BiPAP OHS-3

OHS Short and Long Term Effects

Key aspect: OHS Short and Long Term Effects-2 CPAP vs BiPAP OHS-

Key aspect: OHS Survival Months CPAP vs BiPAP OHS- (18 months) Months after diagnosis of OHS

Risk of Mortality OHS CPAP-vs BiPAP

Key aspect: Obesity-OHS Long-term Outcome OHS-5 (6 months) Factors influencing long-term survival in OHS Key aspect: Obesity-OHS Long-term Outcome OHS-5 (6 months) Relative risk of death CPAP vs BiPAP OHS-

Methodology and Practice OHS CPAP and PAP

Initial therapy, Acute, chronic Situations Ph/pCO2 trends

Key aspect: OHS Initial therapy, Acute, chronic Situations Ph/pCO2 trends CPAP vs BiPAP OHS-

Noninvasive Ventilation

Key aspect: Inspiratory Muscle Activite- Methodology-2 Pressure-time products of diaphragm OHS OSA Simple Obese CPAP vs BiPAP OHS- OHS OSA Obese OHS OSA Obese

Backup Respiratory Rate factor

Key aspect: Backup Respiratory Rate factor CPAP vs BiPAP OHS-

Key aspect: CPAP vs BiPAP OHS- Backup Respiratory Rate factor-3 Case A=central apnea-hypopnea Case B=Mixed apnea-hypopnea (No. of events/h) (No. of events/h) BURR: Backup Respiratory Rate

OHS Response Hypercapnic Failure after PAP therapy

Hypercapnic Failure after PAP therapy Inadequate adherence IPAP therapy Inadequate PAP titration Sleep disordered breathing other than OSA (central hypoventilation) Associated respiratory disease (COPD, interstitial lung disease) Metabolic alcalosis ( ie; due to high doses of loop diuretics) Key aspect: Obesity-OHS Hypercapnic Failure after PAP therapy CPAP vs BiPAP OHS-

Compliance and non compliance

Key aspect: OHS Interface CPAP vs BiPAP OHS-

Acute Hypercapnic Respiratory Failure Interface- clinical-technical factors

Key aspect: OHS Compliance And non compliance CPAP vs BiPAP OHS-

Summary and conclusions for practical decisions OHS CPAP versus BIPAP

2-OHS Clinical- Methodology Use of Health care resources 1-Obesity It is a global disease. Increasing prevalence of OHS-OSA overlap 2-OHS 3-Overlap disease associations OSA (*) predominat failure during sleep), OHS, COPD, CHF (*) comorbidities ( cardiovascular) Clinical- Methodology Lung mechanics-Volume –Failure-Pathways-Expiratory reserve Implications-Initial therapy Acute (non PSG study) Chronic ( PSG study) Situations Hypoxemic------------------------------------------------------------------------------------------pH/pCO2 trends

Hypoxemic---------------------------------------Ph/pCO2 trends 1 Situations   Hypoxemic---------------------------------------Ph/pCO2 trends 1 (OSA-OHS= Acute hypercapnic during Sleep) (CO3h trends) 2 OHS= Awake daytime hypercapnic Upper airways compromise-Sleep Hypercapnic mechanisms Leptin-factor PCO2 trends-follow up

Noncompliance Compliance Short-term Long term effects NPPV-Interface-Pressure positive selection Goals theory [Gas exchange, Sleep parameters, Pulmonary function, TST SatO2 response] CPAP-------------------------------------------------------------------------------------BiPAP Hypoxemic Hypoxemic-hypercapnic O2 therapy hypercapnic 2-Respiratory breathing patterns 3-Apnea –hypopnea limitation--- (Back up respiratory rate, ST mode) Noncompliance Compliance Hypercapnic failure after IPAP strategy Low VT? Consider AVAPS Short-term Long term effects Mortality