Obesity hypoventilation syndrome (OHS) is defined as the combined presence of obesity (BMI > 30kg/m2) with awake arterial hypercapnia (pCO2 > 6.0 kPa / 45 mmHg) in the absence of other causes of hypoventilation. The exact prevalence of OHS in the general population remains unknown, and most prevalence data describe subjects with obstructive sleep apnoea, wherein its prevalence has been estimated to range from 10% to 38% in different groups. On the other hand, patients with OHS often suffer from sleep-related breathing disorders. Prevalence of obstructive sleep apnoea may reach up to 90-95% in OHS patients.
Are the case reports useful for you? Would you also require case reports from other clinical disciplines? Do you have any comments or suggestions for improvement? Please provide your feedback by filling out a short questionnaire.
Sleep anamnesis: 48-year old patient underwent overnight polysomnography and arterial blood gases analysis and was diagnosed with obesity hypoventilation syndrome. At the time, he refused therapy by noninvasive ventilation. Two years later he sought respiratory specialist and was admitted to deparment of respiratory diseases. He reported fragmented sleep with 4-5 awakenings per night, snoring, daytime sleepiness, exertional breathlessness.
Personal history: chronic obstructive pulmonary disease, obesity hypoventilation syndrome, obstructive sleep apnoea, cor pulmonale chronicum, pulmonary hypertension, compensatory polyglobulia, cardiomegaly, arterial hypertension, upper back pain, heterozygote for the MTHFR gene
Medication: furosemide, tiotropium, budesonide, formoterol, theophylline, roflumilast, acetazolamide
Habits: exsmoker for 15 years, previously smoked 10 cigarettes per day for 10 years
Anthropometry: Height: 172 cm Weight: 135 kg BMI: 45.63 kg/m2
Physical examination: hypersthenic, extremely obese, eupnoea, cyanotic, trophic changes of skin on the lower limbs
Epworth sleepiness scale: 7 points
Spirometry and bodyplethysmography: mild restrictive ventilatory impairment (Figure 1) – inconsistent with chronic obstructive pulmonary disease
- Saturation by pulse oximetry: 75%
- Arterial blood gases: pH 7.344, pCO2 7.20 kPa, pO2 6.48 kPa, HCO3 28.70 mmol/L, SaO2 81.50% - chronic hypoxemic-hypercapnic respiratory failure with severe hypoxemia and moderate hypercapnia, retention of bicarbonates with borderline acidosis
Chest X-ray: no infiltration, accentuated hilar shadows with signs of pulmonary hypertension, wide heart shadow (Figure 2)
Polysomnography: severe obstructive sleep apnoea with apnoeic-hypopnoeic index of 103.4 episodes/h, with severe desaturations (desaturation index 115.4 episodes/h), with mean saturation 45% in REM sleep and 60% in NREM sleep, time under 90% saturation 414.9 min, with reduction of slow wave sleep and REM sleep, with severe snoring 49.5% of sleep (Figure 3 and 4)
Noninvasive ventilation with bilevel positive airway pressure (BiPAP) in spontaneous-timed mode with oronasal mask (Figure 5). Ventilator delivers set expiratory pressure during expiration and when patient´s inspiratory effort is recognised it delivers higher inspiratory pressure. The difference between inspiratory and expiratory pressure sets the pressure support that makes patient´s ventilation deeper. Expiratory pressure at the same time maintains the patency of upper airways and prevents occurrence of obstructive apnoeic episodes, thus comorbid obstructive sleep apnoea is treated simultaneously.
Changes of pressure depend on patient spontaneous breathing. However, when patient breathing frequency drops or central apnoea occurs, backup frequency is used to force inspiration. Thus, adequate minute ventilation is assured.
The patient was treated with inspiratory pressure 18 cmH2O expiratory pressure 10 cmH2O, and backup frequency 13 breaths per minute. In these settings, we achieved reduction of apnoeic-hypopnoeic index from 103.4 to 3 episodes/h, average tidal volume of 525 ml and average minute ventilation of 9.8 L/min (Figure 6). In arterial blood gases, we observed a reduction of pCO2 from 7.20 to 5.15Pa, bicarbonates from 28.70 to 24.10 mmol/L, and a rise of pO2 from 6.48 to 11.40 kPa and saturation from 81.50 to 97.40%. pH was quickly normalized.
Chronic hypoxemic-hypercapnic respiratory failure
Obesity hypoventilation syndrome
Severe obstructive sleep apnoea
Obesity hypoventilation syndrome (OHS), sometimes referred to as Pickwickian syndrome, is a combination of obesity and chronic hypercapnic respiratory failure. However, not all obese patients develop respiratory failure. This suggests that the pathophysiology of OHS is more complex than anticipated. Excessive fat accumulation over the chest and abdomen leads to loss of expiratory reserve volume, reduction in total lung capacity and functional residual capacity. Moreover, basal atelectasis predisposes to localized hypoventilated areas, resulting in shunting and ventilation/perfusion mismatching. Secondly, adipose tissue produces leptin, the satiety hormone. In OHS patients we observe leptin resistance and hyperleptinemia. Hyperleptinemia reduces respiratory drive, thus contributing to hypoventilation. Thirdly, often concomitant obstructive sleep apnoea adds to blood gases dysbalance.
Clinically, major symptoms include daytime sleepiness and neurocognitive dysfunction, poor sleep quality, morning headaches, other symptoms are overlapping with obstructive sleep apnoea. In case of pulmonary hypertension and right-sided heart failure, patients might report symptoms like exertional dyspnoea and lower limb oedema.
The first step in successful management starts with making the diagnosis of OHS and referring the patient for sleep study.
The approach for treatment of OHS patients consists of 3 points. The first is inevitable weight loss. The second is resolution of respiratory failure, nowadays mainly, and successfully, with noninvasive ventilation with positive airway pressure (PAP) which relieves the obstructive component, it can effectively alter chest wall and lung mechanics and it could be acting by improving central ventilatory drive. Oxygen supplementation should be added if the patient continues to have hypoxemia despite complete elimination of the obstructive respiratory events and hypoventilation.
Affected subjects require the input from internists and endocrinologists regarding their diabetes mellitus, hypertension, hyperlipidaemia, heart failure and hypothyroidism therapy.
Authors declare the case report will not be published in any national or international publications.
E66.22 Extreme obesity with alveolar hypoventilation BMI: 40 and more, J96.11 Chronic respiratory failure type II - hypercapnic, G47.31 Obstructive sleep apnoea
Textbooks and manuals
Educational websites and atlases
Presentations and animations
Casuistics in images
E-learning courses (LMS)
Please select achieved education degree and then evaluate the teaching material particularly in light of material suitability for self-learning.
Student – student of bachelor or master degree
Graduate – graduate of bachelor or master degree
PhD. Graduate – Ph.D. student, Ph.D. graduate, researcher, ...
this contribution first!
Contribution content is subject to licence Creative Commons Uveďte autora-Neužívejte dílo komerčně-Nezasahujte do díla Attribution 3.0 Czech Republic
citation: Ivana Paraničová: Obesity hypoventilation syndrome. Multimedia support in the education of clinical and health care disciplines :: Portal of Pavol Jozef Šafárik University in Košice Faculty of Medicine [online] , [cit. 06. 06. 2023]. Available from WWW: https://portal.lf.upjs.sk/articles.php?aid=325. ISSN 1337-7000.