Obesity Hypoventilation Syndrome (original) (raw)
Related papers
Obesity Hypoventilation Syndrome as a Spectrum of Respiratory Disturbances During Sleep
Chest, 2001
Objective: To identify the spectrum of respiratory disturbances during sleep in patients with obesity hypoventilation syndrome (OHS) and to examine the response of hypercapnia to treatment of the specific ventilatory sleep disturbances. Designs and methods: Twenty-three patients with chronic awake hypercapnia (mean [؎ SD] PaCO 2 , 55 ؎ 6 mm Hg) and a respiratory sleep disorder were retrospectively identified. Nocturnal polysomnography testing was performed, and flow limitation (FL) was identified from the inspiratory flow-time contour. Obstructive hypoventilation was inferred from sustained FL coupled with O 2 desaturation that was corrected with treatment of the upper airway obstruction. Central hypoventilation was inferred from sustained O 2 desaturation that persisted after the correction of the upper airway obstruction. Treatment was initiated, and follow-up awake PaCO 2 measurements were obtained (follow-up range, 4 days to 7 years).
Obesity hypoventilation syndrome – The big and the breathless
Sleep Medicine Reviews, 2011
s u m m a r y Daytime hypercapnia that develops in morbidly obese individuals in the absence of concurrent lung or neuromuscular disease is referred to as the obesity hypoventilation syndrome (OHS). The characteristic polysomnographic (PSG) abnormality is marked sleep hypoxemia. Although the likelihood of hypoventilation increases with increasing body mass index (BMI), it is too simplistic to think of this disorder arising merely from chest wall restriction due to excess weight. Rather, this is a disorder which emerges when the compensatory mechanisms that normally operate to maintain ventilation appropriate for the level of obesity are impaired. OHS develops from a complex interaction between abnormal respiratory function, sleep disordered breathing and diminished respiratory drive. Irrespective of the mechanisms underlying the development of this disorder, early recognition of the problem and institution of effective therapy is important to reduce the significant clinical and societal repercussions of OHS. While therapy directed at improving sleep disordered breathing is effective in reversing daytime respiratory failure, it is not universally successful and information regarding longer term clinical outcomes is limited. Attention to weight reduction strategies are also necessary to reduce comorbid conditions and improve quality of life, but data regarding how successful and sustained this is in obesity hypoventilation are sparse.
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine, 2018
Hypoventilation in obesity is now divided into five stages; stage 0 (pure obstructive sleep apnea; OSA), stages I/II (obesity-related sleep hypoventilation; ORSH) and stages III/IV (awake hypercapnia, obesity hypoventilation syndrome; OHS). Hypercapnia during the day may be preceded by hypoventilation during sleep. The goal of this study was to determine the prevalence and to identify simple clinical measures that predict stages I/II ORSH. The effect of supine positioning on selected clinical measures was also evaluated. Ninety-four patients with a body mass index > 40 kg/m and a spirometric ratio > 0.7 were randomized to begin testing either in the supine or upright seated position on the day of their diagnostic sleep study. Arterialized capillary blood gases were measured in both positions. Oxygen saturation measured by pulse oximetry was also obtained while awake. Transcutaneous CO monitoring was performed during overnight polysomnography. Stages I/II ORSH had a prevalence ...
Obesity hypoventilation syndrome : Hypoxemia during continuous positive airway pressure. Commentary
Chest, 2007
http://chestjournal.chestpubs.org/content/131/6/1678.full.html services can be found online on the World Wide Web at: The online version of this article, along with updated information and ISSN:0012-3692 ) http://chestjournal.chestpubs.org/site/misc/reprints.xhtml Background: Polysomnography findings between matched groups with obstructive sleep apnea (OSA) and OSA plus obesity-hypoventilation syndrome (OHS) before and after continuous positive airway pressure (CPAP), particularly in the extremely severe obese (body mass index [BMI] > 50 kg/m 2 ), are unclear. Design: Prospective study of subjects (BMI > 50 kg/m 2 ) undergoing diagnostic polysomnography. Subjects with an apnea-hypopnea index (AHI) > 15/h underwent a second polysomnography with CPAP. The effect of 1 night of CPAP on sleep architecture, AHI, arousal indexes, and nocturnal oxygenation was assessed. OHS was defined as those subjects with obesity, PaCO 2 > 45 mm Hg, and PaO 2 < 70 mm Hg in the absence of lung disease.
Patients With Obstructive Sleep Apnea Determinants of Hypercapnia in Obese
2009
2009;136;787-796; Prepublished online June 30, 2009; Chest and Babak Mokhlesi Roop Kaw, Adrian V. Hernandez, Esteban Walker, Loutfi Aboussouan Patients With Obstructive Sleep Apnea Determinants of Hypercapnia in Obese http://www.chestjournal.org/content/136/3/787.full.html and services can be found online on the World Wide Web at: The online version of this article, along with updated information ) ISSN:0012-3692 http://www.chestjournal.org/site/misc/reprints.xhtml ( of the copyright holder. may be reproduced or distributed without the prior written permission Northbrook, IL 60062. All rights reserved. No part of this article or PDF by the American College of Chest Physicians, 3300 Dundee Road, 2009 Physicians. It has been published monthly since 1935. Copyright CHEST is the official journal of the American College of Chest
Obesity and the lung: 2 {middle dot} Obesity and sleep-disordered breathing
Thorax, 2008
As the prevalence of obesity increases in both the developed and the developing world, the respiratory consequences are often underappreciated. This review discusses the presentation, pathogenesis, diagnosis and management of the obstructive sleep apnoea, overlap and obesity hypoventilation syndromes. Patients with these conditions will commonly present to respiratory physicians, and recognition and effective treatment have important benefits in terms of patient quality of life and reduction in healthcare utilisation. Measures to curb the obesity epidemic are urgently required.
Hyperleptinaemia, respiratory drive and hypercapnic response in obese patients
European Respiratory Journal, 2007
Leptin is a powerful stimulant of ventilation in rodents. In humans, resistance to leptin has been consistently associated with obesity. Raised leptin levels have been reported in subjects with sleep apnoea or obesity-hypoventilation syndrome. The aim of the present study was to assess, by multivariate analysis, the possible association between respiratory centre impairment and levels of serum leptin. In total, 364 obese subjects (body mass index o30 kg?m-2) underwent the following tests: sleep studies, respiratory function tests, baseline and hypercapnic response (mouth occlusion pressure (P0.1), minute ventilation), fasting leptin levels, body composition and anthropometric measures. Subjects with airways obstruction on spirometry were excluded. Out of the 346 subjects undergoing testing, 245 were included in the current analysis. Lung volumes, age, log leptin levels, end-tidal carbon dioxide tension, percentage body fat and minimal nocturnal saturation were predictors for baseline P0.1. The hypercapnic response test was performed by 186 subjects; log leptin levels were predictors for hypercapnic response in males, but not in females. Hyperleptinaemia is associated with a reduction in respiratory drive and hypercapnic response, irrespective of the amount of body fat. These data suggest the extension of leptin resistance to the respiratory centre.
Obesity Hypoventilation Syndrome: New Insights in Diagnosis and Management
Indian Journal of Sleep Medicine, 2020
Obesity hypoventilation syndrome (OHS) is a syndrome characterized by a constellation of obesity [body mass index (BMI) ≥ 30 kg/m 2 ], daytime hypercapnia (arterial carbon dioxide tension ≥ 45 mm Hg), and sleep-disordered breathing (SDB), provided other conditions leading to alveolar hypoventilation have been objectively ruled out. Delayed diagnosis can precipitate significant cardiorespiratory morbidity in the form of pulmonary hypertension, heart failure, and coronary disease. Sleep fragmentation, oxidative stress, and obesity-related deconditioning are the predominant mechanisms of the clinical predicament and the poor quality of life. The diagnosis requires a due awareness about its presence and a prone index of suspicion in the suitable clinical context. The diagnosis is conclusively established on basis of a sleep study and arterial blood gases (ABGs). Management requires a holistic approach focusing on weight reduction, lifestyle modification, treatment of comorbidities, and control of the SDB by means of continuous positive airway pressure (CPAP) or noninvasive ventilation (NIV) and pulmonary rehabilitation. Opportune therapy facilitates an optimistic prognosis and improves the quality of life.
Respiratory care, 2015
Arterial blood gas (ABG) analysis is not a routine test in sleep laboratories due to its invasive nature. Therefore, the diagnosis of obesity hypoventilation syndrome (OHS) is underestimated. We aimed to evaluate the differences in subjects with OHS and pure obstructive sleep apnea (OSA) and to determine clinical predictors of OHS in obese subjects. Demographics, body mass index (BMI), Epworth Sleepiness Scale score, polysomnographic data, ABG, spirometric measurements, and serum bicarbonate levels were recorded. Of 152 obese subjects with OSA (79 females/73 males, mean age of 50.3 ± 10.6 y, BMI of 40.1 ± 5.6 kg/m(2), 51.9% with severe OSA), 42.1% (n = 64) had OHS. Subjects with OHS had higher BMI (P = .02), neck circumference (P < .001), waist circumference (P < .001), waist/hip ratio (P = .02), Epworth Sleepiness Scale scores (P = .036), ABG and serum bicarbonate levels (P < .001), apnea-hypopnea index (P = .01), oxygen desaturation index (P < .001), and total sleep ti...